Manual of clinical periodontics

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ACKNOI/VLEDGMENTS
The Manual of CΙinical Periodontics exists in its present form as the result of the concerted efforts of the following individuals:
Robert D. Kerscheη pub|isher and president of Lexi_Comp, lnc; Lynn D. Coppinger, managing editor; David C. Marcus, director
of information systems; Brad Bolinski, product manager; and Tracey J. Reinecke, cover art design.
NoτlcE
This handbook is intended to serve the user as a handy, quick reference and not as a complete reference source on
periodontics. While great care has been taken to ensure the accuracy of the information presented, the reader is advised that
the authors, editors, reviewers, contributors, and publishers cannot be responsible for the continued currency of the information
or for any errors, omissions, or the application of this information, or for any consequences arising therefrom. Therefore, the
author(s) and/or the publisher shall have no liability to any person or entity with regard to claims, loss, or damage caused, or
alleged to be caused, directly or indirectly, by the use of information contained herein. Because of the dynamic nature of clinical
and drug information, readers are advised that decisions regarding treatment and/or drug therapy must be based on independent
judgment of the clinician, changing information about a treatment or drug (ie, as reflected by the literature and drug
manufacturer's most current product information), and changing dental practices. The editors are not responsible for any
inaccuracy of quotation or for any false or misleading implication that may arise due to the text or formulas as used or due to the
quotation of revisions no longer official. The editors, authors, and contributors have written this book in their private capacities.
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3. TABLE OF CONTENTS
About the Authors
Preface. ..-.......4
Chapter 1:Problem-Based Periodontal Diagnosis and Disease Management. ...........5
Ηealth and Disease ... ....... 5
Disease Categories ... ....... 5
Diagnosis and Classification ... ... ... 5
Evidence-Based Thinking ......... .. . I
Equivalence Testing ...... 8
Superiority Testing ....... 8
Parameters of Care ... ....... I
Chapter 2: Anatomy, Ηistology, and Physiology of the Periodontium. ............ 9
Functions of the Periodontium.. ......9
Surface Characteristics of the Periodontium. ......... 9
Histology of the Periodontium .. . 10
Clinically Healthy Gingiva .... . 10
Supporting Structures Beneath the Gingiva .... ..... 11
Blood Supply ........ 12
lnnervation ..........13
Biologicνη/idth.. .....13
AttachmentΑpparatus . . 13
Gingival Crevicular Fluid... ..........13
Chapter 3: Etiology and Classification of the Periodontal Diseases 15
Concepts of Etiology . . 15
Biofilms. .... . 15
Features of Periodontal Pathogens. ......... 16
Dental Calculus .... .. .......17
Risk Factors - Local and Systemic ...... .. . 18
Classification of Periodontal Diseases. ......22
1999 Classification System. .........23
Distinguishing Characteristics of Gingivitis, Periodontitis, and Other Periodontal Diseases
and Conditions...... ......29
Chapter 4: Clinical Αssessment, Diagnosis, and τreatment Pιanning . . '.. 31
RiskΑssessment.... ........31
Components of the Clinical Periodontal Examination .. . . 31
lnstruments and Materials for Periodontal Assessment ..... 34
Radiographic Examination. ..........34
Periodontal Screening and RecordingτΜ Examination....... . ''.'' 34
Adjunctive DiagnosticTechniques ...........35
Periodontal Treatment Planning . .. . . 36
SamplePeriodontal ΤreatmentPlans. ..'...36
Periodontal Prognosis ....... 39
chapter5: Prevention of Disease and Maintenance of Ηealth ''''.''''' 41
Toothbrushing Methods ..... 41
lnterproximal Cleaning ...... 41
Antimicrobial Agents ........ 42
Dentifrices . . ..43
Therapeutic Endpoints . .. 43
Clinical Parameters of Success .43
Maintenance of Periodontal Health. ......... 44
Components of the Maintenance Visit. ..........45
Chapter 6: Nonsurgical Treatment: Scaling and Root Planing, occlusal Therapy, and Αntibiotic
Therapy .......47
Scaling and Root Planing ......... .. 47
occlusal Τrauma ...'..' '.. ' ' 52
occlusal τherapy. . '''''52
Force Control ...... .... .. 55
Antibiotic τherapy ..... ...... 58
Suggested Systemic Αntibiotic Regimens ........... 59
Local AntibioticΤherapy. ............60

4. Chapter 7: Surgical Treatment: Principles .... 61
Basic Principles...... ....61
Categories of Surgery ...... ..... 61
When ls Surgery Necessary? .. .... . 61
Flap Surgery ... .... . 63
Basic Approaches .... ...... .... . 63
Types of Flaps .. .... . 63
Anatomic Landmarks ... ..... 66
Wound Closure. ..... 68
Wound Healing . .70
Chapter8: Surgical τreatment: Repair, Resection, and Regeneration .... '.'''.73
Gingivectomy. .......7g
Electrosurgery ...... .74
Apically-Positioned Flap . . .,. 75
Classification of Osseous Defects ...........77
Crown Lengthening . ........ 82
Periodontal Regeneration ........... 83
Meοhanisms for Bone Grovvth ....... 83
Materials for Regenerative Therapy . ........ 87
Techniques Used in Regenerative τherapy ..... .... 88
Chapter 9: Surgical Treatment: Periodontal Plastic Surgery ..... 91
Defects Treated by Periodontal Plastic Surgery Procedures ........ 91
Aesthetic Εvaluation. .....91
Gingival Recession .. ........ 92
Alveolar Ridge Defects ...... 93
Εxcessive Gingival Display- DiagnosisandTreatment...... '''.''.94
Procedures Used in Periodontal Plastic Surgery . .. .... 94
Chapter 10: Periodontal Emergencies . . .. 1ο5
Diagnosis of Periodontal Emergencies . .. 105
Signs, Symptoms, and Treatment of Periodontal Emergencies. ... 105
Periodontal Abscess ... 106
Pericoronitis .... 106
Αcute Herpetic Gingivostomatitis ... . .. 106
Necrotizing Ulcerative Gingivitis . ....... 1O7
Differential Diagnosis of an Endodonticand Periodontal Abscess. .......107
Chapter 11: Considerations in lmplant Dentistry . . . 109
Biomechanics of Modern lmplants . . 109
Signs of a Healthy and Αiling lmρlant ...... 109
Protocol for lmplant Maintenance .......... 110
APPENDIX
Medical Considerations in the Periodontal Patient ......... 114
Calcium Channel Blockers and Gingival Ηyperplasia ....'. 115
Dental Drug lnteractions: Update on Drug Combinations Requiring Special Considerations........ 116
Occupationsl Exposure to Bloodborne Pathogens (Universal Precautions) ......... 121
Predominant Cultivable Microorganisms of the Oral Cavity . . . .. . . . 124
Reference Values for Adults .. . . . 125
Dentifrice Products . .. ...... 128
Oral Rinse Products. .......133
Prescription Writing ......134
Safe Writing Practices. .....'136
lnsurance Coding for the Periodontal Patient .. . . .. 137
Selected Readings - General .......141
Selected Readings - Specific .......142

5. ABoUτ τHE AUτHoRs
ABOUT THE AUTHORS
FRANCIS G. SERIO, DMD, MS
Dr. Francis G. Serio is Professor and Chairman of the Department of Periodontics at the University of Mississippi
School of Dentistry. He is a Diplomate of the Αmerican Board of PeriodontoΙogy. He received his B.A. from The
Johns Ηopkins University, D.M.D. from the University of Pennsylvania, and M.S. and Certifiοate in Periodontics from
the University of Maryland. Dr. Serio has been involved in education, research, and international volunteer activities
since 1981 . He has published 30 articles, 3 books, several book chapters, and numerous abstracts. He has lectured
throughout the United States and in six other countries on various aspects of Periodontics.
Dr. Serio is the founder of the Dominican Dental Mission Project, a volunteer program that provides dental care to
the rural poor in the Dominican Republic. ln 1991 , the project received the President's Volunteer Action Award from
President George H.W. Bush, and was named one of the Points of Light in 2001 by President George W. Bush. ln
addition to his academic responsibilities, Dr. Serio maintains a private practice limited to Periodontics and lmplant
Dentistry.
CHARLES E. HAνVLΕY, DDs, PhD
Dr. Hawley was Professor in the Department of Periodontics, Dental School, University of Maryland from 1982-
2001. During that time period, Dr. Haw|ey directed, at one time or another, every eduοational program the
department offered to predoctoral and postdoctoral students. He was Director of the Αdvanced Dental Education
Program in Periodontics from 1996-2001. He is Professor Emeritus in the Department of Periodontiοs at Maryland
and also Visiting Professor, Department of Periodontology, Tufts University. Dr. Hawley is a consultant in periodon-
tics to the Commission on Dental Accreditation of the Αmerican Dental Association. He has published over 70
manuscripts, abstracts, and book chapters.
From 1962-1982, Dr. Hawley νvas a career dental officer in the U.S. Army Dental Corps. Dr. Hawley \Λ,as the first
Director of the U.S. Army Residency Program in Periodontics at Ft. Gordon, GA. He retired from the Army at the
rank of Colonel, and at that time, Dr. Hawley was awarded the Legion of Merit.
Dr. Hawley received a Bachelors degree from The Johns Hopkins University, a DDS from the University of
Pennsylvania, a Certificate in Periodontics and a Masters degree in Histology from the University of lllinois, and a
PhD in Microbiology and lmmunology from the University of Maryland. He is a Diplomate of the American Board of
Periodontology. During his professional life, Dr. Ηawley was elected to the lnternational College of Dentists, the
American College of Dentists, and the Pierre Fauchard Αcademy.

6. PFEFACE
PREFACE
TheManuatofCtinicatPeriodonticsisu/rittenasaquickreferenceforgeneraldentists,dentalhygienists,dental
students, and dental hygiene students. Both basic and clinical science topics.are arranged in a tabular form to
allow for easy access to each chapιer.
Each chapter is presented in a "Question & Answer'' format, providing a stepwise approach to thal particular area.
This book has been written in a straighforward manner, making it a practical resource both in clinical practice and in
an educational setting. Chapters are arranged by basic principles, disease entities, diagnosis, treatment planning,
and then various treatment options.
The authors intend that this book be a quick and easy reference to many of the clinical problems that challenge all
practitioners and students of periodontics.
:'.

7. CHAPτEB 1
-
CHAPTER 1: PROBLEM-BASED PERIODONTAL
DIAGNOSIS AND DISEASE MANAGEMENT
The framework of effective periodontal therapy includes a
working diagnosis and classifiοation of disease, the identifi-
cation of pertinent etiologic factors, and a treatment plan that
addresses eaοh of the etiologic agents in a logical sequence.
Τo ignore pertinent etiologic factors in the treatment plan will
translate to undertreatment and failure in therapy. Treaι
ment of etiologic factors that either do not exist, or that have
been incorrect|y identified, wiΙl produce overtreatment and
unnecessary financial or physical hardships for the patient.
Problem-based periodontal therapy begins wiih an under-
standing ot health and knowing what it means to diagnose
and classify a disease.
What ls Health? \Mhat ls a Normal Periodontium?
What ls Meant by the Term "Disease"?
Health is the absence of disease or abnormality. Periodontal
health then is defined by the absence of marginal periodontal
inflammation, the absence of inflammation in the periodontal
ligament, or evidence of periodontal deformities. Success-
fully treated and maintained gingivitis patients may be both
free of disease and have a normal periodontium.
Periodontitis patients who have received successful perio-
dontal and maintenance therapy (ie, patients who are appar-
ently free of periodontal inflammation with no ongoing injury
in the periodontal ligament) may, by definition, be considered
healthy as well. However, these patients may not have a
normal periodontium.
DiSeaSe is defined aS a ρrocess that is οharacterized by a
series of morbid pathobiologic events that produce cliniοal
signs and symptoms in the affected host. The process
ocοurs in response to known or unknown etioΙogic factors.
What Are the Fundamental Periodontal Disease
Categories? Do These Periodontal Diseases
Conform to the Definition of Disease?
The basiο categories of periodontal diseases are:
. Gingivitis. The gingival diseases are periodontal
diseases in which the process is gingival inflammation,
the primary etiologic factors may be microbiologic,
systemic diseases, or physical injury, and the signs and
symptoms are gingival bleeding, increases in probing
depths, and pain. Loss of periodontal attachment, tooth
mobility and/or fremitus of teeth, and tooth migration,are
not ordinary features of gingivitis. As it is with all inflam-
matory diseases, the pattern and severity of gingival
inflammation in a given patient is affected qualitatively
and quantitatively by local and/or systemic contributing
factors.
. Periodontitis. The types of periodontitis are periodontal
diseases in which the process is periodontal inflamma-
tion, the primary etiologic factor may be microbiologiο,
systemic diseases, or physical injury, and the signs and
symptoms are gingival bleeding, increases in periodontal
probing depths, destruction of periodontal attachment,
pain, and tooth loss. Mobility and/or fremitus and migra-
tion of teeth are consequences of forces on teeth with
reduced/lost periodontal attachment (see occlusal trau-
matism below). The pattern and severity of periodontal
inflammation in a given patient is affected qualitatively
and quantitatively by local and systemic contributing
faοtors.
. Occlusal traumatism. Occlusal traumatism is a perio-
dontal disease in which the process is inflammation
ιΛ/ithin the periodontal Ιigament and the alveolar bone
(the lesion of trauma from occlusion), the primary etio-
logic factor is force acting on teeth, and the signs and
symptoms are pain, tooth mobility and/or fremitus, and
pathologic migration of teeth. The pattern and severity of
the lesion of trauma from occlusion in a given patient is
affected quantitativeΙy and qualitatively by local and
systemic contributing factors.
Each one of these categories conforms to the definition of
disease. ln each disease, there is a process, there is a series
of morbid pathobiologic events that are outcomes of the
process, and there is a reΙated set of clinica| signs and symp-
toms.
What ls Meant by the Expressions "Diagnosis"
and "Ctassification"?
F|GURE 1. Photomicrograph of the ρrocess of inflammation in the marginal
periodontium. τhe morbid outcome of the process is histologically repre-
sented as evidence of resorbed alveolar bone and the level of attachment
on cementum.
Diagnosis is the aιt of identifying the disease process. lt is
the product of a careful evaluation of the patient's history, the
array of symptoms presented by the patient, and the clinical
signs revealed during a clinical examination. For instance,
the diagnosis of periodontitis is ordinarily achieved by
detecting gingival bleeding with a periodontal probe, destruο-
tion of periodontal attachment using radiographs and/or a
probe, mobility and/or fremitus digitally, determining any
pathologic migration and/or loss of teeth. Figure 1 represents
histologically the process of marginal periodontal inflamma-
tion and the morbid outcomes (ie, loss of both alveolar bone
and periodontal attachment) of periodontitis.
-

8. PRoBLEM-BASED PERloDoNτAL D|AGNoSΙs AND D|SEASE MANAGEMENτ
CΙassification is the art of categorizing individual clinical
cases of disease according to treatment requirements. Clas-
sification systems are frequently used by third pafty prov-
iders to help understand treatment needs. For over 20 years,
dentists have been using a classification system developed
by the Αmerican Αcademy of Periodontology (AΑP) to facili-
tate dialogue among dentists and between third party individ-
uals concerning the severity of periodontal diseases, and by
direct extension, treatment needs. This classification system
consisted of:
. Type l. Gingivitis where gingival inflammation \νas
present without radiographic evidence of intΘrproΧimaΙ
bone loss.
FIGURE 2. An artistic represenιation ot gingivitis" There is gingival erythema
and edema. τhe clinical attachment levels are at the cementoenamel
iunction. The alveolar bone height wilh respect to the cementoenamel
iunction is normal. Restoraιion of a healthy periodontium without further
loss of attachment may be predictably achieved with nonsurgical
therapy. (Couftesy of Kala Addess, MS, RDH)
. Type ll. Early periodontitis where gingival inflammation
was superimposed over clinical evidence of mild bone
loss without furοation invasions.
FIGURE 3. An artistic representation of earιy periodon lfis. τherΘ is gingival
erythema and edema. τhere is early loss of clinical attachment and
reduclion of alveolar bone height. Furοation invasions wilι probably not
be clinically or radiographically apparent. Periodontal health and func-
tion may usually be restored by nonsurgical and/or surgicaΙ therapy.
(cour1esy of Kala AddeSS' ΜS' RDH)
. Type lll. Moderate periodontitis where gingival inflam-
mation was superimposed over clinical evidence of
moderate bone loss with early furcation invasions and
possible tooth mobility.
FiGURΕ 4. An artistic representation ot moderate periodontitis. τhere is
gingival erythema and edema. τhere is moderate lοss of clinical atιach-
ment and reduction of alveolar bone height. Furcation invasions are
evident both cιinicaΙly and radiographically. Affected teeth may show
degrees of mobility. Shaded area on the adiacent tooth indicates that
regeneration ot Ιost periodontal tissues may be one outcome of
successful periodontal theraρΥ. (courtesy of Karla AddeSS' Ms' RDH)
. Type lV. Αdvanced periodontitis where gingival inflam-
mation was superimposed over severe bone loss with
extensive furcation invasions and tooth mobility. Cases
of this type could display tooth loss due to periodontitis,
pathologic migration of teeth, posterior bite collapse,
and/or loss of occluding vertiοal dimension.
FΙGUBE 5. An artistic representation oΙ advanced periodontitis. τhere is
gingival erythema and edema. τhere is advanced loss of clinical attach-
ment and alveolar bone height. Furcaliοn invasions are θxtensive. τooth
mobilily and/or pathologic migration may be seen. τeeth with advanced
periodontitis frequently have a poor prognosis, and decisions abοut
therapy often include the placement of implants. (Couιlesy of Κarla
Addess, MS, RDH)
While the terms that defined each type were intentionally
vague, the system did provide the framework for dialogue
among therapists, allied personnel, and third party payers

9. CHAPTER 1
over treatment needs for each case. For instance, a treat-
ment plan for a Τype lll moderate periodontitis case
dispΙaying the osseous defects and furcation invasions
shown in Figure 6 would be expected to include resective
and/or regenerative surgical therapy. Τhe treatment plan for
a Type ll early periodontitis οase, such as that shown in
Figure 7, would probably not include resective or regenera-
tive therapy.
FIGURE 6. A dried human mandible showing periodontaΙ osseous defects and
furcation invasions that are οonsistent with a type lll moderate periodon-
titis case.
FIGURE 7. A dried human mandible showing minor periodontal osseous
deformities that are consistent with a type ll early periodontitis case.
As the knowledge base about the patterns of periodontal
diseases improved, this system of classification became
inadequate. Models of periodontitis had emerged sug-
gesting that not all cases of periodontitis behaved the
same clinically, that small (<1 mm) changes in attachment
level were difficult to detect clinically, and that there was
evidence that all cases of periodontitis did not respond the
same to therapy.
An attempt to overcome many of these shortcomings
occurred during the 1999 lnternational Workshop for a Clas-
sification of Periodontal Diseases and Conditions. Here,
scientists and clinicians agreed upon a reclassification
system to improve the understanding of periodontal diseases
among scientists, clinicians, and allied dental healthcare
agencies. Each new or revised category of disease was
based, in part, upon its etiology and the particular healthcare
requirements to control etiology.
The new System includes eight major οategories of perio-
dontal diseases or conditions, and each of the categories is
subdivided into specific etiology-based diseases or condi-
tions. This new Classification System for Periodontal
Diseases and Conditions was adopted by the AAP in 2000.
Τo facilitate its use in every-day periodontiοs, the new
system would be modified over time.
How Are Scientifically-Based Decisions Made in
Successful Periodontics? What ls Meant by the
Expression "Art of Decision-Making in
Periodontal Therapy"?
Successful periodontal therapy is based upon scientifically-
based decisions involving: the disease process, the identifi-
cation of aΙl etiologic factors, a correct diagnosis, controlling
the etiologic factors, and correcting deformities produced by
disease.
The arl of decision-making in periodontal therapy involves
the synthesis of:
1. Clinical experience of the therapist
2. Τechnical ability of the therapist
3. lntuition
4. Experiences of others (type lll information) as
reported and presented at professional forums
5. Evidence-based thinking
F|GURE 8. οlinical decision_making in periodontics can be multifaceted.
Evidence-based thinking b.ings the outcomes of sοientificalιy sound
cΙinicaΙ trials into the process.
While the traditional components of a deοision process
remain impoftant ingredients (ie, a clinician will not ordinarily
make a treatment decision that will involve a technique that
is beyond the scope of his/her abilities), the fact remains that
the knowledge base in a|l aspects of periodontiοs is rapidly
expanding. lt is incumbent that clinicians keep current with
new science and technology, evaluate reports in the litera-
ture criticalΙy, and utilize new information in their practices
when appropriate.

10. PRoBLEM-BASED PERloDoNτAL DlAGNosls AND DlsEAsE MANAGEMENτ
What ls Meant by the Expressions "Evidence-
Based Thinking", "Equivalence Testing", and
"Superiority Testing"?
Εvidence-based thinking occurs when the therapist logically
and systematically utilizes scientifically-based clinical
evidence in the process of making decisions about diag-
nosis, prognosis, and treatment.
Εquivalence testing in c|inical trials may show that a method
is at least as effective as a commonly employed "gold stan-
dard". Superiority testing may show that a given method will
produce outcomes that will be more beneficial than another
to a patient.
lf there is evidence that a technique or concept of therapy is
predictably equivalent or superior in a given clinical scenario,
then, within the scope of experience and ability, it should be
considered as a treatment option. ln doing so, the number of
options available to the patient are increased, and the poten-
tial for placebo effects, personal biases, or clinical experi-
ences of the therapist that have no controls are kept to a
minimum.
The fallout of evidence-based thinking in clinical periodontics
will inevitably be an increased number of treatment options,
increased patient confidence, practice gro\λ/th, and improved
therapeutic outcomes.
What Are the Parameters of Care?
The AAP took a leadership role in developing diagnostic and
therapeutic guidelines for what might be considered the stan-
dard of care for periodontal patients. The resulting Parame-
ters of Care describe the scope of possible active treatment
plans for the following clinical situations:
ο Plaque-associated gingivitis
o Chronic periodontitis with slight to moderate loss of peri-
odontal support
o Chronic periodontitis with advanced loss of periodontal
support
. Refractory periodontitis
. Mucogingivalconditions
ο Acute periodontal diseases
. Αggressive periodontitis
. Placement and management of the dental implant
. Occlusal traumatism in patients with chronic periodontitis
o Periodontitis associated with systemic conditions
. Systemic conditions affected by periodontal diseases
o Periodontal maintenance
The emphasis of the current parameters is treatment and
what therapeutic entities might be appropriate for given peri-
odontal conditions. Each parameter is inclusive so as to give
the reader (clinician, patient, third party healthcare provider,
etc) an appreciation of the scope of acceptable care in each
category. The parameters do not prescribe the care that
every periodontal patient in a given category should receive.
The final decision over what will constitute a treatment plan
in a given case remains, as it should be, in the hands of the
clinician and the patient.
Definitions of terms and details of each of these parameters
of care may be obtained at the web site of the American
Αcademy of Periodontology, www.perio.org.

11. CHAPτER 2
CHAPTER 2: ANATOMY, HISTOLOGY, AND PHYSIOLOGY OF THE
PERIODONTIUM
Α οlear understanding of the structure and function of the
periodontium is necessary in order to appreciate the disease
process and treatment. The periodontium consists primarily
of noncalcified and οalcified connective tissues covered by a
protective layer of epithelium. lt is the destruction of the
calοified conneοtive tissues due to the host response to the
exogenous and endogenous periodontal pathogens that
gives rise to a ιoss of periodontal Support and eventua| tooth
loss.
What Are the Functions of the Periodontium?
. Attach the tooth to the alveolar bone proper
. Resist and dissipate the forces generated by mastica-
tion, speech, and deglutition
. Αdjust to οhanges in functional demands through contin-
uous remodeling, regeneration, and repair
o Defend against the external pathogenic and environ-
mental influences present in the oral cavity
What Are the Surface Characteristics /
Landmarks of the Periodontium?
FlGURE 1Α. surface characteristics and Landmarks of the Periodontium.
Free gingivat margin: This is the most coronal edge of
the gingiva.
Free gingival groove: A groove seen on the facial
gingiva that approximates the location of the base of the
sulcus. The free gingivaΙ groove is not always present
(estimated in only 30% to 40"λ ot adults), nor is it an
exact landmark for the base of the sulcus.
Keratinized tissue: The surface of the tissue that
comprises the free and attached gingiva. Τhe boundaries
are from the free gingivaΙ margin to the mucogingival
iunction on the facial and lingual surfaces. The
keratinized tissue is continuous with the rest of the
mastiοatory mucosa of the palate. The keratin is found in
the stratum corneum of the epithelium and may be
parakeratin (cell nucΙei remaining) or orthokeratin (thick
layer of keratin without remaining cell nuclei). The
epithelium covering is also referred to as the oral
epithelium.
Free gingiva: The gingiva from the free gingival margin
to the base of the sulοus' This tissue is continuous with
the attached gingiva but is not bound down to any
underlying structure.
Attached gingiva: Gingiva that is firmly bound down to
underlying tooth structure, periosteum, and bone. Τhe
boundaries of the attached gingiva are from the base of
the sulcus to the mucogingival junction. The width of
facial attached gingiva ranges from 1-9 mm and is
greatest on the facial surface of the maxillary lateral
incisor and narrowest on the facial surfaces of the
mandibular canine and first premolar. On the lingual,
attached gingiva was widest near the first and second
molars and narrowest adjacent to the incisors and
canines. The thickness of attached gingiva averages
1.25 mm + O.42 mm.
Mucogingival junction: The demarcation between the
attached gingiva and the alveolar mucosa apical to the
attached gingiva. The mucogingival junction often
appears as a distinct line between the two structures. lf
the mucogingival junction is difficult to see, it may be
identified as the fold area when the alveolar mucosa is
gently pushed in a coronal direction.
Alveolar mucosa: Part of the lining muοosa. The
a|veolar muοosa is located apical to the attached gingiva
on the facial and lingual surfaces. This tissue is loosely
attached to the underlying bone, freely moveable, and
relatively fragile compared to the gingiva. There are
more elastic fibers in the alveolar mucosa. This tissue
extends into the vestibule of the mouth and is continuous
with the labial, buccal, and lingual mucosa. There is no
alveolar muοosa on the hard palate'
Masticatory mucosa: Keratinized tissue including the
gingiva and the tissue covering the hard palate.
Frenum (frenulum): The narrow band of tissue that
attaches the labial and buccal mucosa to the alveolar
mucosa. There is also a lingual frenum that attaches the
anterior part of the tongue to the lingual aspect of the
alveolar process and the floor of the mouth in the anterior
region.
FIGURE
'1
B. Surface Characteristics and Landmarks of the Periodontium.
-

12. ANAToMY, ΗtsτoLoGY, AND PHYsloLoGY oF τHE PERloDoNτlUM
. Rugae: The irregular ridges found on the anterior part of
the hard palate adjacent to the incisors, canines, and first
premolars.
. Stippling: The irregular surface texture of the attached
gingiva, similar to the surface of an orange peel, found in
40% ot adults. Stippling occurs at the intersection of
epitheΙial ridges that causes the depression and the
interspersing of connective tissue papillae between
these intersections giving rise to the small bumps.
. Sulcus: This is the space bounded by the free gingival
margin, the tooth, and the most coronaΙ attachment of
the junοtional epithelium. ln health, the sulcus usually
measures from 1-3 mm deep. ln disease, this space is
referred to as a pocket.
. Col: This is the saddle-like depression in the interdental
gingiva as seen from buccal to lingual apical to the
contact of two adlacent posterior teeth.
What Are the Layers of Cetls That Comprise the
Oral Epithelium? What Are a Keratinocyte,
Langerhans Cell, and a Melanocyte?
The oral epithelium consists of four layers of cells:
1. Stratum basale: Basal layer of cuboidal cells along the
basement membrane. This is where epithelial οell rep|i-
cation occurs. Melanocytes are found in this layer.
2. Stratum spinosum: These cells appear to have cyto-
plasmic spines when viewed by Ιight microscopy.
Langerhans cells, involved in the processing of antigens,
are found in this layer. Keratin synthesis begins in the
stratum spinosum.
3. Stratum granulosum: Keratohyalin granules may be
seen in this layer. Keratin synthesis is ongoing. Cells
appear to be fΙattened.
4. Stratum corneum: This is the layer where para- or
orthokeratinization are found.
Keratinocyte: A cell of the epidermis and parts of the
mouth that produce keratin. Because of their ability to
produce keratins, epithelial cells are referred to as kerati-
nocytes. Keratins are a family of approximately 30
proteins that form the intermediate filaments of the
epithelial cell cytoskeleton. Keratins may be found eΧtra-
celluΙarly in the stratum corneum and contribute to the
protective function of epithelium.
Langerhans cell: A dendritic cell in the epidermis.These
cells are found in the suprabasal layers of the epithelium,
Τhey do not have desmosomal attachments to adja-
cent cells. Τhey move in and out of the epithelium, are
derived from bone marro\,v, and probablyhave an immu-
nologic function for recognizing and processing antigens.
. Melanocyte: Α celΙ of the basal layer that produces
melanin pigment granules (melanosomes) that are trans-
ferred to surrounding keratinoοytes for transpoι1' There
are similar numbers of melanocytes in the epithelium re-
gardless of the skin or gingival pigmentation present.
What Does Clinically-Healthy Gingiva Look Like?
FlGURE 2. characteristics of the Heaιthy Pefiodontium. τhe hea,thy periodon-
tium is genefally coral pink, possibly with natural pigmentation. τhe
gingival margins are scalloped to a fine edge. τhe tissue is firm, usually
with a stippled surface.
Color: The normal οolor of gingiva is often described as
coral pink. Gingiva may also have slight to significant
brown pigmentation from the melanoοytes located in the
basal layer of the epithelium.
Size: Gingival contours generally follow the cemento-
enamel junctions of the teeth. Tissue thickness is in the
0.25-0.5 mm range. Α wider zone of gingiva is normally
seen in the maxillary anterior region, with the narrowest
zone of gingiva on the buccal surface of the mandibular
first premolars. On the lingual, it is narrowest in the
mandibular region and widest in the molar area.
Contour: Gingiva has been described as being either
thin and scalloped, or thick and flatter in contour. The
contour of the gingiva depends on the οontour of the
cementoenamel junction of the teeth, the amount of em-
brasure space, and the nature of the contact between
teeth. The gingiva appears prominent over the tooth root
and may have a slightly concave appearance in the inter-
proximal area.
Consistency: Gingiva is generally firm to the touch and
attached to the underlying bone and/or tooth.
Surface texture: Gingiva may have either a smooth or
stippled surface. Stippling is not an indicator of health nor
is the absence of stippling an indiοator of disease. The
reappearance of stippling during therapy may be an indi-
cation of tissue returning to health.

13. CHAPτER 2
What Supporting Structures Lie Beneath the
Gingiva?
F|GURE 3A. τhe supporting structures Beneath the Tissue surface. side
view, A. oral epithelium, B. suιcular epithelium, c. Junctional epithelium,
D. Dentogingivaι fibers, E. circular fibers, F. Dentoalveolar fibers' G.
Acellular cementum, H. Alveolar crestal fibers of the PDL, ι. cellular
cementum, J. Horizontal fibers of the PDL, κ. Alveolar bone, L. oblique
fibers of the PDL.
FIGURE 38. lnterproximal view. A. Dentogingival fibers, B. Circular fibers, C"
τransseptal fibers, D. Alveolar crestal fibers of the PDL, E. Horizontal
fibers of the PDL, F. Oblique fibers of the PDL, G. Apical fibers of the
PDL' Η. Alveolar bone, lnterradicular fibers not shown.
. Sulcular epithelium: The epithelium that lines the
sulοus. ln health, sulcular epithelium does not have
epithelial ridge formation.
o Junctional epithelium: The epithelium that attaches the
gingiva to the surface of the tooth, or to compatible
restorative materials' Τhe special part of the junctional
epithelium that actually provides the attachment is called
the epithelial attachment. τhis attachment consists of a
lamina lucida, lamina densa, and hemidesmosomes.
Connective tissue: The predominantly collagenous
tissue found beneath the epitheΙium. The connective
tissue contains collagen fibers (60%), fibroblasts (5%),
and interfibrillar substanοe οomposed of noncollagenous
proteins and mucopolysaccharides, small numbers of
neutrophils and lymphocytes, blood vessels, lymphatics,
and nerves (the remaining 35%). Τhe overlying epithe-
lium must have intact connective tissue in order to
survive. Most of the coΙlagen found in the periodontium is
type I collagen.
Gingival fibers: These are specially oriented fibers in
the connective tissue. Also known as Ιhe supracrestal
connective tissue fibers, these fibers are designated by
their orientation: Dentogingival, dentoperiosteal, circular,
and transseptal (connecting tνvo adjacent teeth) fibers.
Some authors inοlude the transseptal fibers in the prin-
cipaΙ fibers of the periodontal ligament, although they are
actually tooth-to-tooth and not tooth-to-bone fibΘrs.
Periodontal ligament (PDL): This is the collagenous
tissue that surrounds the tooth root and attaches the
tooth to the alveolar bone proper. The principal fibers of
the periodontal ligament have been cΙassified as the
alveolar crest, horizontal, oblique, apical, and interradic-
ular (in the furcation area of multirooted teeth) fibers. Τhe
oblique fibers are the most numerous. Fibroblasts, osteo-
blasts, cementoblasts, osteoclasts, epithelium, and
nerve celΙs are also found in the periodontal ligament
space. The width of the PDL space is about 0.25 mm in
normal function. Α tooth in hypofunction may have a
narro/er PDL space and a tooth in hyperfunction may
have a considerably wider PDL space.
FlGURE 4. τhe Attachment Apparatus. From the left: Dentin, cementum, perio-
dontal ligament fibers, alveolar bone.
. AIveolar bone: Αlso known as Ιhe alveolar process, this
is the portion of the maxilla and mandibΙe that form and
support the tooth sockets. The alveolar process gives
Support to the alveoΙi and consists of coιtical bone,
cancellous trabeοulae, and the alveo|ar bone proper.
A
D
c
11
-

14. Ξ
ANAToMY. HlsτoLoGY. AND PHYsloLoGY oF τHE PERloDoNTlυM
F|GURE 5A. The Alveolar Bone. τhis section shows the relationship of the
roots of this molar to the alveolar bone proper and the rest of ιhe alveolar
prοcess.
FlGURE 58. τhe Alveolar Bone. ln cross section, corticaι bone can be seen on
the surface of this mandible with trabecular bone within the confines of
the iawbone. τhe density of the trabeculaιions can vary markedly from
one area of the iaw to another and among individuaΙs.
. Alveolar bone proper: That part of the alveolar bone
that lines the tooth socket. lt is a perforated cribiform
plate through which vessels and nerves pass between
the PDL and marrow.
. Basal bone: That part of the maxilla and mandible that
supports the alveolar process. Basal bone is all that
remains once all of the alveolar process is resorbed after
the teeth are lost from the arch.
. Cementum: The thin, calcif ied tissue of ectomesen-
chymal origin covering the roots of teeth in which
embedded collagen fibers attach the teeth to the alveo-
lus. There are t\ivo types of cementum: Αcellular and
cellular cementum. Acellular cementum does not con-
tain cementocytes and is found on the οoronal half of the
the tooth rooΙ. Cellular cΘmentum contains cementocytes
and is found primarily on the apical third of the root. lt is
continuously deposited throughout life.
What ls the Blood Supply to the Periodontium?
FlGURΕ 6Α. Local Blood supply to the Periodontium. supraperiosteal blood
vessels and PDL vessels coalesce into the gingival plexus.
F|GURΕ 68. Loοal Blood supply to the Periodontium. lnterseptal vessels
supply the alveolar bone, PDL, and gingiva.
The blood supply to the periodontium arises from the
terminal branches of the internal maxillary aftery. Locally, the
blood supply to the gingiva consists of supraperiosteal
vessels. Vessels from the alveolar bone and periodontal liga-
ment also contribute to the coalescence of vessels in the
gingival papillae, known as Ιhe gingivaΙ plexus. The alveolar

15. CΗAPTER 2
bone is supplied by branches of the anterior, middle, and
posterior superior arteries to the maxilla and branches of the
inferior alveolar artery in the mandible. lntra-alveolar or inteμ
dental vessels supply the interdental bone. Arterial blood
generally flows in an apical-to-coronal direction. Large
numbers of capillary loops that resemble renal glomeruli are
found beneath the iunctional epithelium and sulcular epithe-
lium near the surface of the gingiva.
What ls the Innervation of the Periodontium?
Nerve supply to the periodontium is derived from terminal
branches of the maxillary and mandibular branches of the
trigeminal nerve. The periodontium contains sensory recep-
tors for pain, touch, and pressure as well as proprioceptors in
the periodontal ligament but not in the gingiva. The sensory
nerves have their center in the semilunar ganglion and the
proprioceptive nerves are centered in the mesencephaliο
nυcleus.
What ls the BioIogic ι,vidth?
duωcτιo*υ
E
SlλPιeAc'ιee'nL
coilωep-I1ν€
Tι'Sιλ'E
ΡιB,Ε!LS
FtGURE 7. Biologic νlridth. Junctional epithelium and supracrestal connective
tissue fibers (dentogingival, dentoalveolar, circular, transseptal) must be
maintained in health.
The biologic width is the apicocoronal distance that the junc-
tional epithelium and supracrestal connective tissue
(gingival) fibers are attached to the tooth. This distance is
measured histologically from the most coronal part of the
junctional epithelium (base of the sulcus) to the crest of the
alveolar bone. The average measurement of the biologic
width is 2.04 mm, approximately 1 mm for the junctional
epithelium and 1 mm for the supracrestal connective tissue
fibers. The sulcus depth is nof part of the biologic width.
ΨVhy Is the BioIogic Vvidth lmportant?
The body maintains the biologic width as a stable dimension.
When the biologic width is encroached upon and iniured by
extension of restorative preparations and materials into this
area, uncontrolled inflammation may result as the body tries
to reestablish this dimension. ln areas of thin gingiva, this
may result in recession or bleeding upon gentle probing even
when the patient has good plaque control and recession.
What ls the Attachment Apparatus?
The attachment apparatus is the alveolar bone proper, perio-
dontal ligament fibers, and cementum that attach the root to
the alveolar bone. Regeneration of the attachment apparatus
is one of the surgical goals in periodontal therapy. Regenera-
tion of the attachment apparatus is the only treatment proce-
dure in dentistry where new tissue is histologically identical
to that which has been lost due to the disease process.
ΨVhat ls Gingival Crevicular Fluid?
ln health, gingival crevicular fluid (GCF) is a transudate that
emerges from the gingival sulcus. The gingival crevicular
fluid may contain a variety of enzymes and cells, particularly
desquamating epithelium and neutrophils, that are being
shed through the sulcus. An increase in gingival crevicular
fluid flow is the first detectable sign of inflammation. Once
inflammation has ocοurred, the GCF is referred to aS an
inflammatory exudate. This exudate contains higher levels of
serum proteins and leukocytes.
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16. Ξ

17. CHAPτER 3
CHAPTER 3: ETIOLOGY AND CLASSIFICATION OF THE
PERIODONTAL DISEASES
The etiology of the periodontal diseases is multifactorial, but
bacterial plaque is necessary for the initiation and progres-
sion of infΙammatory periodontal disease. Αs indicated by the
neνι Ctassification System for Periodontal Diseases and
Conditions, etiologic faοtors have become the framework for
periodontal diagnosis and classification
What ls lnflammation?
lnflammation is a soft tissue cellular and vascular response to
local iniury of physical, thermal, chemical, or microbial origin.
lnflammatory periodontal diseases are no exception to this
paradigm as local periodontal etiologic factors may be phys-
ical (factitial habits such as toothbrush abrasion or occlusal
trauma), thermal, chemical (epithelial disorders associated
With some mouth\ivashes, smokeless tobaοco, aspirin, and
coοaine), and microbial (dental plaque induced gingival
diseases). The most common inflammatory periodontal
diseases are caused by a locaΙ accumulation of baοteria.
What ls Meant by EtiologY?
ΕtioΙogy is "the study or theory of the causation of any
disease; the sum of knowledge regarding causes." Therefore,
etiology is a noun that defines the science of disease causa-
tion, but in common usage, etiology is a cluster of faοtors that
contribute to disease (ie, the etiology of periodontal
diseases).
What Are the Microbiologiο Etiologic Factors in
Periodontal Diseases?
Τhe microbiologic etiologic factor in periodontal diseases is
dental plaque with dental calculus as probably the most
significant local contributing factor. Food debris and the
bacteria it contains is probably a major etiologic factor in root
caries.
F|GURE 1. A photomicrograph showing severe marginaΙ inllammation and
local etiologic factors of bacteriaι origin.
There is littΙe dispute over the concept that bacteria are the
primary etiologic factors in inflammatory periodontal
diseases. ln 1965, Loe and co-workers published their classic
work that demonstrated that gingival health could be reliably
achieved with immaculate oral hygiene and that gingival
inflammation could be caused by the aοcumulation of plaque
on the teeth. Light microscopiο examination of tooth scrap-
ings revealed that plaque \ivas an adherent mat of bacteria,
epithelial cells, and leukocytes encased in an amorphous
protein and polysaccharide matrix, and that cocci, filamen-
tous bacteria, spirochetes, and vibrios accumulated on teeth
in an ordered sequence. The knowledge produced in this and
later studies of plaque morphology and microbiology
emphasied that plaque was a heterogeneous community of
bacteria (see Figure 2).
Generally speaking, bacteria assoοiated with periodontal
health are characterized as Gram-positive, nonmotile faculta-
tive anaerobes. Bacteria assoοiated with disease are gener-
ally Gram-negative, motile, Strictly anaerobiο speοies. Τhe
cell wall of Gram-negative bacteria consists of a lipopolysac-
charide base, aΙso known as endotoxin, that has significant
pathogenic potential. νγhile over 350 distinct speοies of
bacteria have been isolated from the oral cavity, relatively
few are associated with gingival or periodontal inflammation.
The list of strongly associated pathogenic bacteria includes:
ο Actinobacillus actinomycetemcomitans
ο Bacteroidesforsythus
. Fusobacteriumnucleatum
. Peptostreptococcusmicros
o Porphyromonasgingivalis
o Prevotella intermedia/nigresens
What ls Meant by the Term "Biofilm"?
B
FIGURE 2. A thin section eleclron photomicrograph of supragingival plaque
(biofilm) showing a heterogeneous popu|ation of resident bacteriaΙ
morphοtypes and bacterial debris. τhe interbacterial matrix permits the
exchange of nutrients between microorganisms.
-

18. I
I
ι
I
ET|oLoGY AND cLASslFlcATloN oF τΗE PERloDoΝτAL DlsEAsEs
Biofilms form on inert surfaces where bacteria to bacteria
cohesive interactions or bacteria to surface adhesive interac-
tions are allowed to occur. Biofilms are heterogeneous
composites of bacterial communities within a nonbaοterial
protein, polysaccharide, and glycoprotein matrix of bacterial
and salivary origin. The matrix allows for a "circulation" of
nutrients and baοterial metabolites betνveen communities and
the environment outside the biofilm. τhere are extreme varia-
tions in oxygen levels ranging from highly aerobic areas
within fluid channels to almost completely anaerobic areas in
microcolonies.
What ls the "Nonspecific Plaque Hypothesis"?
The basic tenets of the nonspecific plaque hypothesis state
that inflammatory periodontal diseases (and possibly caries)
are caused by composite effect of bacterial colonization and
maturation on the surfaces of teeth, not by specific bacteria
themselves. Gingival disease is the outcome from release of
bacterial metabolites (such as butyrate or other short chain
fatty acids) and immunogenic bacteriaΙ antigen components,
such as lipopolysaοcharide (endotoxin) from Gram-negative
cell walls during plaque growth. lnflammatory disease is the
outcome of a microbial mass that is in excess of the local
defense mechanisms of the host.
What ls the "Specific PIaque Hypothesis"?
The specific plaque hypothesis states that periodontitis is an
infection caused by a limited number of periodontal microor-
ganisms, and that these microorganisms characterize the
plaque biofilms associated with periodontitis but not gingivitis
or gingival health. lt appears that of the 300+ identifiable
species found in the oral cavity, only a small proportion (10-
12 species) are actually found in active periodontitis sites.
The bacteria believed to be pathogens in periodontitis do not
conform to the classic dogma for microbial pathogenicity (ie,
Koch's Postulates). The current understanding of mixed
infections, bacterial invasion, virulence factors, conducive
bacteria habitats, the role of so-called "beneficial species",
and the susceptibility of the host have rendered Koch's
Postulates obsolete when it comes to periodontitis.
What ls Meant by "Putative Periodontal
Pathogen"?
The criteria for implicating oral microorganisms as perio-
dontaΙ pathogens are:
1. The microorganism must be associated in high numbers
in active periodontitis lesions and either absent (not culti-
vable) or in low numbers in gingivitis or healthy sites. The
numbers of the microorganism should have increased to
a threshold level before the onset of disease.
2' Ιhe elimination of the microorganism, or its numerical
reduction below threshold levels, should parallel remis-
sion of active disease.
3. There should be a specific host immune response
against the organism (ie, elevated serum, salivary, and
crevicular fluid antibody titers).
4. The microorganism should evoke virulence factors that
contribute to its pathogenicity or explain disease pathobi-
ology.
5. The microorganism should produce periodontitis in
animal model systems.
What Features Do Most Periodontal Pathogens
Have in Common? What Are the Exceptions to
the Paradigm?
This smalΙ group of putative periodontal pathogens possesses
certain features in common. Most of them have a Gram-
negative cell wall. The outer membrane of the Gram-negative
cell wall contain lipopolysaccharide (LPS) \Λ/hich has endo-
toΧin activity (see Figure 3). Typically, LPS οontaining Gram-
negative cell waΙl extracts are capable of promoting bone
resorption, inhibiting osteogenesis, οhemotaxis of neutrophils,
and other events associated with active periodontitis. Some
pathogens release a LPS that suppresses the innate immune
response. Many periodontal pathogens are strict or faculta-
tive anaerobes and are asaccharolytic, permitting survival in
the restricted ecosystem of the periodontal pocket. Among
the strict anaerobes is the only presumptive periodontal path-
ogen with a Gram-positive οell ν'ιall, Peptostreptococcus
micros.
F|GUHE 3- A terminaΙ outer membrane vesicle at the tip of Fusobacterium
nucιeatum. High concentrations of lipopolysaccharide (endotoxin) are
present in the outer membrane of Gram-negative cell walls,
Actinobacill us actinomycetemcomitans and Porphyromonas
gingivalis are the best studied and have been designated,
along with Bacteroides forsythus, as true etiologic agents in
periodontitis because of the host of virulence they produce
and their ability to invade gingival tissues. Prevotella inter-
media/nigrescens and Fusobacterium nucleatum have been
widely studied as well, and appear to satisfy all criteria for
periodontal pathogenicity. Because P. intermedia and strains
ot F. nucΙeatum have also been found in areas of Severe
gingival inflammation without evidence of attachment loss,
controversy exists as to their true periodontal pathogenicity.
Campylobacter rectus, Εikeneila corrodens, Εubacterium
species, SeΙenomonas species, enteric rods/Pseudomonas
speοies, and Treponema species satisfy some, but not all,
criteria with any degree of confidence. Nonetheless, they
remain among the list of periodontal pathogens, and microbi-
ology testing serviοes commonly report their presence
among cultivable flora.
Relative risk values of periodontal pathogens in periodontal
sites have emerged from archival reviews of data bases
located in commercial testing facilities. The relative risk of a

19. CHAPτER 3
microorganism as a pathogen is often expressed as percent
of total cultivabιe bacteria in a given culture. For example, the
cultivability of A. actinomycetemcomitans at levels at or
above 0.01% indicates a periodontal site at risk for active
disease. The risk for P. gingivalis, C. rectus, P. intermedia,
and P. micros in periodontal sites is 0.1%, 2%,2.5%, and 3"/",
respectively.
What ls Dental Calculus?
Dental calculus is mineraΙized, mature plaque covered on its
suface with nonmineralized plaque, material alba, desqua-
mated epithelial cells, and formed blood elements. The
bacterial components are largely branched and unbranched
filamentous microorganisms that are usually nonvital or
display minimal metabolic activity. These bacteria probably
play a role in the mineralization of calculus as inorganic crys-
tals are frequently found within and around microorganisms.
Structurally, calculus retains much of the histologic
morphology of its plaque precursor.
Calculus may be classified as supragingival or subgingival
based on location. lt may also be classified as salivary or
serumal based on the source of inorganiο salts that comprise
calculus. Root calculus is usually more strongly adherent to
tooth surfaces than that found on enamel sudaces (see
Figures 4 and 5).
The inorganic components of calculus deposits are primarily
organized into crystalline struοtures that vary according to the
age of the deposit. For instance, in mature calculus (>6
months), the major crystalline structure is hydroxyapatite
(Ca16[PO4]6(OH)r) with lesser amounts of octacalcium phos-
phate (Cas[HPOa]a), whitlockite (Ca3[POo]r), and brushite
(Ca[HPOo]2HrO). ln younger deposits (<3 months), brushite
predominates, but with progressive aging, octacalcium phos-
phate, whitlockite, and finally hydroxyapatite become more
abundant.
FlGURE 4. A heavy deposit of suρragingival, salivary calculus on the buccal
and occlusal surfaces of nonfunctional maxillary premolar and molar
teeth.
Calculus deposits have also been desοribed as radiographi-
cally apparent. The radiographiο detection of calculus is posi-
tively influenced by the thickness of the deposit, the amount
of surface area covered by the deposit, and the anatomy of
the tooth. Only 40% to 50% of calculus deposits will be radio-
graphicaΙly apparent. Therefore, radiographs should not
solely be used to measure the presence or absence of
calculus.
How Does Calculus Attach to Teeth? Do the
Attachment Mechanisms Have Any Clinical
Significance?
Calculus will attach to tooth suι'faces by several mechanisms.
The most common mechanism of supragingival calculus
attachment to smooth enamel surfaces is salivary pellicle,
and it is usually easily removed using ultrasonic or hand
instrumentation. The irregularities of unrestored caries and
defective dental restorations complicate the removal of
supragingival calculus. The attachment of subgingival
calculus is further complicated by microscopic irregularities in
cementum such as cementaι tears, cemental voids once
occupied by Sharpey's fibers, resorption bays, and other
surfaοe cemental defects. lt is for these reasons that clini-
cians will further designate calculus deposits as either
coronal or radicular to reflect the relative tenaciousness of
radicular and coronal calculus, and in the οase of radicular
calculus, the difficulty they may have in achieving total
calοulus removal during root planing.
FlGURE 5. serumnaι calculus deposits that have become supragingival due to
gingival reοession caused by advanced periodontitis. Note the more
generalized distribution of the deposits with no apparent relationship or
proximity to ma,or salivary ducts.
What ls the Pathogenic PotentiaΙ of Calculus?
The current view is that calculus exerts its pathogenic poten-
tial as a contributing factor that fosters plaque formation and
promotes its retention on teeth. Also, there is little question
that the microbiaΙ composition of calculus provides bacterial
factors that, by themseΙves, produce an inflammatory reac-
tion in tissue. Bacterial οomponents (outer membrane vesi-
cles containing LPS, cell \ivall material containing lipoteichoiο
acids, periplasmic and cytopΙasmic enzymes, and bacterial
metabolic factors) are all suspect pathogenic factors in dental
calculus. The persistent inflammation in gingival tissue
predictably seen adjacent to reasonably plaque free calculus
is unequivocal evidence of the pathogenic effect of calculus.
17
-

20. EτloLoGY AND clAsslFlcAτloN oF τHE PEBloDoNτAL DlsEAsEs
F|GURE 6. τhe exposure of subgingival' serumnal calculus aΙter a period of
improved plaque control. Marginal inflammation has been reduced but
erythema and edema persist. τhis is the same patient as seen in Figure 1'
Aside from this, the rough surface of dental calculus is
usually covered with a layer of plaque biofilm. Αs such,
calculus tends to "present" plaque to periodontal soft tissues
and interfere vvith efforts to improve plaque control. The phys-
ical removal of dental calculus remains a critical component
of mechanical periodontal inflammatory disease control.
What Are the Risk Factors for Periodontal
Diseases? What ls Meant by "Risk"?
The expression risk in this context means that, in the pres-
ence of a given factor, injury to or loss of periodontal tissue is
a possibility. Risk factors may be local or systemic in nature.
Local contributing factors to the etiology of periodontal
diseases fall into two general categories: Anatomic or iatro-
genic. They share in common their ability to either facilitate
bacterial plaque, and therefore calculus, accumuΙation/reten-
tion or their ability to interfere with plaque/calculus removal.
Τhe loca| anatomic risk factors include:
1. Furcation anatomy. ln many instances, the entrance
of bifurcations or trifurcations is restricted enough to
limit access for mechanical root instrumentation.
once access to the intrafurcaΙ space has been
achieved, concavities in the furcal aspects of molar
roots wiΙl limit instrumentation as well (see Figure 7).
2. lntermediate bifurcation ridges extending from the
mesial furcation surfaοe of the distal root across the
roof of the bifurcation to the distal sudace of the
mesial root of mandibular molars. Τhese common
anatomic deformities interfere with a patient's ability
to effeοtively remove plaque biofilm.
3. Cervical enamel projections (CEP). CEPs are tooth
developmental deformities of the CEJ found on
molars. They are classified according to their involve-
ment in tooth furcations. Α Grade l CEP presents with
minimal projection of enamel tov/ard the entrance of
the furcation. Α Grade ll οEP approximates the
entrance of the furcation, and the tip of a Grade lll
CEP is well within the furcation (see Figure 8).
FlGURΕ 7. A maxiΙlary moΙar displaying a buccal to distal furcation invasion
with a Nabers probe in place. The narrowness of the furcation entrances
and the tortuousness of the furcation invasion mitigate against access for
scaling and root planing. (Courtesy of Dr. Jeanne Salcetti)
F|GURE 8. A human dried maxilla with a grade ll cervical enamel proiΘction
(cEP) in the buccal furcation of the maxilΙary sΘcond molar. τhe cEP
could have been partially responsible tor the furcation invasion and local-
ized severe bone loss around the tooth.
4. Palato-gingival grooves (PGG). PGGs are tooth
develοpmenta| deformities of maxilΙary central and
lateral incisors. They begin in lingual piis and extend
vertically onto root suιJaces. PGGs could, on rare
occasions, extend to the root apex. PGGs are
commonly associated with increased gingival inflam-
mation, plaque aοcumulaiion, and probing depth (see
Figure 9).

21. CHAPτER 3
FlGURE 9. A palatogingival groove on a maxillary lateral incisor. τhe gfoove
couΙd have been partially responsible for the sΘvere attachment loss
around the tοoth. Note that because of its loss of support, the lateral
incisοr has undergone pathologic migration.
5. Open contacts and food impaction. Open contacts
between teeth may be anatomical in origin, iatrogenic
in origin, or be due to caries and pathologic migration
of periodontally involved teeth. Food impaction is
defined as the forceful wedging of food between
teeth. Any other accumulation of food or food debris
around teeth should be categorized as food retention
and is probably less threatening to the periodontium.
Food impaction and subsequent retention may
contribute to root caries in individuals who do not
perform proper oral hygiene interdentalΙy. open
contacts by themselves probably do not contribute to
periodontal pathology, but, in the presence of food
impaction, open contacts have been associated with
periodontal destruction. This may be particularly
noticeable in periodontitis cases where the progress
of disease is in its early stages or particularly obvious
where periodontitis is isolated to sites of open
contacts/food impaction.
F|GURE 10. surgical exposure of an anomalous maxillary first moΙar. The
palatal root is bifurcated and the distopalatal root curues into the mesial
furcation of the second molar. on the bucca| aspect, the mesiobuccaΙ
root of the second molar is in close approximation to the distobuccal root
of the first molar. Access for effective scaling and root planing is
extremely limited.
6. Other anatomic risk factors of potential etiologic
importance are: The width of the space between
teeth and root proximity (so-called "kissing roots").
The iatrogenic risk factors are:
1. Overhanging dental restorations. Since dental
restorations remain the mainstay of dental practice, it
is not surprising that overhanging dental restorations
are arguably the most common form of iatrogeny to
affect marginaΙ periodontal health (see Figure 11).
Overhanging and improperly placed dental restora-
tions can be physicaΙly irritating' be pΙaque retentive,
foster the growth of periodontal pathogens, alter the
morphology of the interdental space, and violate the
dentogingival junction (see 2 below). By virtue of their
roughness and overall bulk, they may also interfere
\ivith interdentaι plaque control.
FIGURE 11. A maxillary first molar with a mesial amalgam overhang that
eπends into the furcation. lt is probable that the preparation Ιor this
restoration impinged upon the biologic width. Note how the attachment
level on the tooth parallels the extension of the overhang onto the
cementum and into the furcation.
Violation of the "biologic width". After overhanging
restorations, iatrogenic invasion of the biologic width
may be the next more serious insult to the periodon-
tium a dentist can make. The impact of this insult is
usually permanent as the margins of dental restora-
tions are inevitably placed in the wake of the insult.
The biologic width is one of nature's constant dimen-
sions. lt is most constant within individuals and less
constant bet\Λ/een individuals. lf it is injured, it will
repair. lf however, restorative materials render the
invasion of the biologic width permanent, periodontitis
wilΙ produce apical migration of the .iunctional epithe-
lium, resorption of crestal alveolar bone, loss of perio-
dontal attachment, and possible vertical osseous
defeοts (Figure 1 1). Α new bio|ogic width will repair a
few mms apical to its original position on the tooth.
This represents a net loss of attachment on the tooth.
Open contacts and food impaction related to
inadequate restorative dentistry. The impact of
food impaction through open contacts created by
2.
3.
Ξ

22. EτloLoGY AND clAsslFlcAτloN oF τHE PERloDoNτAL DlsEAsEs
4-
5.
iatrogeny offers the same threat to the periodontium
as food impaοtion associated with open contacts that
have resulted from growth and development or
occlusal \Λrear.
Occlusal traumatism associated with inadequate
dentistry in 1, 2, and 3 above.
Additional local iatrogenic risk factors for perio-
dontal diseases include: Removable partial 2.
dentures and overdentures, fixed bridges, removal of
third molar teeth in older adults, placement of fixed
orthodontic appliances, and orthodontic movement of
periodontally involved teeth.
Uncontrolled diabetics, poorly controlled diabetics, or
diabetics whose control is unknown should only
receive emergency periodontal therapy, and that
treatment should be performed \,vith intraprocedural
and/or postoperative antibiotic coverage. The
patient's physician may also prescribe insulin or other
antihyperglycemic agents to help limit post-operative
infections or complications in wound healing.
Ηlv/AlDs. Given the immunosuppressed state of
these individuals (decreased CD4 lymphocytes), an
expectation for severe periodontitis in patients with
HIV/AIDS is reasonable. lndeed, these individuals
suffer from other bacterial, viral, and fungal diseases
more than those νvithout HIV infection. Many
sucοumb to these infections. Early studies of the peri-
odontal status in AIDS patients indicated that these
individuals showed increased severity of periodontal
diseases. H|V-gingivitis (linear erythema) and HIV-
periodontitis (necrotizing ulcerative periodontitis)
categories of periodontal diseases were quickly
proposed to designate the unique cΙinical characteris-
tics of periodontal diseases in this group. RecentΙy,
the issue has been challenged by those who report
no increases in the prevalence or extent of perio-
dontal diseases among HlV-positive individuals.
Smoking. Due to the vasoconstrictor effect of nico-
tine and the paralysis by carbon monoxide on the
ability of hemoglobin to transport oxygen, it is under-
standable that smoking is a serious environmental
risk factor for periodontal diseases. The length of time
an individual has been smoking and the frequency of
smoking play contributory roles in the severity of peri-
odontal disease in smokers. Smokers also have a
greater accumulation of plaque and οaΙcu|us than
nonsmokers and may be more at risk to harbor perio-
dontal pathogens.
While probing depth reduction following conventional
nonsurgical and surgical periodontal therapy has
been reported in smokers, the amount of reduction
has been reported as less than that achieved in
nonsmokers. A growing body of evidence suggests
strongly that the failure rate of implant therapy is
higher in patients who smoke. lt is not uncommon for
a therapist to recommend against the placement of
dental implants in smokers. Patients must be coun-
seled in this regard and supported in their attempts to
overcome their addiction.
Sex hormone imbalances. The most notable
changes in the periodontium that are affected in part
by hormonal changes occur in \Λ/omen in their child-
bearing years. ln the case of pregnancy, proges-
terone and estrogen levels increase to levels that are
several orders of magnitude greater than those seen
during a normal menstrual cycle. Varying degrees of
a reversible "pregnancy gingivitis" are common
during pregnancy. The biologic impact of hormone
changes range from the release of inflammatory
mediators that increase vascular permeability (pros-
taglandins), the alterations in immunoregulation and
pro-inflammatory reguιators, the imbalances in the
fibrinolytic system, and the abundant growth of the
periodontal pathogen, P. intermedia. Because the
duration of pregnancy is relatively short, hormonal
changes associated with pregnancy have little effect
on the more irreversible progress of periodontitis.
What Are the Systemic Diseases and/or
Conditions That Are Contributing Factors for
Periodontal Diseases?
Aside from the medications that affect the clinical presenta-
tion of plaque-induced gingival diseases (nifedipine for
control of hypertension, phenytoin for control of epileptic
seizures, and cyclosporine to control organ transplant rejec-
tion), most systemic diseases and conditions that may affeοt
periodontal diseases generally alter host barrier and host
defense mechanisms. The impact of diminished host suscep-
tibility, along with the diverse virulence mechanisms invading
microorganisms possess, help to explain the individual varia-
tions in periodontal disease patterns \Λ,e See in systemically ill
periodontal patients. An assessment of systemic contribu-
tions to periodontal diseases in our patients is critical to perio-
dontal diagnosis and/or treatment planning.
The systemic diseases and conditions that commonly affect
periodontal diseases are: Uncontrolled type I and type ll
diabetes mellitus, HIV/AIDS, hormone imbalances, genetic
predisposition, medications, smoking, and malnutrition.
1. Diabeιes mellitus. Diabetes mellitus (DM) is
atfecting a growing number of Americans. The inci-
dence of the disease seems to vary according to
ethnic origin, but it is estimated that 5% to 10% of
individuals in the United States are affected with
diabetes. DM is an aberration in carbohydrate, lipid,
and protein metabolism. Most of the morbid compli-
cations of DM stem from longterm impaired glucose
metabolism. The characteristic hyperglycemia of
uncontrolled DM is the basis for most of the vascular,
cellular, and immune changes assoοiated with the
disease.
Epidemiologic data has made clear associations
between increased severity of periodontal diseases
and uncontrolled type I and type ll diabetes mellitus.
Type I and type ll uncontrolled diabetics tend to
present with more gingiva! inflammation, more loss of
periodontal attachment, and radiographic evidence of
more bone loss than controlled or nondiabetic individ-
uals. There is agreement that periodontal patients
whose DM is welΙ controlled may receive periodontal
therapy without restriοtions' incΙuding periodontal
surgery and implant placement.
3.

23. CHAPτER 3
Oral contraceptives mimic the hormonal levels seen
during pregnancy, and it is not uncommon to find
pregnancy-like changes in patients using birth οontrol
pills (BCP). Because gingivaΙ sex hormone concen-
trations tend to be lower during normal menstruation,
it is not unexpected that women in their childbearing
years may present with "cyclic" episodes of increased
gingival inflammation.
F|GURE'12. τhis lesion is a pyogenic granuloma in a 17-year-oιd femaΙe
patient as a result in changes in sex hormone levels and plaque
accumuιation.
The most important οoncern of the dentist in
managing patients who present with gingival disease
related to hormone imbalances is to be certain that
inflammatory disease control measures are effective
(Figure 12).
This is particularly important in women who are preg-
nant because data exists to suggest a relationship
bet\Λ/een periodontal infections (periodontitis) and
preterm low birth weight babies. Antibiotiοs should be
used only after a medical consultation in patients who
are pregnant. Although οontroversial, there are
reports of decreased effectiveness of oral οontracep-
tives in individuals taking certain antibiotics. lndivid-
uals who are taking BCPs should be advised that the
use of prescribed antibiotics such as tetracyclines
and some penicillins may interfere with the action of
BCPs. To avoid unwanted pregnancy, these individ-
ua|s should be so warned and use aΙternative
methods of birth control \ivhile taking antibiotics.
5. Genetic predisposition for periodontal diseases.
There is general agreement that individual responses
to plaque bacteria vary. lt has been suggested that
disease pattern variations could be based, in part, on
underlying genetically based differenοes in immune
function. lndeed, the association of:
a. Neutrophil receptor defects
b' Αntibody responses (lgGr) to periodontal patho-
gens
c. οertain histoοompatibility antigens (HLΑ)
d. Lymphocyte immune regulatory defeοts in patients
with aggressive periodontitis adds credibility to this
conοept.
Studies in twins indicate that many of the clinical
variations seen in chronic periodontitis can be attrib-
uted to individual genetic differenοes. Recent reports
of genetic pleomorphism in lL-1 genes and the
elevated production of proinflammatory mediators,
such as lL-1 , add another dimension to the impact
genetic variations among individuals have on the
patterns of chronic periodontitis.
-

24. EτloLoGY AND cLAsslF|cATloN oF TΗE PERIoDoNτAL DlsEAsEs
CLASSIFICATION OF PERIODONTAL DISEASES
Concepts about the etiology, pathogenesis, and treatment of
the periodontal diseases have changed significantly over the
years. Ne\Λ/ levels of understanding are reflected in the clas-
sification systems for these diseases and conditions. The
t\Λ/o most recent widely accepted classification Systems of
the periodontal diseases and conditions were developed in
1989 and 1999. The current system, more comprehensive
than any of its predecessors, is admittedly still a work in
progress.
Ηoνv Has the Understanding of Periodontal
Diseases Changed Over the Years?
For many years, the periodontal diseases were thought of as
degenerative diseases. Early confirmation of the role of
bacterial plaque in the initiation and progression of gingivitis
was only presented in the 1960s. Since that time, many of
the earlier tenets have fallen by the wayside. Currently, it is
clear that both gingivitis and periodontitis in their varied
forms are caused by the accumulation of a bacterial plaque
biofilms on the teeth and in the subgingival area, the host
response to that aοcumulation, and the various systemic and
local factors that may affect the host response. lt is also clear
that only a relatively few bacteria are associated with inflam-
matory periodontal disease. The exact role of these bacteria,
their relationship with each other and their interaction with
the immune system in the initiation and progression of
disease is still not clearly understood. There also appears to
be a genetic component to the initiation and progression of
disease in some patients. At this iuncture, controlling the
acοumulation of plaque is the first line of defense in
preventing disease, no matter what other factors may be
present.
What ls the Difference BetιΛreen Gingivitis and
Periodontitis?
FlGURE
'|3.
Gingivitis in a 12-year-old female. τhe severe gingivitis was due to
the interaction of increased levels of progesterone and plaque.
Gingivitis is inflammation of the gingival tissues in the
absence of οlinical attachment loss (Figure 13). lt may be
οharacterized by edema, erythema, increased gingival
temperature, and oοcasionally pain. As the inflammation and
loss of connective tissue is confined to the soft tissues, teeth
are not in jeopardy of being lost. Gingivitis is ordinarily
reversible with appropriate therapy. Periodontitis is infΙam-
mation that affects and destroys the attachment apparatus
(Figure l4). The histology is marked by apical migration of
the junctional epithelium from the οementoenamel junction,
Ιoss of connective tissue attachement, loss of periodontal
Ιigament, and destruction of bone. lncreased probing depths
may occur or the gingiva may recede as attachment is lost.
Continuation of this loss of attachment will eventually lead to
the loss of the tooth. The progress of periodontitis may be
arrested \Λ/ith proper therapy. ln certain Situations, lost
attachment apparatus may be surgicaΙly regenerated.
FIGURE 14. Periodontitis in a 37-year-old male. Note the significant calculus
and plaque accumulations, severe gingival inflammatiοn, and recession
associated with the mandibular anterior teeth.
What ls the "Traditional" Classification of the
Periodontal Diseases?
The 1989 World Workshop in Clinical Periodontics recom-
mended the following categories of periodontitis. This system
iS the one most familiar to a majority of cliniοians'
l. Αdult periodontitis
ll. Early-onset periodontitis
A. Prepubertal periodontitis
1. Generalized
2. Localized
B' JuveniΙe periodontitis
1. Generalized
2. Localized
C. Rapidly progressive periodontitis
lll. Periodontitis associated with systemic disease
lV. Necrotizing ulcerative periodontitis
V. Refractory periodontitis
One of the generally accepted classifications for gingivitis
vι/as:
l. Plaque-associated gingivitis
ll. Αcute necrotizing ulcerative gingivitis (ANUG)
lll. Hormonal gingivitis
lV. Drug-induced gingival overgrowth
V. Desquamative gingivitis (associated with vesiculo-
bullous diseases)

25. CHAPτER 3
During the ensuing decade, it \Λ/as determined that this
disease classification system exοluded many of the diseases
and conditions of the periodontium that clinicians and
researοhers confront on a dai|y basis. Further work was
necessary to develop a neνv, more inclusive system.
VVhat Is the 1999 Classification of Periodontal
Diseases?
The American Academy of Periodontology convened the
1999 lnternational Workshop for a Classification of Perio-
dontal Diseases and Conditions to reassess the disease
classification system that \ivas developed by the 19B9 νvorld
Workshop in Clinical Periodontics. Based on current knoννΙ-
edge and philosophies, a more comprehensive classification
system of diseases and conditions that affect the periodon-
tium \Λ/as proposed. Major οhanges include the addition of a
section on gingivaΙ diseases, changing the names of adult
periodontitis to chronic periodontitis, early onset periodontitis
to aggressive periodontitis, and the elimination of refractory
periodontitis as a distinct disease class. Periodontitis as a
manilestation of systemic disease has been further clarified,
new categories added on periodontal absοesses, perio-
dontic-endodontiο lesions, and the developmental or
acquired deformities and conditions, and the replacement of
necrotizing ulcerative periodontitis with necrotizing perio-
dontal diseases.
l. Gingival Diseases
A. Dental Plaque-lnduced Gingival Diseases
.l
. Gingivitis associated with dental plaque only
a. Without Ιocal contributing factors (Figure 15)
FIGURE 15. Gingivitis associated with dental plaque only. Note that the
gingival inflammation is worse on the maxillary left side than the
right side. τhis may be relatθd to the hand with which the patient
biushes his teeth. As the patient turns his hand to maneuver the
brush, the lateral incisor and canine are ofιen missed.
b. V/ith local contributing factors
2. GingivaΙ diseases modified by systemic factors
a. Αssociated with the endocrine System
1. Puberty-associated gingivitis (Figure 16)
FIGURE 16. Puberty-Associated Gingivitis. τhis is related to the patient in
FigurΘ 13.
2. Menstrual cycle-associated gingivitis
3. Pregnancy-associated
- Gingivitis
- Pyogenic granuloma (see Figure 12)
4. Diabetes mellitus-associated gingivitis
b. Associated with blood dyscrasias
1. Leukemia-associated gingivitis
2. Other
3. Gingival diseases modified by medications
a. Drug-influenced gingival diseases
1. Drug-influenced gingival enlargements
(Figure 17)
FlGURE'17Α. Drug-lnfluenced Gingival Enlargements. Gingival enlarge-
ment due to phenytoin the,aPy.
23
-

26. EτloLoGY AΝD cLAsSlFlcATloN oF THE PER|oDoΝTAL DlSEASES
FIGURE 178. Drug-lnfluenced Gingivat Enlargements. Gingival enlarge-
ment due to nifedipine therapy superimposed on chronic periodon-
titis.
2. Drug-influenced gingivitis
- Oral contraceptive-associated
gingivitis
- Other
4. Gingival diseases modified by maιnutrition
a. Αscorbiο acid-deficiency gingivitis
b. Other
B. Nonplaque-lnduced Gingival Lesions
1. Gingival diseases of specific baοterial origin
a. Νeisseria gonorrhea-associated lesions
b. Treponema pallidum-associaied lesions
c. Streptococcal species-associated lesions
d. Other
2. Gingival disease of viral origin
a. Herpesvirus infections
1. Primary herpetic gingivostomatitis
2' Reοurrent oraΙ herpes (Figure 1B)
FIGURE 18A. Recurrent Oral Herpes. General herpetic outbreak on the
gingival tissues.
F|GURE 188. Recurrent oraι Herpes. Herpes outbreak localized to one
side of the hard palate several days after periodontal surgery on the
same side ot the maxilla.
- VaricelΙa-zoster infectionS
b. Other
3. Gingival diseases of fungal origin
a. Candida-sρecies infections
- Generalized gingival candidiasis
b. Linear gingival erythema (Figure 19)
FIGURE
'19.
Linear Gingival Erythema. Seen in some HIV+ patients.
ο. Ηistoplasmosis
d. Other
Gingival lesions of genetic origins
a. Ηereditary gingival fibromatosis
b. Other
Gingival manifestations of systemic conditions
a. Mucocutaneousdisorders
5.

27. CΗAPτER 3
'1 . Lichen planus (Figure 20)
F]GURΕ 20. Erosive Lichen Planus. Ιn its ulcerative form, this disease
can be quite painful for the patient.
2. Pemphigoid (Figure 21)
fe #j
FlGURΕ 21Α. Benign Mucous Membrane (cicatricial) Pemphigoid. A posi-
tive Νikolsky sign is seen over the maxillary right lateral incisor.
τhis indicates that a vesiculobullous disease is present.
FlGURE 21B' Benign Mucous Membrane (cicaιricial) Pemphigoid. lmmu-
notluorescence contirms the diagnosis ot pemphigoid.
3. Pemphigus vulgaris
4. Erythema multiforme
5. Lupus erythematosus
6. Drug induced
7 " Other
b. Αllergic reactions
1. Dental restorative materials
- Mercury
- Nickel
- Acrylic
- Other
2. Reactions attributable to
- Toothpastes/dentifriοes
- Mouthrinses/mouthwashes
- Chewing gum additives
- Foods and additives (Figure 22)
3. Other
FlGURΕ 22Α. Allergic Reactions Attributable to Food. This patient
presented With severe gingival infΙammation associated with perio-
dontal disease. The patient had no history or cΙinical findings
suggesιive of sysιemic disease.
9q
FΙGURΕ 22B' AΙlergic Reactions Atlributable to Food' After contrοl of
local factors, there was still a signiricant amount of inflammation.
-

28. EτloLoGY AND cLAsSIFlcAT|oN oF τHE PER|oDoNTAL DlsEAsEs
FIGURE 22C. Allergic Reactions Attributable to Food. An incisional
biopsy revealed a diagnosis of plasma ceΙl gingivitis (allergic reac-
tion)-
FIGURE 22D. Allergic Reactions Attributable to Food. After eliminating
curry peppers from her diet, this patient's gingiva returned to
health.
6. Traumatic lesions (factitious, iatrogenic, acci-
dental)
- Chemiοal injury
- Physical injury
- Thermal injury
7. Foreign body reaction
8. Noi otherfise specified (NOS)
ll. Chronic Periodontitis (Figure 23)-
FlGURΕ 23Α. Generalized chronic Periodontitis. A' ln spite of significant
plaque and calculus accumulations in the mandibular arch, ιhis
palient had minimal gingival intlammation.
FiGURE 23B. Generaιized chronic Periodontitis. τhe right buccal
segment showed minimal soft tissue infΙammation buι probe depths
ranged from 7-10 mm.
FlGURE 23c. Generalized chronic Periodontitis. τhe radiographs
showed significant bone loss in this area.
F|GUΗΕ 23D. Generalized chronic Periodontitis. once a full thickness
mucoperiosteal flap was reflected, the extent of bone loss was
apparent.
Α. Localized
B. Generalized
26

29. CHAPτER 3
ll!. Aggressive Periodontitis*
A. Localized (Figure 24)
FιGURES 24A and B. Localized Αggressive Periodontitis. clinical and
radiographic evidence of localized severe periodontal destruction.
FlGURΕ 24ο. Localized Aggressive Periodontitis. Note the severe bone
loss on the mesial of the tirst molar and no bone loss on the adia-
cent distal of the second premolar.
B. Generalized (Figure 25)
FΙGURE 25. Generalized Aggressive Periodontitis. τhis 1g-year-old
patient has already lost several teeth due to periοdontal disease.
τhe entire dentition has been affected by disease.
Periodontitis as a Manifestation of Systemic Diseases
Α. Αssociated With Ηematologic Disorders
1. Acquired neutropenias
2. Leukemias
3. Other
B. Αssociated With Genetic Disorders
1. Familial and οyοιic neutropenia
2. Down syndrome
3. Leukocyte adhesion deficiency syndromes
4. Papillon-Lefevre syndrome
5. Chediak-Higashisyndrome
6. Histiocytosis syndromes
7. Glyοogen siorage disease
8. lnfantile genetic agranulocytosis
9. Cohen syndrome
10. EhΙers-Danlos syndrome (Types lV and VlΙl)
1 1. Hypophosphatasia
12. Other
Necrotizing Periodontal Diseases
Α. Necrotizing Ulcerative Gingivitis (NUG) (Figure 26)
FlGURΕ 26. Νecrotizing Ulceraιive Gingivitis. These lesions are quite
painful and exude a distinctive unpleasant odor.
tv.
v.
-

30. EτloLoGY AΝD cLAsslFιcAτloN oF THE PΕRloDoNτAL D|SEASES
B. Necrotizing Ulcerative Periodontitis (NUP) (Figure
27)
FlGURE 27. Necrotizing Ulcerative Periodontitis' τhis lesion is often seen
in an Hlv+ patient or a patient with fully developed ΑlDs.
Vl. Abscesses of the Periodontium
A. Gingival Abscess
B. Periodontal Αbscess (Figure 28)
FiGURE 28. Periodontal Abscess. τhis lesion is associated with some
popcorn that was trapped in the subgingival area.
C. Pericoronal Abscess
Vll. Periodontitis Associated With Endodontic Lesions
Α' Combined Periodontic-Endodontic Lesions
Vlll. Developmental or Acquired Deformities and
Conditions
A. Localized Tooth-Related Factors That Modify or
Predispose to Plaque-lnduοed Gingival Diseases/
Periodontitis
1. Tooth anatomic factors
2. Dental resiorations/appliances
3. Root fraοtures
4' Cervical root resorption and οemental tears
B' Muοogingival Deformities and Conditions Around
Teeth
1. GingivaΙ/soft tissue recession (Figure 29)
F|GURE 29. Gingival/soft Tissue Recession. τhe recession is related to a
lack οf attached gingiva and the buccaι frenum altachment.
a. Facial or lingual surfacΘs
b. lnterproximal (papillary)
2. Lack of keratinized gingiva
3. Decreased vestibular depth
4. Αberrant frenum/muscle position
5. Gingival excess
a- Pseudopocket
b. lnconsistent gingival margin
c. Excessive gingival display
d. Gingivalenlargement
6. Abnormal color
C. Mucogingival Deformities and Conditions on
EdentuΙous Ridges
1. Vertical and/or horizontal ridge deficiency
2. Lack of gingival/keratinized tissue
3. Gingival/soft tissue enlargement
4. Aberrant frenum/muscle position
5. Decreased vestibular depth
6. Abnormal color (Figure 30)
FTGURE 30. Abnormal Color. This abnormal gingival color is due to retro-
grade endodontic surgery and a resultant amalgam tattoo.

31. CHAPτER 3
D. occΙusal Trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
"Cases of chronic and aggressive periodontitis may be
generally described by the extent and severity of the
disease. Localized disease would be <30o/o of sites involved
and generalized disease as >30% of sites involved. Slight
disease would have 1-2 mm of clinical attachment loss
(CAL), moderate disease 3-4 mm CAL, and severe disease
>5 mm CAL.
What Are Some of the Distinguishing
Characteristics of the New Classifications of
Gingivitis?
Gingivitis associated νιrith dental plaque only. As the
name implies, bacterial plaque must be present to initiate the
gingival infΙammation. This inflammation may be character-
ized by changes in gingival color, contour, and possibly
consistenοy; slight elevation of intrasulcular temperature;
bleeding on gentle probing; an increase in gingival crevicular
fΙuid flow (now as an exudate); and the inflammation is
confined to the soft tissues. Local factors may include resto-
ration overhangs, open contacts, and other plaque traps and
impediments to good oral hygiene.
Gingival diseases modified by systemic factors:
Pubefiy-associated gingivitis, menstrua! cycle-associ-
ated gingivitis, and pregnancy-associated gingivitis.
These conditions are all associated with changes in steroid
hormone levels, primariΙy progesterone and estrogen. Τhey
have been associated with increased levels of Prevotella
intermedia in the infΙamed sites. ln puberty-associated gingi-
vitis, the inflammation may be exaggerated even with appar-
ently minimal amounts of plaque. Menstrual cycle-associated
gingivitis may appear in a very mild form. lncreased gingival
crevicular fluid flow has been seen in a majority of subjects
during ovulation. Pregnancy-associated gingivitis has
perhaps the most radical changes, vith the possible appear-
ance of a pyogenic granuloma. lt is an extreme response to
gingival inflammation, characterized as a painless protuber-
ance of the gingiva that bΙeeds readily at slight provocation.
Gingival diseases modified by medications. There are
three major drugs that can induce an overgro\Λ/th of gingival
tissues. Phenytoin is used as an antiseizure medication,
nifedipine and several of the other calcium channel blockers
are antihypertensive/antiarrhythmic drugs, and cyclosporine
Α is an immunosuppressant. overgrowth appears to be
related to the level of plaque accumulation. Approximately
50% of phenytoin patients are susceptible to this overgro\,νth.
lt has been estimated Ιhat 2o"/" of patients on calcium_
channel blockers, and 2O/" to 30% of patients on cyclo-
sporine A are susceptible to drug-induced gingival over-
growth.
Nonplaque-induced gingival lesions. Many of these
lesions are relativeΙy rare with the exception of the herpes-
virus and Candida infections. Herpesvirus infections must be
cautiously treated due to their contagious nature \Λ/hile the
lesions are shedding virus. Treatment must be deferred
νvhen the patient presents with a weeping lesion. Candida
infections may be problematic if there is no apparent cause
(reοent antibiotic use' illness) for the infeοtion. Candidaintec-
tions have a high association /ith human immunodeficiency
virus (HlV) infection, so a thorough patient work-up may be
necessary in the face of an unexplainable Candida infection.
Gingival manifestations of systemic conditions. Muco-
cutaneous disorders: These disorders include the dermato-
logic/autoimmune diseases of lichen planus, pemphigoid,
pemphigus vulgaris, erythema multiforme, lupus erythema-
tosus, and drug-induced disorders. These disorders at one
time were classified as desquamative gingivitis, a descriptive
term signifying desquamation or falling away of the surface
epithelium of the gingiva. These disorders are actually auto-
immune in nature with no clear etiology. lt is critical that a
definitive diagnosis be obtained, for while they all may have
a similar appearanοe, pemphigus has a higher morbidity,
while the mucocutaneous disorders are difficult to manage
for patient comfort.
Gingival manifestations of systemic conditions: Linear
gingival erythema. This lesion is characterized by a bright
erythematous margin of the free gingiva. lt is associated with
immunosuppression, particularly ΗlV infection. The
erythema does not resolve with the removal of plaque.
Gingival manifestations of systemic οonditions: Aller-
gies' Αllergic reactions may take on a Variety of forms from
mild erythema and edema to severe inflammation to an
apparent lichenoid appearance. The challenge is to be sure
that the inflammation is not plaque related. A diagnosis of
plasma cell gingivitis may be made by biopsy. The allergen
must then be identified and, if possible, eliminated from the
oral cavity. Allergens incΙude amalgam, base metals used in
fixed prosthodontics, flavoring agents in dentifrices and
cheνving gum' chili peppers, and other foodstuffs. lt may be
difficult to identify the offending agent. Changes must be
made one at a time, often a time-consuming process, in
order to identify the allergen.
What Are Some of the Distinguishing
Characteristics of the New Classifications of
Periodontitis?
The new classifiοation system for periodontitis is more
descriptive and not temporal as νvas the previous system.
The terms adult, juvenile, early onset, and prepubertal have
been replaced with various forms of chronic and aggressive
disease. ln addition, many periodontal conditions that νvere
not addressed in any previous classification system have
been described. The term refractory periodontitis has been
removed as a distinct disease entity, as the current thinking is
that any type of periodontitis may be refractory.
Chronic periodontitis. As the name implies, this type of
periodontitis has a relatively long-standing history in a
patient. This disease is characterized by relatively slow
progress, loss of attachment and underlying bone with
increased pocket depth. lt may have periods of rapid attach-
ment Ιoss foΙlowed by prolonged periods of inactivity. Ιt is
related to the presence of plaque and calculus, \ι/ith a variety
of associated bacteria involved. There may be modifying
local factors, such as restorative overhangs, food impaction,
or open contaοts, and systemic factors, such aS uncontrolΙed
diabetes mellitus or cigarette smoking. Most often, chronic
periodontitis is responsive to mechanical therapy. lt is no
longer referred to as adult periodontitis as this disease may,
albeit rarely, be seen in οhildren.

32. EτloLoGY AND clAsslFlcAτloΝ oF τHE PER|oDoNTAL DlsEASEs
Aggressive periodontitis. This category replaces what
used to be known as the early-onset periodontal diseases.
Localized aggressive periodontitis replaces the older term,
juvenile periodontitis, that is manifest by rapid and severe
attachment loss in the incisor and permanent first molar
regions. Actinobacillus actinomycetemcomitans is assoοi-
ated with a majority of cases. Τhese patients have shown
abnormalities in neutrophil function that may be related to a
hyperimmune effect of their macrophages. This type of
aggressive periodontitis has a fairly clear inheritance pattern.
Τhe loοalized ρattern affects 14 or fewer teeth, mostly
confined to the incisors and first molars. The generalized
form of aggressive periodontitis, formerly known as rapidly
progressive periodontitis, affects 15 or more teeth with
possible immunologic changes as well. lt is characterized by
episodic, rapid, and severe attachment loss. At times, this
disease may be difficult to control.
Periodontitis as a manifestation of systemic diseases.
\Λ/ith the exception of Down syndrome, most of the listed
genetic disorders are relatively rare. τhe Down syndrome
patient is a challenge because of the difficulty in maintaining
good oral hygiene. The prevalence and severity of periodon-
titis is high compared to unaffected siblings, and attaοhment
loss may appear in the deciduous dentition. As the roots of
teeth are often short, these patients may lose teeth earlier
due to the early onset of disease and the root anatomy.
What Are Some of the Distinguishing
Characteristics of Some of the Other Periodontal
Diseases and Conditions?
Necrotizing periodontal diseases. Τhis οategory includes
both necrotizing ulcerative gingivitis (NUG) and necrotizing
ulcerative periodontitis (NUP). NUG and NUP have been
classified together as they may be different stages of the
same disease. NUG is characterized by necrosis of the tips
of the interdental papilla with a pseudomembrane appear-
ance, pain, foul odor, spontaneous bleeding, and possible
fever and lymphadenopathy. There is no attachment loss
associated with NUG. Fusiforms and spirochetes, as well as
Prevotella intermedia,haνe been implicated in the etiology of
NUG. Significant contributing factors include stress, fatigue,
poor oral hygiene, smoking, and poor nutrition, basically
factors associated with immunosuppression. NUG and NUP
are also associated with HIV infection. NUP shares many of
the clinical characteristics of NUG along \Λ/ith attachment
loss.
Abscesses of the periodontium. Periodontal abscesses
are local infections of the gingival or periodontal tissues. The
etiology may be a foreign object such as a popcorn hull or
loose piece of calculus. This type of abscess is marked by
localized swelling and tenderness or pain. As the marginal
gingiva begins to heal ιΛ,ith treatment, the orifice to deeper
drainage of infection may be closed off. lt may be drained
either externally or through the wall of the periodontal pocket.
Periodontitis associated with endodontic lesions. Endo-
dontic and periodontal Iesions may coexist separately asso-
ciated with the same tooth or may communicate with each
other. Two separate lesions may coalesce or there may be a
root fracture or root perforation. Occasionally, an isolated
endodontic lesion may masquerade as a periodontal lesion,
such as in an isolated furcation defect on a mandibular first
molar. ln this case, proper endodontic therapy will heal the
furοation lesion as weΙl. ln a true combined lesion, the endo-
dontic therapy must be performed first in order for the even-
tual periodontal therapy to succeed as well.
Developmental or acquired deformities and conditions.
Most of the deformities and conditions classified here are
self-explanatory by name. Specific conditions such as
mucogingival deformities, edentulous ridge deficiencies, and
ocοlusal trauma are described elsewhere in Ιhis Manual.
How ls a Periodontal Case Type Formulated
Using the American Academy of Periodontology
Case Type System?
The case type refers to the level of disease sΘverity, not the
specific diagnosis. Case type may be applied to each type of
gingivitis and periodontitis (also see Chapter l).
Case Type 1: Gingivitis. lnflammation confined to the
soft gingival tissues only. All gingivitis, irrespeοtive of
the level of inflammation, is considered to be in this
category.
Case Type 2: Mild Periodontitis. This category signifies
the beginning of attachment loss, up to approxi-
maΙely 2o"/" of the attachment apparatus on the root.
τhere may be some pocketing and initial mobility.
Furcation involvement, when present, is confined to
a Class I involvement.
Case Type 3: Moderate Periodontitis. This category
signifies further loss of the attachment apparatus, up
to approximately 40% Ιo 45"/o. There is increased
bone loss, pocket depth, mobility, and furcation
involvement. Furcas may have Class ll involvement.
Case Type 4: Severe Periodontitis. There is severe
attachment loss, deep pocketing, mobility, pathologic
migration of teeth, and Class ll and possibly Class lll
f urcation involvement.
30

33. CHAPTER 4
GHAPTER 4: CLlNlcAL ASSESSMENT, DlAGNoSlS, AND τREATMENT
PLANNING
A comprehensive periodontal examination is necessary to
ascertain the presenting condition of the patient. ln addition
to examining the patient's periodontal status, information
regarding the patient's medical history, past dental history,
and a thorough soft and hard tissue examination will allow the
practitioner to formulate a complete set of diagnoses and a
comprehensive treatment plan.
What ls the Risk Assessment in the Examination
and Diagnosis of the Periodontal Diseases?
Risk is defined as the possibility of loss or iniury. While it is
well established that bacterial plaque is the etiology of inflam-
matory periodontal disease, there are many factors that
increase risk of periodontal attachment loss. These contrib-
uting factors may alter the host response to the bacterial
οhallenge. Contributing factors may be systemic or local in
nature. Uncontrolled diabetes, smoking, or the use of certain
medications may adversely affect periodontal health. Open
interproximal οontacts, caries, restorative overhangs, and
invasion of the bioΙogic width may contribute to periodontal
inflammation. The combination of these factors in coniunction
with the host response is responsible for the manifestations
of disease. As risk is assessed, the resulting periodontal
condition must also be assessed.
What Are the Components of the Clinical
Periodontal Examination? How ls Each
Component Completed?
Patient interview. The patient interview would elucidate the
patient's chief complaint and desired outcomes of treatment.
The patient's state of mind relative to dental treatment may
also be determined. Often, the patient will relate previous
dental experiences, both positive and especially negative
experiences that have shaped their perception of dentistry
and dental care. Soοial habits such as smoking and
frequency and technique of oral hygiene may also be
discussed.
Medical history. A complete medicaΙ history must be
obtained. The adage, "Never treat a stranger," is appropriate
to remember. Medical problems such as uncontrolled
diabetes, smoking, arthritis, uncontrolled hypertension, infec-
tious diseases such as hepatitis or HlV, allergies, bleeding
disorders, anticoagulation therapy, prophylaxis vs subacute
bacterial endocarditis, and certain medications may alter the
course or treatment of periodontal disease. A complete list of
medications must be obtained. lnformation on medications
may be obtained from the Drug lnformation Handbook for
Dentistry, Tth ed, a companion Lexi-Comp book to this
manual. Often, the dentist may be the only healthcare
provider who has a complete picture of a patient's medical
care. Αs more patients live longer and see multiple health-
care providers, polypharmacy (concurrent use of many
drugs) of both prescribed and self-administered medications
will be an increasing problem.
Dental history. The dental history will provide a picture of
both the progress of the current conditions and the patient's
previous efforts at maintaining their oral health. A history of
bleeding gums, change in tooth position, pain, halitosis or a
bad taste, oral habits, and previous periodontal care and
maintenance may all οontribute to a proper diagnosis and
determination of prognosis. Copies of previous records and
radiographs will also contribute to a more complete picture of
the patient's clinical condition.
Extraorat and intraorat examination. Both the external
surfaces of the head and neck and internal suι'faces of the
mouth are examined for abnormal growths, lumps, bumps, or
other signs of pathology. A complete bimanual and visual
examination will uncover unusual gro\Λ/ths or lesions for
further analysis. Baseline vital signs: Blood pressure, respira-
tions, and pulse should be obtained. Α complete muscle and
TMJ examination should be completed for patients with
temporomandibular dysfunction signs and/or symptoms.
Dental examination. Numbers of teeth, missing teeth, resto-
rations and their condition, caries, tooth position, and pulpal
status \Λ/hen indicated should all be recorded"
FIGURE 1. Severe Caries. A hard tissue and dental examination are part of the
comprehensive periodontal examination. Caries such as this can
contribute to the gingival inflammation sΦn here by harboring pΙaque.
Plaque score. There are many methods by which to quantify
plaque accumulation on the teeth. One of the simplest
methods is to use a plaque disclosing dye that visualizes the
plaque and then count the percentage of surfaces that have
plaque accumulated or those surfaces without plaque.
Sequential recording of plaque and bleeding scores may be
used to show patients improvement in their level of oral
hygiene and clinical health.
F|GURE 2. Disclosing Dye. Red dye may bΘ used to help visualize plaque for
the patient and practitioner.
-

34. cLlNlcAL ASSESSMENτ, DlAGNosls, AΝD TREAτMENT PLANN|ΝG
Bleeding scores. BΙeeding is still the most reΙiable indicator
of the presence of gingivaΙ or periodontal inflammation.
Bleeding on gentle skimming examines the health of the
marginal gingiva. Bleeding on probing examines the health at
the base of the sulcus or pocket. The amount of bleeding and
the time bet\,veen stimulation and the appearance of blood
may also be used to judge the severity of inflammation.
Bleeding scores may be οaΙcuΙated as a percentage of sites
around a tooth that bleed or do not bleed.
Periodontal pocket probing. Α periodontal pocket is a path-
ologic space between a tooth and pocket wall and its depth
measured from the gingival margin to the οlinical attachment
level. The depth of a periodontal pocket may only be
is measured by using a calibrated periodontal probe (see
Figures 3A and 38). The probe is inserted along the long axis
of the tooth into the pocket \,γith gent|e (approximately 25
grams) of force until resistance is met. τ\Λ/enty-five grams of
force is necessary to indent the pad of the thumb about 1-2
mm (see Figure 4). The probe is walked around each sur-
face of the tooth. Errors in probing may arise from stopping
the probe on a piece of calculus coronal to the base of the
pocket, using excessive probing force, using a probe greater
than 0.5 mm in diameter at the tip, the angulation of the
probe, and the health of the tissue.
F|GUΒE 3Α. PeriodontaΙ Probes. Periodontal probes come in a variety of
designs and markings. lt is important to have uniform instruments
throughout the practice as the same style probe may have different
dimensions from different manufacturers.
Figure 38. Periodontal Probes. Plastic probes may be used to examine around
implants. τhe probe on the left has PsB markings. τhe probe on the right
is a pressure-sensitive probe set at 25 g of force.
FlGUHE 4. Probe νιrith Gently Pressure. τhe correct probe force depresses the
ιhumb pad approximately 1_2 mm as seen here.
Εach tooth is examined at 6 locations: The mesiobuccal,
buccal, distobuccal, distolingual, lingual, and mesiolin-
gual surfaces. The probe may be angled approximately
10" on each interproximal surface so that the tip of the
probe is placed apical to the contact point of adjacent
teeth and may deteοt any interdental crater but, in most
instances, the direction of probing is paralΙel to the long
axis of the tooth. ln a healthy site, the tip of the probe
stops v/ithin the junctional epithelium and in a diseased
site it penetrates into the connective tissue. ln severe
disease, the probe tip may penetrate to the alveolar
bone. Therefore, the cliniοal probing depth is always
greater than the histologiο sulcus or pocket depth. Among
examiners, or from one time point to another, probing
acοuracy is only within + 1 mm (see Figure 5).
FlGURE 5. Probing' τhe periodontaΙ probe is angled to the intefproximal under
the contact point to dΘtect any interproximal pocketin9.
Recession measurements, Recession is the measurement
of the migration of the free gingival margin apiοal to the
cementoenamel junction of the tooth. Recession is measured
as a positivΘ value. The recession measurement added to
the probe depth at a particular site indiοates the amount of
periodontal attachment that has been lost at that site. When
the gingival margin is οoronal to the cementoenamel junction,
the recession measurement has a negative value.
Progressive recession from one examination to the next may
indiοate the need for surgical intervention.
δz

35. cHAPτER 4
Amount of attached gingiva. The attached gingiva is
measured from the projection of the base of the sulcus or
periodontal pocket onto the suι'face of the gingiva to the
mucogingivaΙ junction. Τhe amount of attaοhed gingiva may
be calcuΙated by Subtracting the sulcus/pocket depth from the
width of the gingiva from the free gingival margin to the
muοogingival junction' The mucogingival .junction may be
identified by sight, by moving the lip or cheek laterally and
detecting where the alveolar mucosa stops moving, or by
using the side of a periodontal probe or other instrument and
gently pushing in a coronal direction. The mucogingival junc-
tion is located where the tissue folds (see Figure 6).
FlGURE 6. ldentification of the mucogingivaΙ iunction. τhe alveolar mucosa
may be gently displaced in an occlusal direction to identΙfy ιhe muco-
ginqival
iunction.
Furcation examination. The furοation, the anatomic area of
a multirooted tooth where the roots diverge, may be exam-
ined with a furcation probe such as the Nabers 2N probe. The
furcation probe is curved with a rounded end (see Figure 7).
The furcation probe should not be confused with the pigtail
explorer in which the probe is shorter than a furcation probe
\νith a sharp tip.
F|GURΕ 7. Furcation Probes. τhe curued furcaιion prοbe has a long shaft and
blunted tip.
Furcations are probed by placing the tip of the Nabers
probe against the tooth and moving it in an apical direc-
tion. Τhe depression of the furca may be felt in this
manner. Maxillary premolars would have the mesial
furcation examined, maxillary molars would have the
buccal, mesial, and distal furcas examined, and mandib-
ular molars would have the buccal and lingual furcas
examined. The mesial furcation of maxilΙary molars must
be approached from the palate due to the shape of the
mesial and palatal roots (see Figures 8Α and BB). The
depth of the furcation may be measured with a perio-
dontal probe or specially marked furοation probe.
FIGURE 84. Examining Furcations.The buccal and lingual furcas are examined
in both a vertical and horizontal direction.
F|GURE 88. Examining Furcations. Τhe mesial furcation of the maxillary first
and second molars may only be detected from a palatal approach.
Glickman furcation classification:
Grade l: lncipient bone loss. The furcation probe
can feel the depression of the furcation
opening.
Grade ll: Partial bone loss (Cul-de-sac). The furca-
tion probe tip enters under the roof of the furca-
tion.
Grade lll: Total bone loss with through-andthrough
opening of the furcation. The furcation entrance
is not visible.
Grade lV: Α Grade lll furcation \Λ/here the furcation
entrance is visible.
Other furcation systems may measure the horizontal
(Lindhe and Nyman) or vertical (Tarnow and FletcheQ
οomponents of furcation involvement.
Mobility. Τhe movement of a tooth in its socket as a result of
an externaΙly applied force. Mobility is measured by the
examiner pushing the tooth gently in a faciolinguaΙ direοtion
-

36. cltΝlcAL AssEssMENτ- DιAGNosls" AND τREAτMENτ PLANNlNG
using the blunt ends of two metal instruments, usually a
mirror handle and handle of a periodontal probe. The use of a
finger is not acceptable when assessing mobility. Mobility
may be recorded on a 0-3 scale, although this scale may be
modified by individual practitioner preference.
Mobility scale:
0: No mobility
1: Mobility that is perceptible
2: Mobility <1 mm faciolingually but no apical move-
ment
3: Αpica! movement as well as lateral movement >1
mm
FIGURE 9. Mobility is measured using gentle force and the handles of two
instruments. A finger should not be used to measure mobility.
Fremitus. A palpable δr visible movement of a tooth when
subjected to occlusal forces. Fremitus may be deteοted both
in centric occlusion and in lateral excursive movements
(lateral fremitus). Fremitus may be detected by placing a
fingertip on the tooth in question or by looking as the teeth
come together or are moved. lt is easier to detect fremitus of
the maxillary teeth than the mandibular teeth. Fremitus is
recorded aS +. τhere is no numerical fremitus scale.
Occlusal analysis. Centric relation, CR-CO slide, excursive
contacts: The centric relation contact may be obtained using
the chin point manipulation, bimanual manipulation, or the
power bite technique. The CR-CO sΙide and excursive
οontacts may be detected using articulating ribbon or
occlusal indicator wax. lf these contacts, particularly
nonworking οontacts, are associated with occlusal pathology
(mobility, fremitus, widened PDL on radiographs), an occlusal
adjustment to minimize excursive forces on each tooth may
be indicated.
What lnstruments and Materials Are Necessary
for a Complete Periodontal Assessment?
Mouth mirror. A front surface mouth mirror is necessary to
see areas that may not be accessible by direct vision, reflect
the lips, buccal mucosa, and tongue, and in the assessment
of mobility. The mirror may also be used to depress the
tongue during the soft tissue examination.
Periodontal probe. The calibrated periodontal probe should
have a tapered shaft approximately 0.5 mm in diameter at the
tip. The tip may be smooth or have a small ball at the end
(PSR probe, Maryland/Moffitt probe) useful for detecting
calculus and root irregularities. ln any practice, all periodontal
probes should be of the same design and from the same
manufacturer in order to ensure as much standardization as
possible (see previous Figure 3).
Furcation probe. Furcations are best examined using a
furcation probe suοh as the Nabers 2N or Hamp probe. The
lf23 exρlorer, periodontal probe, and pigtail explorer are not
properly shaped to adequately explore a furcation (see
previous Figure 7).
Articulating ribbon and articulating ribbon forceps
(holder), occlusal indicator wax. Occlusal contacts must be
highlighted in order to be properly identified. This may be
done either with articulating ribbon or occlusal indicator wax.
Occlusal indicator wax has the advantage of being
completely perforated only where opposing teeth are in
contact. Often, articulating paper leaves stray marks that
makes proper interpretation more diffiοult.
What ls Necessary for a Periodontal
Radiographic Examination?
Α periodontal radiographic examination consists of a full
mouth series of radiographs including vertical bitewing films.
A long cone paralleling technique is utilized and the apices of
all roots must be visible. ln many instances, particularly when
there is significant bone loss or the films are misaligned,
standard horizontal bitewing films do not adequately eΧpose
the interproximal bone between the posterior teeth. Bone
loss, widened periodontal ligaments, caries, calculus, root
proximity, and unusual radioluοencies and radiopacities may
be detected. The true topography of vertical osseous defeοts
cannot be determined by radiographic examination alone.
F|GURΕ
'10.
vertical bitewing radiographs, seen here with well-executed
posterior periapical films, will show the interproximal crest of the alveolar
bone that is often missed on horizontal bitewing films.
VVhat Is a Clinical Periodontal Screening
Examination?
The Periodontal Screening and RecordingτM (PSR) Examina-
tion \Λ/aS developed in order to streamline the data gathering
and recordkeeping for the screening periodontal examina-
tion. The PSR Exam is patterned after the Community Perio-

37. CHAPτER 4
dontal lndex of τreatment Needs (CPITΝ) of the World
Health organization (\Λ/Ho). This exam is completed with a
periodontal probe that has a ball at the tip and a black or
colored band from 3.5-5.5 mm. While six sites are examined
per tooth, a score for eaοh sextant is determined and
recorded.
PSR Godes:
Code 0: The deepest probing in the sextant is less
than 3.5 mm (the colored band on the probe
remains completely visible) and there is no
bleeding, οalοulus, or defeοtive restorations. The
patient needs preventive care only.
Code 1: The colored band on the probe remains
completely visible. There is no calculus or
defective restorative margins but there is
bleeding at the gingival margin. Plaque must be
removed and the patient instructed in proper
oral hygiene.
Code 2: The colored band on the probe remains
completely visible. There is detectable calculus
and/or defective restorative margins. Treatment
consists of plaque and caΙculus removal, correc-
tion of plaque retentive factors, and oral
hygiene instruction.
Code 3: The colored band on the probe is partially
submerged in the pocket. This indicates a
comprehensive periodontal examination and
charting for the sextant in question. Two or
more sextants with a score of 3 indicates a full
mouth examination and chaιting.
Code 4: The colored band on the probe is
compΙete|y submerged at one site. This indi-
οates a comprehensive full mouth periodontal
examination and charting.
Code
*:
An asterisk is added to the numerical
sextant score when furcation involvement,
mobility, mucogingival problem, or recession is
present.
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How ls Periodontal Examination Data Recorded?
The periodontal examination data may be recorded on paper
or saved in a digital format. There are many examples of
periodontal charts. One example may be seen in Figure 11.
What Adiunctive Techniques Are Available to
Help in the Diagnosis of the Periodontal
Diseases or Other Periodontally-Related
Diseases or Conditions?
Bacterial culturing and sensitivity. Bacterial culturing is
considered to be the "gold standard" of bacterial identifica-
tion. ldentification of bacteria associated with ongoing perio-
dontal inflammation is indicated when the use of systemic or
locally delivered antibiotics is contemplated. Culturing
requires the harvest of live bacteria from the pocket or
pockets in question, placing these bacteria in a suitable
transport media, and then shipment of the sample to a micro-
biological laboratory for analysis. Bacteria identified are those
that survived the transport and are οultivable. lt is assumed
that the identified bacteria are associated with the periodontaΙ
inflammation. An estimation of antibiotic sensitivity and resis-
tance may also be determined with this method. Bacterial
samples must be harvested on a Monday, Tuesday, or
Wednesday and sent by overnight delivery to the selected lab
in order to maximize the numbers and variety of cultivable
species. Reports are generally available about 7 days after
delivery to the laboratory.
DNA probe analysis. DNA probe analysis uses special tech-
nology to identify bacterial DΝA within a sample. The advan-
tage to this technique is that time is not a factor as live
bacteria are not necessary for analysis. Smaller absolute
numbers of bacteria may be detected with this method.
Probes identify ActinobacilΙus actinomycetemcomitans,
Bacteroides forsythus, Campylobacter rectus, Εikenella
corrodens, Fusobacterium nucleatum, Porphyromonas gingi-
valis, PrevoteΙΙa intermedia, and Treponema denticola' AnΙi-
biotic sensitivity testing is not possible with this technique.
lnterleukin-1 (lL-I) genotype testing. This test, the Perio-
dontal Susceptibility τest (PSττ") determines if a patient
possesses a combination of alleles in two interleukin-1
genes. A specifiο interleukin-1 genotype is associated with
increased production of lL-1 in periodontal inflammation with
subsequent increased attachment loss. Smoking significantly
increases the amount of attachment loss in patients found to
have an increase in lL-1 production.
Enzymatic meιhods of bacterial identification. While the
analysis of gingival crevicuΙar fluid for enzymes related to
specific bacteria or for the presenοe of infΙammatory media-
tors is of scientific interest, there has yet to be οonsistent
practiοal application developed for this technology.
Biopsy. The biopsy is used when a sample of tissue is
needed for histopathological analysis. Biopsies may be inci-
sional, where only a piece of the lesion and adjacent normal
tissue is removed, or excisional, where the entire lesion is
removed with healthy tissue margins. The biopsy should be
done as atraumaticaΙly as possible to ensure intact tissue for
analysis. Tissues to be submitted for immunofluorescence
testing to rule out the vesiculobullous diseases must be
placed in special fixative such as Michel's solution.
Nikolsky sign. Apparently normal epidermis or gingiva may
be separated at the basal layer and rubbed off when pressed
with a sliding motion. This is done using the end of a mirror
handle or a moist οotton swab. Τhis technique is helpful in
cP000709 ΦΦΦs*
FIGURE 1 1. Periodontal Chart, All clinical information may be recorded on one
well-designed chart. The chart may be a paper or electronic record.

38. Ξ
cLlNlcAL AssESsMENτ. D|AGNosls. AΝD TREAτMENτ PLANN|NG
identifying the vesiculobullous diseases. Distinction among
the diseases may be made only by biopsy.
Exfoliative cytology. This technique may be used to identify
abnormal cells on the surface of a lesion. Several commer-
οially available tests can be used to sample suspicious-
looking red lesions.
What Are the Dento-Legal Considerations of a
Complete Examination and Diagnosis in
Periodontal Therapy?
The patient record should contain a complete periodontal
charting, diagnosis, and treatment plan for all patients with
periodontal disease. Studies have shown that fe/er than
20% ot records in general practice οontain these necessary
elements. lt is significantly easier for a practitioner to support
claims of a complete examination, diagnosis, treatment, and/
or specialty referral if this documentation is present. "lf it isn't
written down, it didn't happen," and that a "Short pencil is
wofth more than a long memory," should be remembered at
all times.
PERIoDoNTAL TREAτMENτ PLANNING
Periodontal diagnosis and treatment planning are critical
steps in the process of periodontal disease management.
Diagnosis and treatment planning are the direct outcomes of
a periodontal assessment. An accurate diagnosis and an
effective treatment plan should be based upon a comprehen-
siye assessment of periodontaΙ signs and patient Symptoms.
The aft of decision-making in periodontal therapy involves a
synthesis of 1) the cΙinicaΙ experience of the therapist, 2) the
technical ability ot the therapist, 3) intuition, 4) the experi-
ences of others as recorded in texts or presented in profes-
sional forums, and 5) evidence-based thinking.
What ls a Working Diagnosis? How Does a
Working Diagnosis Differ From a Differential
Diagnosis?
A working diagnosis is the "pencil" diagnosis generated by
the cΙiniοian that is based upon the scientific signifiοance of
the signs and symptoms recorded during the comprehensive
examination. lt is the οlinician's best estimate of the patho-
logic process, the etiologic factors for that process, and the
morbid outcomes of the process present at the time of the
examination. Τhe working diagnosis is the basis of the
patient's initial treatment plan. lf later assessments are made
at the re-evaluation of initial therapy, or for that matter,
assessments are made at any time during therapy indicate
that the working diagnosis may be incorrect, the working
diagnosis may be changed to reflect the new information.
A differential diagnosis is one that includes t\ivo or more
possible processes that may be consistent with initial clinical
assessments. Rather than commit to one νvorking diagnosis,
the clinician may choose to provide a differential diagnosis
and either perform or request additional diagnostic testing. ln
this instance, the clinician fully expects that a working diag-
nosis will emerge from the differential diagnosis.
The initial treatment plan is based upon the periodontal disease
identified in the working diagnosis. The treatment plan
addresses itself to each etiologic agent in a logical sequence.
Pertinent etio|ogic factors that are not addressed in the treaι
ment plan result in undertreatment and failure of therapy.
The treatment of etiologic factors that either do not exist, or
have been incorrectly identified by the clinician, leads to over-
treatment, which prolongs treatment, or in the οase of an
incorrect assessment, undertreatment, which prevents
disease οontrol. Both oveftreatment and undeιtreatment are
outside the standard of care for any patient. Assuming that
the clinical assessments are complete, control of the etiologic
factors should effectively manage the periodontal disease
(identified in the working diagnosis). Simply stated, οontrol of
etiologic factors translates to disease control.
SAMPLE PERIODONTAL TREATMENT PLANS
While all periodontal treatment plans share a common goal
(ie, control of inflammatory periodontal diseases), the
path\Λ/ay to that goaΙ from patient to patient is rarely the
same. For discussion purposes, models of treatment plans
will be presented for each of the three basic periodontal
disease categories: Gingivitis, periodontitis, and occlusal
traumatism.
Gingivitis. The presence or absence of dentaΙ plaque as the
primary etiologic factor distinguishes the two major catego-
ries of Class I Gingival Diseases. There are four categories of
dental plaque-induced gingival diseases and eight categories
of nonplaque-induced gingival lesions. Since the majority of
gingival diseases seen in a dental practice are related to the
presence of pΙaque, the framework of a treatment plan
designed to manage these common disorders is included
here.
The correct working diagnosis is the critical first step in the
treatment planning process. The therapeutic "mindset" of the
provider should be based upon that diagnosis. For example,
a diagnosis of gingivitis associated with dental plaque
only should ordinarily not include resective periodontal
surgery, but a diagnosis of drug-influenced gingival
enlargement might include a gingivectomy, apiοally posi-
tioned flaps, or systemic antibiotics as a therapeutic
possibility if the gingival enlargement persists following
nonsurgical mechanical therapy and/or attempts to modify
the patient's medication protocol.
AcTlvE TREATMENτ oF A DENTAL
PLAQUE-INDUCED GINGIVAL DISEASE
Working diagnosis. Gingivitis associated \Ιvith dental plaque
only.
FIGUFIE 12. Gingivitis Associated livith Dental Plaque Only. Severe gingivitis
that displays the clinical signs of necrotizing ulcerative gingivitis is
present in the maxillary incisor and canine area.
JO

39. cHAPτER 4
The patient is a well-kempt 26-year-old systemiοally healthy
female. She sees a physician annually and has been on oral
contraceptives for 2 years. She is married and works as a
vice-president in a local banking institution. Her chief
complaint is "bleeding gums." She also presents with severe
gingival inflammation consistent with localized necrotizing
ulcerative gingivitis (NUG) around the maxillary right incisors
and canine. With treatment, the prognosis for keeping her
periodontium in health and comfortable function for a lifetime
is good to excellent.
TREATMENτ PLAN
lnitial τherapy
ο Presentation and discussion of diagnosis and treatmenι
plan.Ιhis step will ensure that the patient understands
her condition and the rationale of therapy. Because so
much of periodontal therapy requires patient involvement
and behavior modification, understanding her disease will
be critical. Commonly, points made here will need to be
re-enforced during the course of therapy.
. Medical consuΙtation. Probably unneοessary in this case.
. Oral physiotherapy. The patient's methods of plaque
control are evaluated and, as probably will be the case,
modifications wiΙl be made. Special emphasis should be
placed on improving plaque control in the maxillary right.
o Coronal debridement. Hand and power-driven scalers νvill
be used to remove coronal calοulus. Since this is a gingi-
vitis case, there will not have been loss of periodontal
attachment to permit root planing.
. Correction of plaque and food retention factors such as
overhanging restorations and open contacts. The clinical
croνvns will be polished with a fluoride-containing mild
abrasive.
. Re-evaluation of inΙtial therapy. After a minimum of 4
weeks (the time for healing and maturation of the dento-
gingival junction), the patient is re-examined and the
results of that examination will be compared νvith those
recorded at the initial examination. Decisions about the
working diagnosis, continuation of periodontal therapy, or
a periodontal maintenance program will depend upon the
answer to the following two questions:
Are thΘre any persistent signs and symptoms of
gingivitis present?
lf so, is there anything that can be done to improve
this patient's gingival health?
lf the answer to both questions is"no", the working diagnosis
is confirmed. The patient's final diagnosis is then: Gingi-
vitis associated with dental plaque only with local con-
tributing faοtors.
lf, however, the answer to the both questions is "yes", then
considerations for improving the patient's oral hygiene, anti-
microbial therapy in the form of antimicrobial mouthrinses,
additional correction of plaque retentive factors, and discus-
sions concerning the effect of oral contraceptives on gingival
health might be appropriate. A gingivoplasty in the maxillary
incisor/canine area may be required if the gingival deformities
continue to be worrisome.
F|GUBE 13. Gingivitis Associated ι,vith Dental Plaque onΙy After Plaque
control, scaling, and Polishing. Residuaι disease and deformities may
require local deΙivery of antibiotic, additional emphasis on plaque control'
and/or gingivoplasty,
AcτlVE τREATMENT oF cHRoNlc PERloDoNτlTls
Periodontitis. Periodontal diseases and conditions that
feature loss of periodontal attachment include chronic perio-
dontitis, aggressive periodontitis, periodontitis as a manifes-
tation of systemic disease, necrotizing periodontitis, and
periodontitis associated with endodontic lesions. Since the
majority of gingival diseases seen in a dental practice are
related to the presence of plaque, the framework of a treat-
ment plan designed to manage these common disorders is
included here. Since chronic periodontitis is a relatively
common disorder, a typical treatment plan for chronic perio-
dontitis will be presentΘd here.
Working diagnosis. Generalized moderate chronic perio-
dontitis with occlusal traumatism.There are >30% of perio-
dontal sites with >3-4 mm loss of periodontal attachment.
Generalized mobility and fremitus patterns are present.
There are areas of gingival recession.
FIGURE 14. Generalized Moderate οhronic Periodontitis lΙvith occlusal τrau-
matism. τhe patient has a 2s-pacιΦear history of cigarette smoking,
Results of a recent medical evaluation were unremarkable.
τhe patient is a robust 47-year-old male \ivho works as a
construction foreman with a chief complaint of "loose
teeth." He reports that the outcomes of a recent physical
examination \Λ/ere unremarkable. He has been divorced
for 3 years and has a 25 pack/year history of cigarette
smoking. His dental treatment has been infrequent. His
last dental appointment was for a "cleaning" four years
ago. \Λ/ith treatment and regular periodontal mainte-
1.
2.

40. cllNlcΔL ΔssEssMENτ- DlAGNοsls- AND τREAτMENτ PLANN|NG
nance, the prognosis for keeping his dentition in health
and comfortable function is excellent for 5 years and
good forl0 years.
TREAτMENτ PLAN
lnitial Therapy
. Presentation and discussion of diagnosis and treatment
plan. Ιhis step will ensure that the patient understands
his condition and the rationale of therapy. Because so
much of periodontal therapy requires patient involvement
and behavior modification, understanding his disease will
be critical. Α concept of co-therapy bet\Λ/een dental health-
care professionals and the patient is stressed because of
the expected lifetime duration of active and maintenance
therapy. The timing and sequence of any endodontic
therapy, minor tooth movement, and/or restorative
dentistry is presented at this time as well. The patient
should be presented with the rationale for periodontal
surgery that will most likely be necessary. Commonly,
points made here will need to be re-enforced during the
course of therapy.
o Medical consultation. Because of the recent physical
examination, it may not be necessary to send the patient
for an evaluation. Α letter to the patient's physician
requesting a copy of recent medical laboratory test
results for his dental record is appropriate. The letter
could also describe the patient's periodontal condition,
outline the periodontal treatment plan, and request any
pertinent medical recommendations.
. Counseling in methods for smoking cessation. Ιhe
patient needs to understand clearιy how continued
smoking u/ill abrogate the effects of periodontal therapy.
Τhe letter to the patient's physician might solicit strate-
gies for smoking cessation. Because smoking is such a
significant etiologic factor, smoking cessation will be a
major element in infΙammatory disease control for this
patient.
. Oral physiotherapy. The patient's methods of plaque
control are evaluated and, as probably will be the case,
modifications will be made.
. Scaling and root planing. Hand and power-driven scalers
will be used to remove coronal and radicular calculus.
Since this is a periodontitis case, there will have been
loss of periodontal attachment.
Because of anatomical limitations (probing depths >4
mm, furcation invasions, root grooves etc), it is under-
stood that surgical access may be required to complete
root debridement. Thermal sensitivity is a common
outcome of scaling and root planing. Desensitizing
agents may be prescribed, but often, "tincture of time" is
adequate.
. Correction of plaque and food retention factors such as
overhanging restorations and open contacts. The clinical
cro\Λ/ns will be polished with fluoride containing mild abra-
sives and desensitizing agents.
. Re-evaluation of inflammatory disease controι' After a
minimum of 4-6 weeks (the time for repair of the dento-
gingival junction), the patient is re-examined and the
results of that examination are compared with those
recorded at the initial examination. This is a critical stage
in treatment as decisions about the working diagnosis
and continuing active therapy are made depending upon
the answers to the following questions:
1. Are there any persistent signs and symptoms of
gingival inflammation or debris present?
2. lf so, is there anything short of periodontal surgery
that can be done to improve the conditions?
3. ls there any residual tooth mobility/fremitus?
lf the answer to the first and second question is "no" and the
ansνver to the third question is "yes", the patient's working
diagnosis o't generalized moderate chronic periodontitis with
occlusaΙ traumatism iS Supported, and treatment should
proceed to the occlusal therapy phase.
lf, however, the answer to the first and second question is
"yes"' then considerations for improving the patιent's oral
hygiene, refining scaling and root planing, instituting antimi-
crobiaΙ therapy, additional correction of plaque retentive
factors, and discussions concerning progress made in
smoking cessation might be appropriate. Because any
residual inflammation may contribute to mobility/fremitus, it is
inappropriate to proceed to occlusal therapy vι/ith persistent
gingival inflammation. The working diagnosis cannot be
confirmed or, for that matter changed, without optimal
nonsurgical inflammatory disease control.
occLUSAL τHERAPY
.
Persistent mobility and fremitus patterns should be re-
evaluated following inflammatory disease control. lf
present, selective grinding of nonworking and working
functional tooth contacts that are contributing to occlusal
traumatism should be adjusted. Ιn addition, parafunc-
tional habits of compulsion, such as bruxism, should be
controlled with occlusal appliance therapy. Force control,
like inflammatory disease control, is an ongoing process
in both active and maintenance periodontal therapy.
RE-EVALUAT|oN oF lNlτlΑL THERAPY
.
After all of the items on the initial therapy treatment plan
have been addressed, decisions about the working diag-
nosis and the need for additional treatment are made
based upon the ansνver to the following questions:
'l . ls there any additional therapy required to control
this patient's periodontitis?
2. ls there anything that needs to be done for this
patient other than periodontal surgery to controι his
periodontitis?
3. Are the outcomes of inflammatory disease control
and force control therapy consistent with the
working diagnosis of generalized moderate chronic
periodontitis with occlusal traumatism?
lf the ans\Λ,er to the first question is "no" and the ans\iver to
the third question is "yes", no additional active treatment is
required and the patient should be placed in periodontal
maintenance. Question 2 is irrelevant.
lf the answer to Questions 1 and 3 are both "yes", and the
ansνver to Question 2 is "no", treatment should progress to
the surgical phase.
38

41. CHAPτER 4
FIGURE 1 5. Generalized moderate chronic periodontitis with occlusal trauma-
tism following initial inflammatory disease control and occlusal force
control. The patient has stopped smoking and should begin the surgical
phase of his treatment plan.
lf the answers to the questions 1 and 2 are "yes", nonsurgical
inflammatory and force control issues may need to be revis-
ited before surgery.
lf at any time that the answer to question 3 is "no", the
vvorking diagnosis should be modified to read refractory
chronic periodontitis or be redesignated as one of the other
οlasses of periodontal diseases or conditions.
sURGlcAL THΕRAPY
The primary purpose of periodontal surgery is to provide
access to root surfaces and osseous defects. The type of
surgical access to root surfaces and bone (eg, apically
positioned flaps, replaced flaps, or modified \iηlidman
flaps) will be determined by what will be done to manage
osseous defects. The options are: Resective osseous
surgery, regenerative surgery, or open flap curettage
(osseous surgery by "ventilation").
The surgical treatment plan should be completed within
3-6 months following initial therapy. Patient compliance
with the surgical schedule and financial commitments
must be understood at the onset. The periodontal surgery
should be performed by a clinician trained and experi-
enced in all aspects of periodontal surgery.
The surgical treatment plan should be based upon the
needs of the case and not on the expefiise or parochial
biases of the surgeon.
onοe healing iS complete, and the periodontitis is
perceived to be under controι, the patient should be
placed in periodontal maintenance.
PERIoDoNTAL MAlNτENANGΕ THERAPY
Periodontal maintenance is performed at an interval
deemed appropriate for the patient's response to initial
and surgical therapy.
Procedures included in periodontaι maintenance are:
Review of mediοal history and an update of medications,
a review of dental history, an update of radiographs, an
intra-oral and extra-oral hard and soft tissue examination,
a dental examination, a periodontal examination, a perio-
dontal debridement with scaling and root planing as indi-
cated, an evaluation of the serviceability of occlusal
appΙiances' and polishing with a stannous fluoride
containing dentifrice.
During the course of periodontaΙ maintenanοe therapy,
areas of deteriorating periodontal health may make it
necessary to initiate active treatment in the form of local
or systemic antibiotics, periodontal surgery, and/or
occlusal therapy.
While periodontal maintenance therapy is performed by
dental hygienists, it is the responsibility of the treating
dentist to assure that the patient's periodontitis is
οontrolled, and that relapses in disease activity are
managed aggressively.
AcTlvE τREAτMENT oF occLUSAL τRAUMATιSM
Occlusal trauma is defined as the "injury resulting in tissue
changes within the attachment apparatus as a result of
occlusal forces." Occlusal traumatism is the "loading of teeth,
usually off axis, that is of sufficient magnitude to induοe
changes to the teeth or supporting structures. The changes
may be temporary or permanent." Conceptual|y, occΙusal
traumatism is a disease, not a condition, as it has a major
etiologic factor (force), a pathologic process (inflammation
within the periodontal Ιigament), and a morbid outcome
(destruction of the attachment apparatus), and an array of
clinicaΙ signs and Symptoms (pain, mobility, fremitus, patho-
logic migration etc).
τREATMENT PLAN
. Τhe management of forces acting on teeth cannot be any
more arbitrary than the management of periodontal
inflammation. The key to occΙusal therapy is the working
diagnosis and the etiologic factors, which deliver the
forces and produce occlusal trauma (lesion of trauma
from occlusion).
. Force control is achieved by limiting the duration and the
strength of traumatogenic forces. A comprehensive plan
of occlusal therapy wilΙ include any or aΙl of the following
items:
1. Occlusal adiustment by selective grinding of
occlusal surface
2. Occlusal appliances such as "night guards"
3. Orthodontics
4. Restorative dentistry
5. Tooth removal (as a last resort)
ln the case of a patient with a working diagnosis of chronic
periodontitis with occΙusal traumatiSm, therapy would be inte-
grated into the initial therapy treatment plan.
PERIODONTAL PROGNOSIS
The general goal of periodontics is the preservation of teeth
and the dentition in health and comfortable function for as
long as possible. Α prognosis is an estimate of hoνv long that
goal can be achieved. lt is nothing more than an educated
guess based upon the presentation of the case and the
perceived impact local and systemic risk (prognostic) faοtors
on its future. Αs it iS \Λ/ith periodontal diagnosis and treatment
planning, a prognosis is weakened when assessments are
incorrect or incomplete.
39

42. cLlNlcAL AssEssMENτ. DlAGNosls. AND τBEAτMENτ PLANN|NG
What ls Meant by Prognosis? ls a Prognosis
Related to the Oltcori'e of a Disease Witn
r A "poor" prognosis will suggest that the goal is
Treatment or Without Treatment?
unachievable for any significant length of time and
that major changes in periodontal health will probably
A prognosis is a forecast of the probable result of an attack of
occur'
a disease - the prospect as to recovery from a disease as
indicated by the nature and symptoms of the (#ftirδ '
A.hopeless" prognosis will offer no chance of main-
case. ln periodontiοs, a prognosis \,lι,ill οommonly n"
"ircrΞi
taining the dentition in health and comfortable func-
for individua| teeth and the complete dentition depending
τlon'
upon whether or not treatment is rendered.
A periodontal prognosis \ivill be rooted in assessments of the
Α prognosis is usually expressed in terms of a finite time initial status of the case (eg, degree and extent of inflamma-
period during which the goal of health and comfortable func- tion, pocket depths, attachment loss, the amount of bone
tion can be maintained. Typically, a 5- to 1O-year timeframe loss, the number of teeth lost due to periodontal disease, and
is typical of a "long-term prognosis", while a 2- to s-year time- the severity of mobility/fremitus patterns). To this information,
frame is typical of a "short-term prognosis". Within each time- an overlay of the systemic, local, and intangible risk (prog-
frame, graded qualitative estimates of success for achieving nostic) factors will be added.
the goal are also made. For example:
Clearly, there is little true science involved in formulating a
o An
,,excellent,,prognosis
will forecast that goal with no
prognosis- Too many prognostic factors are out of the direct
significant change in periodontal health.
control of the therapist and the patient. ln addition, the
predictability of treatment outcomes is almost always weak-
. A
,,good,,
prognosis will forecast that goal with only
ened by the severity of the disease. A prognosis can be
minor changes in periodontal health.
helpful to the patient in decision-making vis-a-vis time and
costs of treatment. ln every case, the patient should/must
. A "fair" prognosis will forecast that goal, but changes understand that for anything other than a "good" prognosis or
in periodontal health might occur that will either a "poor'' prognosis, forecasts for treatment outcomes can be
downgrade or reduce the timeframe of the forecast. extremely unreliable.
40

43. CHAPτER 5
CHAPTER 5: PREVENTION OF DISEASE AND THE MATNTENANCE OF
HEALTH
Prevention of disease and the maintenance of health once
the disease process has been controlled are the corner-
stones of periodontal therapy. As plaque is the primary etio-
logic agent of gingivitis and periodontitis, personal plaque
control is the s,ne qua non of dental therapy. A patient must
be able to control the etioΙogiο agents of both caries and
periodontal disease on a daily basis for therapy to be
successful. As plaque can reorganize on the teeth and sub-
gingivally within 24 hours, daily plaque removal is essential.
What Are the Components of Personat PIaque
Control?
Personal plaque control consists predominantly of the
mechanical disruption of plaque on the facial, lingual, and
interproximal surfaces of the teeth. This disruption may be
achieved using a manual toothbrush, powered toothbrush,
floss, interdental brush, specialized brushes, and other
instruments. Antimicrobial agents such as chlorhexidine or
the essential oils may be used as adjuncts to mechanical
plaque removal.
VVhat Methods of Toothbrushing May Be
Recommended to a Patient?
The toothbrush can remove plaque on accessible surfaces.
No matter what toothbrushing method is chosen, the manual
toothbrush should have soft nylon bristles and a small head,
either a child's size brush or a size 20 or the equivalent. A
smaller brush head allows the brush to be properly adapted
to the irregularities of tooth anatomy and arrangement. A
SmalΙer head also lessens the potential for activating the gag
reflex and may reach posterior surfaces more comfortably
and effectively than a larger headed brush. For use in deli-
cate areas, the bristΙes may be softened by running the brush
head under hot νvater before use.
There are many toothbrush designs available today. Each
brush manufacturer presents claims νVhy that particuΙar brush
is superior to others. ln reality, brushes of many different
designs will effeοtively remove plaque when used properΙy.
Bass Method. The bristles of the toothbrush are placed at a
45" angle to the tooth surface at the gingival margin, trying to
get the bristles into the gingival sulcus. The brush is then
moved in short back-and-forth motions for about 20 strokes.
The brush head is then moved around the arch, both on the
facial and lingual surfaces. The occlusal surfaces are cleaned
by manipulating the bristle ends into the pits and fissures of
the tooth crown. This is the currently preferred method of
manual brushing.
Other Methods:
Modified Stillman Method. The brush bristles are
resting partially on the cervical area of the teeth and
partially on the gingiva pointing toward the gingival
margin. Pressure is applied to the brush to cause the
gingiva to blanch. The brush head is then moved in short
back-and{orth strokes with the brush moving οoronally at
the same time. The sides of the bristles, instead of the
bristle tips, are used to disrupt the plaque. This method is
classified as a "roll" technique.
Charters' Method. The brush is placed against the
surface of the teeth with the bristles pointing away from
the gingival margin. The back-andJorth motion is a
massaging stroke for the gingiva. This method may be
used for gentle plaque removal.
What Methods of Interproximal Cleaning May Be
Recommended to a Patient?
For the patient with no or minimal attachment loss, flossing is
the interproximal technique of choice. There is no clear-cut
difference in effectiveness between waxed and unwaxed
floss. lt should be stressed to the patient that fιoss be used in
an up-and-down motion, not in a "shoeshine" motion. Many
patients will revert to improper technique even after proper
instruοtion. Dental tape, basically a wider version of floss,
may also be used.
Once attachment loss has occurred and root concavities are
accessible, floss loses its effeοtiveness. lnterproximal
brushes, toothpicks, and rubber tips may be used in these
circumstances. With moderate to severe attachment loss, a
manual brush and an interproximal brush will outperform the
manual brush and floss in plaque removal.
Interproximal brushes may be cylindrical or conical in shape.
The advantage of an interproximal brush is that the bristles
may be worked into root concavities and furcation areas
exposed by attachment loss. The interdental brush should be
used in both a back-and{orth and rotary motion to ensure
maximum adaptability of the bristles. The brush should be
used from both a facial and lingual or palatal approaοh to
remove all plaque.
FIGURE 1. lnterproximal Brushes. Either cylindrical or cone shaped are more
effective in removing plaque that is lodged in the exposed concavities or
furcations of tooth roots.
The end-tuft brush (Figures 2Α and 28) may be used on
interproximal surfaces \Λ/here there is no adjacent tooth and
on the distal areas of the most posterior teeth. With a bend in
the handle and tapered bristles, the end-tuft brush fits almost
perfectly in the distal furcation of the most posterior maxillary
molar.
-

44. PREvENτloNoFDl
manual brushing along with appropriate interproximal
cιeaning with floss or an interproximal brush'
Powered brushes may be useful as a motivationaι tool to
assist patients in cleaning their teeth on a daily basis' These
brushes may also assist patients with arthritis or other debili-
tating conditions that make holding or manipulating a manual
brush difficult or impossible. While there are several distinc-
tive designs of po\Λ/ered brushes, each design has its strong
points and weaknesses, but all of these brushes perform at
similar levels of effectiveness.
FlGURES 2A and 2B' End-Tuft Brush. τhe end-tuft brush, particu|ar|y When the
'- -
nanαε is υent approximately 3o", is quite effective at removing
PlaqΨ9 9η
iii;'li;gr;i;r;i;ces of th6 mandi6ular anterior teeth and the distal
surtaces οf the most posterior teeth.
What Role Do Powered Toothbrushes Have in
Personal Plaque Control?
F|GURE 38. τhe smalι head of this powered brush adapts w
smoolh surface and interproximal areas ot teeth'
What Antimicrobial Agents Can Assist in
Controlling PIaque ani Gingival lnflammation?
When seleοting a chemotherapeutic agent, it is important to
distinguish bδtween the ability to remove plaque and
substΞntiated evidenοe of a therapeutic effect' Many
mouthrinses οan reduce the amount of plaque over rinsing
with water, but wiihout a positive therapeutic effect, the justifi-
cation for recommending such an agent is minimal'
To date, two basic agents have been shown to have a signifi-
cant therapeutic effect on gingivitis over a 6-month period'
Chlorhexidine gluconate, O.12Yo' in an alcohol-containing
vehicle, now aviilable in generic as well as brand name form'
and phenolic compound/essential oil-based mouthrinses can
be used to help control gingivitis. Chlorhexidine kills bacteria
rn sifu when used for 30 seconds twice daily' Side effects
include increased calculus formation, staining of teeth and
restorations, and altered taste. Caution should be taken \νhen
recommending a chlorhexidine rinse for a patient with
composite resin restorations.
The essential oils, thymol, menthol, and eucalyptol, along
Vvith methyl sa|icylate for flavoring, constitute the aοtive ingre_
dients in most phenol-based mouthrinses. These rinses also
contain betv/een 20"λ Ιo 27"/" alcohol in the vehicle' Discre-
tion should be taken in recommending these rinses to recov-
ering alcoholics.
There are other mouthrinses and mouthwashes that show a
therapeutic effect for periods of time shorteτ than the 6
montλs stipulated by the U.S. Food and Drug Administration
for approval as a therapeutiο agent. Some agents have a
detergent effect to remove plaque and contain glycerin or
other compounds that leave teeth feeling smooth to the
tongue. These agents have noi been shown to have any
significant therapeutic benefit to the patient'
42
F|GURE 3Α. Powered toothbrushes come in a variety ot shapes and with
different plaque disruption principles.
It has been demonstrated that powered toothbrushes remove
more plaque than manual toothbrushing alone, when both
are used properly. There is no evidence to suggest that the
use of a powered brush alone is as effective as appropriaie

45. CHAPτER 5
What Are the Ingredients in a Dentifrice
(Toothpaste)?
Toothpaste, in conjunction with toothbrushing, serves to:
. Minimize plaque buildup
. Provide an anticaries effect
. Remove stain
r Freshen breath
Τhe ingredients found in most toothpastes include:
ο Polishing or abrasive agent. May be silica, calcium
carbonate, alumina, or other mild abrasive. The
polishing agent removes stain, stained pellicle,
and plaque.
. Binder or thickener. May be the carrageenates,
alginates, or carboxymethyΙcellulose. Τhese
binders give the toothpaste its consistency and
flowability when expressed from the tube.
. Surfactant. Detergent such as sodium lauryl sulfate
that foams to aid in debris removal. Detergents
may also have inherent antimicrobial properties
that contribute to plaque control.
. Ηumectant. May be glycerin, sorbitol, or polyethy-
Ιene glycol. Provides moisture to the paste and
keeps it from drying out, even when left exposed
for short periods of time.
ο F]avoring. May be spearmint, Wintergreen, or
peppermint. Some patients may have allergic
sensitivity reactions to certain flavoring agents,
particularly those νvith a cinnamon base.
. Active (therapeutic) ingredient. May be fluoride for
caries protection, triclosan as an antiplaque
agent, pyrophosphate as an anticalculus agent,
potassium nitrate as a desensitizing agent, or
peroxide compounds as whitening agents.
Vhat is the American Dental Association Seal of
Acceptance?
The American Dental Αssociation (ADΑ) Seal of Acceptance
is earned by product manufacturers after submitting their
products to rigorous testing under standards defined by the
ΑDA. As this is a costly and lengthy process, manufacturers
of consumer products more often seek approval than those of
professional products. This Seal may be carried on product
packaging.
THERAPEυτIc ENDPolNTs
Ηow much treatment is enough? Τhe answer to that question
is found in an understanding of the endpoints of therapy.
These endpoints must be practical and realistic for each indi-
vidual patient. Once the goals of therapy have been
achieved, frequent and regular re-evaluation and periodontal
maintenance become integral parts of periodontal therapy. lt
has been well documented that patients retain more teeth for
longer periods after therapy with appropriate maintenance
care than \λ/ithout that care.
ls Periodontal Therapy Successful?
This question goes to the core of periodontics as a discipline
in dentistry. There are many studies that have proven that
periodontal therapy, when appropriately executed and with
good patient compliance to oral hygiene regimens and
scheduled maintenance wbifs, can reduce tooth loss due to
periodontal disease by up to 7o"λ. ln one group of treated
patients with periodontal disease followed an aνerage ot 22
years, overall tooth loss νιas7.1"/o. occasionally, teeth Will be
lost in even the most compliant patient. Those few patients
(<10% of the total) that fall into the "extreme downhill" group,
may continue to lose attachment and subsequently lose teeth
in spite of all efforts.
What Are the Goals of Periodontal Therapy?
The primary goal of periodontal therapy is the maintenance of
the natural dentition in health, comfortable funοtion, with
pleasing aesthetics and satisfaction for the life of the patient.
This goal persists even in the face of the expanding use and
success of endosteal implants. lmprovements in implant
therapy have given the practitioner neνv treatment planning
and decision-making challenges regarding the retention or
removal of natural teeth. ln spite of these successes, the
overarching goal must still be the prevention of disease and
maintenance of the natural dentition when practically
possible.
What Teeth Can Be Expected to Ηave the
Greatest Longevity and \Ιvhich Teeth Are Lost
Most Frequently Due to Periodontal Disease?
Excluding third molars, maxillary second molars are lost most
often to periodontal disease. This would be expected both
due to complex root anatomy and the difficulty in performing
effective oral hygiene because of the tooth's location.
Mandibular canines and first premolars are the teeth most
likely to be retained.
What Clinical Parameters May Be Used to Judge
the Success of Periodontal Therapy?
There are several clinical and radiographic parameters that
may be used to judge the success of periodontal therapy,
including:
Reduction or absence of bleeding on probing.
Bleeding on gentle probing (25 g of force) is still the best
prognostic indicator of the potential for future attachment
loss. Absence of bleeding on probing is a
g8% negative
predictor that the site will lose attachment in the future.
Conversely, approximately 3O/" ot sites that bleed at
consecutive maintenance visits over one year are at risk
for future attachment loss. Since it is impossible to predict
exactly which site will lose attachment, the thrust of
therapy is to control inflammation at all sites.
Reduction of probing depth and gains in periodontal
attachment. Periodontal therapy is focused on the
removal of etiologic agents and contributing factors and
the subsequent maintenance of health. One way to
improve this possibility for both the patient and practi-
tioner is to reduce probing depths. Greater success is
achieved in creating and maintaining a plaque-free envi-
ronment with shallow pockets compared to pockets
greater than 5 mm in depth. Persistence of periodontal
pathogens and progressive loss of attachment is associ-
ated \Λ,ith deeper pockets' Pocket depth may be reduced

46. Ξ
PREvENτloN oF DlsEAsE AΝD τHE MA|ΝτENAΝcE oF HEALτH
by inflammatory control achieved with initial therapy,
resective surgery (eg, gingivectomy, apically positioned
flap with osseous surgery), or by repair or regeneration of
lost periodontal attachment.
Positive radiographic changes. Positive radiographic
changes related to the success of periodontal therapy
include the reappearance of a crestal lamina dura at the
interproximal osseous crests, evidenοe of bone fill in
areas of regenerative therapy, narrowing of the perio-
dontal ligament Spaοe in teeth subiect to occlusal trauma,
and the absence of calculus on coronaΙ and root
surfaces. While radiographs made in clinical practice are
not standardized, valuable comparisons may still be
made betνveen pretreatment and post-treatment films-
Occtusal stability. Tooth mobility is caused by the pres-
ence of edema in the gingival and periodontal tissues,
loss of attachment, and the effects of occlusal forces on
the attachment apparatus. Αfter inflammatory control iS
οompleted, teeth often exhibit decreased mobility. This is
due to the elimination of edema and the reformation of
the supragingival connective tissue fibers that contribute
to tooth stability' particularly when there has been attaοh-
ment loss. Judicious occlusal adjustment by selective
grinding to relieve fremitus may also contribute to
increased tooth stability. Mobile teeth may be success-
fully maintained in a state of health. lncreasing mobility or
hypermobility are indicators that an occlusion remains
unstable even after therapeutic intervention. Τargeted
occlusal therapy, removable or fixed splints, may be indi-
cated in this case.
What Are the Limitations of Periodontal Therapy?
There may be significant limitations to \ivhat periodontal
therapy can accomplish. First and foremost, the patient must
be dedicated to a daiΙy ritual of personal plaque control.
Without this, successful treatment becomes an uphill battle.
There may be limitations due to the amount of attachment
Ιoss, root anatomy, uncorrectable local or systemic factors,
uncontrollable occlusal forces, mobility, and last but not least,
the diagnostic aοumen and skiΙl of the c|inician.
What Can Be Done for the Patient Who Fails to
Respond to Periodontal Therapy?
It is important to identify those factors that may contribute to a
patient's continued attachment loss. Failures in therapy may
be related to either diagnostic or therapeutic shortcomings.
Even with accurate diagnoses and flawless treatment, the
occasional patient \Λ/ill continue to lose attachment.
Diagnostic def iciencies:
o Related to health history: Undetected diabetes,
immune compromise, or other systemic disorder
. lmproper use, or nonuse, of the periodontal and
furcation probe
. lmproper radiographic examination: Particularly the
use of bitewing films of less than a diagnostic quality
to detect interproximal bone loss; vertical bitewing
films are recommended to adequately visualize
posterior interproximal bone height
ο Abnormal anatomy rendering complete root detoxifi-
cation impossible
o Unidentified microbes not eradicated by conventional
mechanical therapy
ο Undeteοted traumatic occlusion
. Pulpal pathosis
Therapeutic deficiencies, failure to:
. lnstruct the patient adequately in plaque control
o Formulate a comprehensive treatment plan
ο Control the etiologiοal agents
o ldentify and correct loοal contributing factors
o Treatment failures related to diagnostic defiοiencies
. Select proper of therapeutic modalities
ο Execute proper initial therapy vvith adequate
follow-up
. Provide adequate surgical techniques
. Utilize an effective maintenance program
How ls Prognosis Determined?
Patients are extremely interested in \Λ/hether or not the
proposed treatment is going to be effective. lt would be
beneficial for clinicians to give their patients a reasonably
accurate prediction of treatment success. Unfortunately,
prognostic acumen is limited. Except for those teeth that
originally have a "good" prognosis, projections were ineffec-
tive at projecting the fate of teeth, acοuraοy in predicting was
in about Ιhe 40"λ range. lnitial mobility, increasing mobility,
and smoking \ivere seen as factors negatively affecting prog-
nosis.
MAINTENANCE oF PERloDoNτAL HEALTH
How Important ls Maintenance in Periodontal
Therapy?
lt is cΙear that regular maintenance visits are a key compo-
nent to successful periodontal therapy. There is a demon-
strated 70% reduction in lost teeth comparing untreated
patients to those who received treatment and followed
through with regular maintenance. Τhere is a 50% improve-
ment in tooth retention when comparing treated patients
without maintenance therapy to those who were both treated
and well maintained. Some studies suggest that with a
regular 3-month maintenance interval, attachment levels may
be maintained even in the face of a patient's poor oral
hygiene.
What Are the Therapeutic Goals of Periodontal
Maintenance?
. To minimize the recurrence and progression of perio-
dontal disease in patients who have been previously
treated for gingivitis and periodontitis
. To reduce the incidence of tooth loss by monitoring
the dentition and any prosthetic replacements of the
natural teeth

47. CHAPτER 5
. To increase the probability of locating and treating, in
a timely manner, other diseases or conditions of the
oral cavity
What Are the Components of the Periodontal
Maintenance Visit?
Τhe basic maintenance appointment should have the
following components:
Update and review the medical history. Τhis aspect is
particularly important related to the onset of Type 2
diabetes mellitus in adult patients, and changes in patient
medications, both prescribed and self-administered.
Queries to the patient must take more than one form, for
simply asking the question, "Has anything related to your
health changed since your last visit with us?" may not
garner the necessary information. Asking patients to list
their current medications, whether or not they are contin-
uing to take previously reported medications, and
inquiring about recent visits to the physician may all elicit
more meaningful answers.
Update the dental history. This review may seem
unnecessary for the patient being treated solely in one
office. Unfortunately, for \ivhatever reason, some recom-
mended treatment may not have been completed and a
periodic review of patient treatment will uncover any
incomplete treatment needs. The patient νvho sees both a
generalist and a specialist or specialists must update
his/her dental history to acknowledge the following, or
decide not to follow treatment recommendations.
Extraoral and intraoral hard and soft tissue examina-
tions' Τhis step will uncover any clinically evident hard
and soft tissue lesions that may require some follow-up
attention.
Dental examination. This step will reveal clinically
evident decay and/or restorations that have outlived their
usefulness.
Periodontal evaluation. This step includes review of
oral hygiene effectiveness (best accomplished before
plaque and οalculus is removed), marginal inflammatory
control as demonstrated by bleeding on gentle skimming,
and reduction or maintenance of probe depths. Use of
the Periodontal Screening and Recording (PSR) system
may simplify documentation of this review.
Radiographic review. Review of existing radiographs
can corroborate clinical findings and the decision for new
radiographs may be made. Vertical bitewing films should
be exposed for patients with posterior interproximal bone
loss.
Removal of supra- and subgingival plaque
Scaling and root planing where indicated
Polishing the teeth. Selective polishing, using a rubber
cup and abrasive prophylaxis paste only where plaque
and stain are evident, has been advocated to maintain
tooth structure, particularly the fluoride-rich layer of
enamel on the surface of the crown. An air abrasive type
of polishing unit may be used as long as the abrasive
stream is not directed onto root surfaces or composite
resin restorations.
Topical fluoride application. This step helps to restore
the fluoride-rich surface that may have been removed
during the polishing step.
Final oral hygiene instructions and the dispensing of
appropriate personal hygiene implements
How ls the Patient's Maintenance lnterval
Determined?
The maintenance interval should be determined on an indi-
vidual basis' Αmong the factors to be considered are the
initial level of disease, the aggressiveness of the attachment
loss, the patient's response to therapy, the patient's ability to
perform effective plaque control, and the post-treatment
stability of gingival inflammation and attachment levels. Main-
tenance intervals may be as shoιt as 1-2 months, up to about
6 months bet\Λ/een appointments. Patients who have already
demonstrated a susceptibility for attachment loss should be
seen no less often than every 4 months.
How Compliant ls the Average Periodontal
Patient?
One study suggests that only about 16% of patients receiving
periodontal therapy comply with recommended maintenance
intervals. other studies have demonstrated a similar Ιack of
compliance. Behavior modification is difficult even when the
patient is faced with a life{hreatening disease. There are
many factors contributing to a lack of compliance including:
. Denial and negligent attitude towards own health
. Αcknowledging the problem means the patient must
participate in his own care
o Many patients \ivant the dental profession to take
responsibility for and fix their problems
. Compliance decreases as treatment time or the
complexity of the required behavioral change
increases
Several steps to improve patient compliance have been
proposed:
. Simplify behavioral change
o Accommodate the patient
. Remind patients of appointments
o Keep compliance records
. lnform the patient about the necessity for and consis-
tency of keeping maintenance appointments
. Provide positive reinforcement
. Ensure the dentist's involvement
What Type of Biological Modulation May Be Used
to Control Recurrent Periodontal Disease in the
Maintenance Patient?
Maintaining stable post-treatment attachment levels may be
difficult. There are several approaches to treating new areas
of attachment loss or to prevent new attachment loss. ln
situations where the attachment loss is localized, local
delivery of antibiotics or antimicrobial agents such as doxycy-
cline, minocycline, or chlorhexidine is possible. For situations
where new attachment loss may be more widespread, the
use of systemic antibiotic therapy may be warranted.

48. PREvENTloN oF DlsEAsE AND τHE MA|NτENANGE oF HΕALτH
Systemic administration of a subantimicrobial dose of doxy-
cycline (SDD) has been advocated to help prevent attach-
ment loss. SDD has been shown to stabilize the activity of
collagenase and other matrix metalloproteinases and there-
fore slow down the destructive inflammatory process. lnitial
cliniοal studies to receive U.S. Food and Drug Administration
approval were of 9 months duration. There is minimal
evidence of the effect of SDD over longer time periods. lt has
been suggested that SDD may be effective in controlling
other collagenase-based inflammatory disorders.
When Should a Patient Be Comprehensively
Retreated for Recurring Periodontal Disease?
Τhere are no clear-cut guidelines as to \Λ/hen a patient should
re-enter comprehensive periodontal treatment. Fortunately,
in most cases, only localized sites remain a problem. One
rule of thumb would be that if the patient's recurrent problems
cannot be addressed in 2-3 appointments, consideration
should be given toward a new round of comprehensive
therapy. ln addition, a patient who has recently completed
surgical therapy but οontinues to have difficulty should be
treated with alternative therapies, such as antibiotics, and
further control of risk factors, with additional surgical therapy
held in abeyance.
When Should a Patient Be Referred for Specialty
Periodontal Care?
Τhe decision on when to refer a patient for specialty care
must be made between the general practitioner and patient,
with the periodontist available to provide the necessary treat-
ment. ln general, most periodontists prefer to treat the patient
from the beginning of initial therapy through advanced
therapy. ln certain situations, particularly when the general
practitioner's office can provide high quality initial therapy or
when there is a questionable need for referral, the patient
may be referred for specialty care after the results of initial
therapy have been evaluated. This arrangement should be
worked out in advance as it is uncomfoιtable for both the
patient and periodontist if additional initial therapy is recom-
mended by the specialist. ln most cases, third party carriers
will not provide benefits for this additional treatment. This
situation also begs the question in the patient's mind as to the
quality of the care received in the generalist's office. Effective
communication between the general dentist and periodontist
is paramount to a clear understanding of the overall course of
the patient's treatment.
46

49. CHAPTER 6
CHAPTER 6: NONSURGICAL THERAPY: SCALING AND ROOT
PLANING, OCCLUSAL AND ANTIBIOTIC THERAPY
What ls Nonsurgical Therapy?
Τhe expression nonsurgical therapy suggests that the
nonsurgical procedure so designated is performed in a
closed environment and, therefore, is not invasive (eg, it does
not break the epithelial seal of the sulcular or iunοtional
epithelium). While the οoncept of scaling and root planing
may be, indeed, nonsurgical, the gingival soft tissue is often
inadvertently invaded. Local anesthesia will often be required
for patient comfoft during scaling and root pΙaning proce-
dures.
Oral hygiene and local antimicrobial procedures, the removal
of iatrogenic factors, occlusal therapy, and systemic antibiotic
procedures are not invasive and, therefore, conform to
nonsurgical concepts.
The term surgical treatment is reserved for those periodontal
procedures that are performed in a deliberately open environ-
ment where incisions are made, periodontal soft tissue is
elevated to expose tooth roots and alveolar bone, and the
soft tissue is either rep|aοed or repositioned over the roots
and bone. During surgiοal access, resective or regenerative
procedures may be performed on the bony defects produced
by periodontitis.
SCALING AND ROOT PLANING
Scaling and root planing are the cornerstones of almost all
initial therapy treatment plans for periodontitis and may be
the only mechaniοal therapy required for the management of
mild (1-2 mm clinical attachment loss) chronic periodon-
titis. WhiΙe sca|ing and root planing procedures are utilized
routinely they remain among the most technically demanding
procedures performed in periodontics. When performed
with optimal access and skill, scaling and root planing wilΙ pro-
duce a decrease in gingival inflammation, a reduction in
periodontal probing depths, and a gain in periodontal attaοh-
ment. With less than optimal access and skill, the outcomes
from scaling and root planing will, by extension, be less
than optimaΙ.
What ls Scaling and Root Planing? What Are the
Goals and Objectives of Scaling and Root
Planing?
Scaling and root planing are tνvo technically similar perio-
dontal procedures. Both involve the mechanical application of
hand- and/or power-driven instruments to tooth suι'faces to
remove plaque, stain, and calculus. Clinically, it is frequently
difficult to separate one from the other. Scaling may be
per{ormed on eithΘr coronal or radicular surfaces in periodon-
titis cases, but in gingivitis cases, scaling should be limited to
coronal surfaces. Root planing is only performed on root
suι'faces that have been denuded of periodontal attachment
by periodontitis. ln addition to the removal of plaque, stain,
and calculus, it also includes the removal of "disease
affected" cementum containing imbedded calculus, whole
bacteria, and toxic bacterial debris such as endotoxin.
The goals and objectives of scaling and root planing are both
technical and biologic. The technical goals and objectives of
scaling and root planing (ie, the mindset of the clinician at the
time), are to produce hard, smooth tooth surfaces free of
calculus and cementum affected with endotoxin and/or other
bacterial contaminants. ln the process, the bacterial load
adjacent to periodontal tissues is reduced.
The biologic aoals and objectives of scaling and root planing
are to produce a tooth surface and sulcular ecosystem that is
biocompatible with periodontal epithelial cell and connective
tissue adhesion. Decreases in gingival inflammation, reduc-
tions in periodontal probing depths, the presence of Gram-
positive beneficial bacterial species, and gains in periodontal
attachment are the outcomes by which effeοtive scaling and
root planing are measured (see below).
What ls Disease-Affected Cementum? What ls
Endotoxin and Where Does it Come From?
Disease-affected cementum is cementum that has been
stripped of periodontal attachment by periodontitis and has
been exposed to the septic contents of the periodontal
pocket. lt contains remnants of embedded calculus, whole
bacteria, and the products of microbial life. Τhe most studied
of these is bacterial endotoxin. Endotoxin and whole bacteria
may be found as deep as 12 microns beneath the cemental
surfaοe (see Figure 1).
F|GURΕ 1. A Photomicrograph of Marginal Periodontitis. τhe associated
deposits o' subgingival, serumnaΙ calculus are firmly attached to and
interlocked with surface irregularities in dentin and cementum.
Εndotoxin is the lipopolysaccharide component of the outer
membrane of Gram-negative cell walls. lt is exported as
membrane vesicles during the lifespan of most Gram-nega-
tive bacteria. The biologiο activity of endotoxin includes
attraction of inflammatory οells, activation of the complement
E

50. NoNsURGlcAL THERAPY: scALlNG AND Rooτ PLANING' occLUsAL AND ANTlBloτΙc τHERAPY
System, Stimulation of bone resorption, fibroblast οytotoxicity,
pyrogenicity, and mitogenic activity with B-lymphocytes.
Endotoxin Will produce a Severe local infΙammatory reaction
\,vhen injected experimentally in tissue (see Figure 2).
FlGURE 2. An electron micrograph of negatively stained Fusobacterium nucιe-
a,Um. The corrugaιed surface is a typical morphological feature of Gram-
negative bacteria. τhe oιher membrane vesicle at the tip of the organism
is a possible source of endotoxin.
What Are the lnstruments Used in Scaling and
Root Planing? \Mhat Techniques Are Employed?
Calculus detection and removal are learned skiΙls that gradu-
ally improve with experienοe. Εxquisite tactile sensitivity,
mediated by hand, sonic, and ultrasonic instruments is
essential. Correct instrumentation is then an essential
prerequislte to detection and removal. There are many
different instruments specifically designed for scaling and
root planing, and there are probably as many personal prefer-
ences for instruments as there are instruments. The following
is a guide to the four general categories of instruments used
in scaling and root planing.
F|GURE 3. τhis is a Moffitt-Maryland periodontal probe detecting subgin-
gival calculus in a narrow subgingival pocket. Calculus removal at this
site will be difficuΙt.
PeriodontaΙ probes and explorers are used to detect calculus
deposits. Probes will also confirm that deposits have been
removed and that the roots have been planed to hard and
smooth surfaces. The uΙtralight Moffitt-Maryland periodontal
probe with Williams markings is an excellent choice for
subgingival calculus detection (Figure 3). The 3A curved
explorer or the Nabers furcation probe may also be used for
οalculus detection and are particularly helpful in root concavi-
ties or furcation invasions.
Scalers are the instruments of οhoice for visible supragingival
calculus removal. Scalers have a bulky working end and a rigid
shank. Both tend to limit their tactile sensitivity. ln cross
seοtion, the most popular scalers (sickle scalers) have a
triangle shaped blade with 2 opposed οutting edges. Scalers
shouΙd not be used in deep (>4 mm) pockets so as to mini-
mize injury to gingival tissues.
Hoes and flles belong with scalers as instruments whose
cutting edges are designed to function at right angles to the
tooth surface and they shouΙd be used almost exclusively for
heavy supragingival deposit removal. Frequently, calculus
removal with sοalers, hoes, and files will be incomplete, and
more delicate instruments with greater tactile sensitivity and
aοcess capability will be required to remove residual deposits
and smooth cementum or dentin. Scalers, hoes, and files are
used with a verlical pulltype stroke.
FIGURE 4. A Gracey curette with calculus and soft tissue debris removed from
a deep periodontal pocket. lncidental tissue removal is common during
subgingival scaling and root pιaning.
Curettes are the instruments of choice for subgingival instru-
mentation and root planing. They are generally smaller than
scalers and are designed to permit atraumatic entry to the
subgingival space. The tactile sensitivity of most curettes is
greater than scalers and, as such, curettes are well suited for
subgingival calculus detection, calοulus removal, and root
planing. Area specific curettes (Gracey and Goldman-Fox)
have a single cutting edge at 60'to the root surface and are
designed to instrument specific tooth surfaces in specific
regions of the mouth. For example, the Gracey 13/14 is
designed to instrument the distal surfaces of molar and
premolar teeth, while the Gracey 9/10 is designed to instru-
ment the buccal or lingual surfaces of the same posterior
teeth. Gracey curettes have been modified for improved
access and reduced tissue injury. Universal curettes (Crane-
Kaplan 6, McOall's 17sl18s, Columbia 4Rl4L) have 2 cutting
edges at 90" to the root surface and may be used in any
48

51. CHAPTER 6
Application
Supragingival calculus removal
Universal scaling and root planing
BuccaΙ and lingua| surfaces
lnterproximal surfaces of anterior teeth
lnterproximal surfaces of posterior teeth
lnstrument
Scalers - Jacquette 34135, τay1or
colUmbia 4Fy4L or 13/14, ΝΙccall's
17sl18s
Gracey 9/1 0
Gracey 112, 314
Gacey 11112 (mesial), Gracey 13/
14 or 15/16 (distal)
region of the mouth. Curettes may be used νvith vertical,
oblique, horizontal, or circumferential pull-type strokes
(see Figure 4).
SUGGESTED SCALING AND ROOT PLANING
lNSTRUMENTs AND APPLlcAτloNs
ments be kept adequately cooled, that the instruments be
kept in constant motion, and that the side (not the tip) of the
instrument be used against tooth structure at all times. Many
ultrasonic units may be used \Λ,ith a variety of irrigants such
as chlorhexidine or povidone-iodine.
Are There Any Medical Risks to the Patient and/
or the Provider When Power-Driven lnstruments
Are Used to Debride Teeth?
Magnetostrictive ultrasonic instruments may "de-program"
some οardiac pacemakers. Αs it is not in the province of
dental health professionals to decide whether or not a patient
with a cardiac pacemaker may be at such a risk, it is recom-
mended that a medical consultation be obtained before
magnetostrictive ultrasonic instrumentation is performed.
Cultivable oral bacteria are present in aerosols created by
sonic and ultrasonic instruments, and there seems to be no
difference in the number of colony-forming units produced
from aerosols generated by magnetostrictive, piezoelectric,
or turbine driven instruments. Antimicrobial mouthrinses
before power-driven instrumentation \Λ/ill reduce the number
of cuΙtivabΙe baοteria in aerosols.
It is beyond the intended scope of this manual to describe the
technical aspects of scaling and root planing. It is recom-
mended that the reader consult one of the textbooks devoted
to the subject listed in the "Selected Readings" section.
How Do Power-Driven Instruments Perform When
Compared to Conventiona] Ηand lnstruments?
Comparison studies of the performance of power-driven
instruments \,vith hand instruments on extracted teeth have
produced equivocal data. Both are partially effective in
removing calculus and cementum. Tests on extracted teeth
suggest that both methods are equally effective in removing
debris from teeth, but that hand instruments alone, or
following power-driven instrumentation, produced the
smoothest tooth surface. Other reports have presented
contrasting data indicating the superiority of power-driven
instruments in producing smooth tooth surfaces.
What Are the Expected Outcomes and
Limitations of Scaling and Root Planing? How
Successful ls Scaling and Root Planing in
Achieving lts Goals and obiectives? νhat Are
the Guidelines for Decision-Making vis-a-vis
Surgical Access for Root Debridement?
Catculus removal. Both hand- and power-driven instruments
have limited utility in calculus removal from periodontal
pockets. As a guideline, calculus removal becomes progrΘs-
sively more inefficient in sites with probing depths greater
than 3 mm, and the limit of any effective instrumentation
occurs in probing depths over 6 mm. These reports support
the notion that closed (nonsurgical) access for scaling and
root planing in pockets less than 3 mm may be as effective as
open (surgical) acοess. When probing depths are greater
than 6 mm, residual calculus is inevitable. These sites wiΙl
require surgical access for effective root debridement.
What Are Power-Driven Scalers? How Are They
Used?
Power-driven scalers are usually used to provide a rapid
calculus and stain removaΙ with a minimum of discomtort to
the patient or trauma to hard or soft tissues. Power-driven
scalers use either ultrasonic or sonic energy for debridement.
Ultrasonic instruments use either magnetostrictive or piezo-
electric technology to convert electrical energy to physical
energy at the instrument tip. lnstrument tips vibrate from
25,000-40,000 cycles per second at an amplitude betvveen
10-30 μm. The heat generated by magnetostrictive instru-
ments requires copious amounts of water for cooling. ln the
cooΙing process, \ivater "cavitation" (similar to the effect
produced by a propeller in water) occurs which releases
dissolved gases. The resulting spray, along with the water
itself, facilitates the removal of dislodged debris. Recent
advances in ultrasonic instrument design, such as thinner
uιtrasonic tips, have improved access in deep pockets and
provide subgingival delivery of antimicrobial agents (Figure
5).
FIGURE 5. An ultrasonic scaler with water cavitation at the tip.
Sonic instruments are classified as air-turbine instruments.
They use the air pressure from high-speed handpiece lines to
produce tip vibrations from 2,000-6,000 cycles per second.
Power-driven instruments may be used in both supragingival
and subgingival areas. lt is recommended that the instru-
49

52. NoNsURGlcAL THERAPY: scALlNG AND Rooτ PLANING. occLUSAL AND AΝτiBloτlc τHERAPY
The limitations in achieving the goals and ob.iectives of
scaling and root planing may be a function of either:
o Probing depth at the time of instrumentation
. The method of access to root surfaces (eg, surgical
versus nonsurgical)
o Root grooves and concavities
o Furcation involvements (Figure 6), and/or
o Technical ability of the operator
F|GUFiE 6. A maxillary premoιar showing retained calculus in the root
concavity and bifurcation. Anatomic features of tΦth frequently limit the
effectiveness and efficiency of calculus remoνal (couι7esy of Dr. Jeanne
Saιcetti)
Scaling and root planing will reduce the biomass of patho-
genic bacteria and calculus in periodontal pockets. The
reduction in bacterial Ιoad will allow improved periodontal
health in most cases of chronic periodontitis. MiΙd cases of
periodontitis may not require additionaΙ surgical therapy. ln
more advanced οases, repeat sessions of scaling and root
planing are not indicated, as they probabΙy will not improve
soft tissue health beyond that achieved by one or two sessions
of therapy. Still, where surgery is indicated, presurgical
scaling and root planing will improve tissue health and
enhance surgical outcomes.
Removat of disease affected cementum. The cementum of
the coronal third of the root ranges from 10-150 μm. lt is
thinnest nearest the cementoenamel junction and becomes
progressively thiοker toνvard the root apex. Because it iS thin
and is readily aοcessibΙe to instrumentation, all cervical
cementum is usually removed in 1-4 strokes of a curette. ln
advanced cases of periodontitis that involve the thicker
cementum at the mid-root, and where cΙinical access may be
reduced by deeper pocket depths or root anatomy, the
removal of cementum is predictably less complete. Other
faοtors that affect the amount of tooth structure removed
during scaling and root pΙaning are the forces applied at the
working end of the instrument and the number of strokes νvith
an instrument against a given root surface. Ultrasonic instru-
ments remove less tooth structure than do hand curettes.
Both hand curettes and power-driven instruments remove
affected cementum containing endotoxin. Curettes are more
effective than ultrasonic instruments in removing endotoxin
from root surJaces, and under ideal conditions, hand curettes
are capable of rendering root surfaces previously in contact
with diseased periodontal tissues totally free of endotoxin.
Decreased probing depths and gains in periodontal
attachment. As a general rule, subgingival scaling and root
planing \Ιvith hand- and/or power-driven instruments wil| yield
decreases in probing depths and, in most cases, gain in
periodontal attachment. Deeper periodontitis sites are more
likely to gain attachment than shallow sites, and there does
not Seem to be a Ιimit to pocket depth where these effects
will not be observed to one degree or another. These changes
usually ocοur within thΘ first month following treatment and
can be maintained with good oral hygiene and monthly
supragingival cleanings for up to three months (Figures
7 and 8).
FIGURE 7. The effect of scaling and root planing on pocket depth. Greater
reduction in pocket depth may be expected following instrumentation of
deeper pockets. (With permission, cercek, et aι, J cιin Periodontol, 1983,
10:46-56)
FlGURE 8. τhe effect of subgingival scaling and root planing on subgingival
attachment levels. Greater gains in attachment may be obtained by
scaling and root planing in deeper pockets. (with permission, Cercek, et al,
J clin Periodontoι, 1983, 10:4σ56)
What ls Meant by Critical Probing Depth?
The downside of scaling and root planing is the observation
that a |oss of οlinical attachment will invariably occur when
shallow pockΘts are mechanically instrumented. Concepts of
critical probing depths have emerged as decision-making
guidelines for nonsurgical and surgical periodontal therapy.
Scaling and root planing initial probing depths <2.9 mm will
50

53. result in a net loss of periodontal attachment \Λ/hile performing
the same proοedures on pockets >2.9 mm will resu|t in a net
gain in periodontal attachment. Similarly, the critical probing
depth for surgical treatment is 4.2 mm.
Judiοious instrumentation to control inadvertent tissue injury
is appropriate in shallow periodontal pockets. Since the injury
produced by instrumentation is a painful blunt tearing of the
tissues of the dentogingival junction, the use of locaΙ anes_
thesia for patient comfort should be avoided to minimize
unwanted soft-tissue injury. Local anesthesia should be
reserved for periodontitis cases where deep pockets (>6
mm) are the rule and where instrument efficiency and effec-
tiveness is limited.
Reduce the load of pathogenic bacteria. Visual clinical
measures of supragingival plaque accumulation on teeth are
usually affected most by supragingival instrumentation and
oral hygiene practices by the patient. Subgingival instrumen-
tation is not a requirement for changes in visual measures.
Subgingival scaling and root planing are effective in reducing
the number of bacterial morphotypes associated with inflam-
matory disease (motile rods and spirochetes) as seen in dark-
field or phase contrast microscopy. Hand, sonic, and ultra-
sonic instrumentation appear to be equally effective in pro-
ducing these changes and in creating an environment \η/here
morphotypes associated with periodontal health (nonmotile
cocci and rods) will predominate. However, these changes
are not permanent, and the proportions of pocket bacterial
morphotypes will return baseline levels in 2-3 months.
Frequent professionally performed supragingival debride-
ments will have little effect on this trend. lt is clear that
subgingival instrumentation is a critical guideline in achieving
the clinical goals and obiectives of scaling and root planing
(Figure 9).
FΙGURE 9. τhe effect of subgingival scaling and root planing on supragingival
plaque scores. lnitial reductions gained following oral hygiene instruction
werδ the same as those obtained by subgingival instrumentation. rwith
ρemission, cercek, et al, J clin Periodontol, 1983' 10:46'56)
The effect of subgingival instrumentation on the cultivability of
plaque microorganisms is limited by the degree of invasive-
ness of P gingivalis and A. actinomycetemcomitans.These t\Λ/o
exogenous periodontal pathogens tend to resist eradication
by scaling and root planing. Because their persistence in high
numbers after mechanical therapy is associated with contin-
uing periodontaΙ deterioration, the eradication of these and
endogenous periodontal pathogens is viewed as a major
criteria for successful periodontal therapy. Systemic antibi-
otics may be used as adjuncts to mechaniοal periodontal
therapy to reduce the levels of periodontal pathogens belo\Λ/
detectabΙe levels.
The requirement for the elimination of periodontal pathogens
does not appear to be absolute as clinical improvements in
plaque levels, inflammation, probing depths, and attachment
levels may be achieved \Ιvith scaling and root planing when
pathogens are reduced, but not necessarily eradicated. The
observations that the goals and obleοtives of scaling and root
planing can be achieved by only reducing the numbers of
periodontal pathogens supports the notion that a critical mass
of pathogenic bacteria are required before the host becomes
susceptible to pΘriodontal diseases.
Control gingival inflammation. Scaling and root planing will
predictably reduce gingival inflammation. As it has been with
other clinical measures of successful scaling and root
planing, the instrumentation must be subgingival to achieve
this outcome. Hand, sonic, and ultrasonic instruments appear
to be equally effective in reducing gingival inflammation
(Figure 10).
F|GUFiE 10. The effect of subgingival scaΙing and root planing on gingival
inflammation (bleeding). Greater reductions in gingivai inflammation may
be expected after the instrumentation of deeper pockets. (With
ρermission,
cercek, et al, J clin Periodontoι, 1983' 10:46-56)
What ls Soft Tissue Management (STM)?
ln its broadest sense, STM refers to local mechanical and
chemotherapeutic approaches to improving and controlling
periodontal health. Αs such, oral hygiene instructions, the use
of antimicrobial agents as mouthrinses or crevicular irrigants,
subgingival scaling and root planing with hand- and power-
driven instruments, correcting unserviceable dental restora-
tions, and supragingival coronal polishing are important
elements of STM. STM bears striking resemblance to the
typical initial therapy periodontal treatment plans that have
been used successfully for inflammatory periodontal disease
control and that are included inthe Parameters of Care. STΜ
should be limited to the management of gingivitis and slight
periodontitis with <2 mm of clinical attachment loss where
bacterial deposits on teeth are usually accessible and can be
removed efficient|y and effectively. Root οoncavities, root
grooves, furcation invasions, and other anatomical factors
that could affect the completeness of debridement are usually
not an issue in these cases. Moderate periodontitis (3 or 4
mm of clinical attachment loss) and severe periodontitis (>5
mm clinical attachment loss) cases should be οonsidered for
referral to a periodontist vι/here issues of force control,
surgical access, pocket elimination, regeneration of lost
attachment, and gingival augmentation can be addressed by
clinicians trained and experienced in the management of
advanced periodontitis.
-

54. NoNsURGlcAL THERAPY: scALlNG AND Rooτ PLANING. occLUsAL AND ANTlBloτlc τHERAPγ
Chairside diagnostic instruments that measure volatiΙe sulfur
compounds, periodontal pocket temperatures, and the
motility of pocket bacteria have been used in patient educa-
tion STM. These methods are not described inΙhe Glossary
of Periodontal Termsnor are they included inthe Parameters
of Care.
Scaling and root planing are fundamental procedures in
nonsurgiοal periodonta| therapy. The target of sca|ing and
root planing is the removal of subgingival bacteria and the
removal of affected cementum. The effectiveness of scaling
and root planing is limited by root anatomy, pocket depths,
the skill and experience of the provider, and the overall
systemic health of the patient. Τhe outcomes of scaling and
root planing include lowered plaque scores, reduοed gingival
bleeding scores, gain in periodontal attachment, gingival
recession, and reductions in probing depths. lnstrumentation
of root surfaces must be subgingival in order to aοhieve these
results.
ln mild and some moderate chronic periodontitis cases, the
clinical outcomes of scaling and root planing may preclude
the need for periodontal surgery.
OCCLUSAL THERAPY
What ls Occlusal Traumatism? How Does
Occtusal Traumatism Conform to the Definition
of a Disease?
ln occlusal traumatism, the etiologic factor is any force in
excess of the adaptive capacity of the periodontium, the
morbid pathobiologic event is injury within the periodontal
ligament and alveolar bone, and the signs and symptoms are
pain, mobility and/or fremitus, pathologic migration of teeth,
excessive occlusal wear, and widening of the periodontal
ligament space in radiographs.
Αs defined in the G/ossary of Periodontal Terms, occlusal
traumatism is the "functional loading of teeth" (force is
primary etiologic factoQ, usually off-axis, that is of sufficient
magnitude (excess of the adaptive capacity) to induce
changes to the teeth (eg, fractures, occlusal wear) or
supporting structures (inflammation in the periodontal liga-
ment and alveolar bone, also known as the "lesion of trauma
from occlusion"). The changes may be temporary (reversible)
or permanent (irreversible).
What is Adaptive Capacity? What Factors Affect
the Adaptive Capacity?
Adaptive capacity is the ability of the teeth and tissues of the
periodontium to sustain the effects of, or adapt to, forces
acting on the periodontium νvithout injury. The adaptive
capacity is affected quantitatively and qualitatively by local
and systemic contributing factors. When it is exceeded,
occlusal traumatism occurs.
Τhe etiologic forces that produce occlusal traumatism may
not always be occlusal in nature, but they may be generated
by orthodontic or prosthodontic appliances and/or habits of
compulsion, such as pipe smoking or fingernail biting. The
more inclusive designation, periodontal traumatism, is
preferred by some over occlusal traumatism because it
allows for nonocclusal forces and occlusal forοes as etio|ogic
factors.
What ls the Nature of the lnjury to the
Periodontal Attachment Apparatus Produced by
Forces Acting on τeeth? What ls Primary
Occlusal Trauma and Secondary Occlusal
Trauma?
The injury to the periodontium caused by forces acting on
teeth is called the lesion of trauma from occlusion or more
simply, occlusal trauma.
o Τhe lesion of trauma from occlusion is located within
the periodontal ligament in areas \Λ/here the ligament
is either under pressure (crushed) or under tension
(torn) (Figure 11). The οrush or tear produces a phys-
ical injury resulting in local necrosis of the periodontal
ligament and a typical inflammatory response. The
histologic appearance of the periodontal ligament is
desοribed as "hyalinization", or a decrease in the
cellular component of the tissue. Resorption of
nearby alveolar bone also occurs as an outcome of
the inflammation. The resorption will occur on the
periodontal ligament side of the alveolar bone proper
with mild injury (frontal resorption) and/or on the
marroνv surfaces of the supporting alveolar bone
(rear resorption). The degree of necrosis, inflamma-
tion, and resorption will depend upon the amount of
force acting on the teeth and the adaptive capacity of
the periodontium (see Figure
'12).
FIGURE 11. A line drawing showing the reciprocal areas of crush and tear
(ιightnin9 bolts) of a p€riodontal ligament when excessive nonaxial forces
are applied to a tooth. τhe tooth rotates within the alveolus around a point
center of rotation located within the root.
52

55. CHAPτΕR 6
that "reduced" the adaptive capacity of the periodon-
tium may be difficult to control or change, secondary
occlusal trauma is difficult to reverse following force
control (Figure 15).
F|GURE 12. A histopathologicaΙ specimen showing a periodontal ligament
,ollowing iniury. τhe disruption in the principal fibe.s of the periodonta|
ligament and the resorption bays containing osteoclasts are typical o, the
lesion of trauma from occlusion.
. Primary occtusal trauma is the injury resulting in
tissue changes (injury to the attachment apparatus)
from excessive (in excess of the normal adaptive
capacity of the periodontium) occlusal (and otheQ
forces to a tooth or teeth With a healthy, anatomiοally
normal, periodontium in a systemically well patient.
Primary occlusal trauma is usually reversible once
the forces that produced it are controlιed (Figure 13).
FIGURE 13. A line drawing showing the morphological requirements fol
primary occlusal trauma. τhere are excessive nonaxial forces acting on a
tooth with a normal, healthy periodontal attachment apparatus. τhe
crown to root ratio is 1:2 and the point center ot totation is in the coronal
1/3 ot the root.
ο Secondary occlusal trauma is the injury resulting in
tissue changes (injury to the attachment apparatus)
from normal or excessive (in excess of the reduced
adaptive capacity of the periodontium) ocοlusal (and
otheQ forces to a tooth or teeth with reduced support
(Figure 14). Because these same contributing factors
FIGURE
'14.
A line drawing showing the morphological requirements for secon-
dary occlusal taauma. τhere a.e normal nonαial forces acting on a tooth
with a periodontal attachment apparatus that has been reduced by perio-
dontiιis. τhe crown to root ratio is 2:1 and the point center of Joιation is in
the apical 1/3 of the .oot.
F|GURE 15. A histopathological specimen showing tΦth with lhree degrΦs of
reduced adaptive capacity. τhe tooth on the right shows marginal inflam-
mation and earΙy loss of attachment. τhe tooth in the cenier has lost
moderate amounts of attachmeπt, the tooth on the left has little, if any,
adaptive capacity remaining. Only the tooth on the right has enough
adaptive capacity to reverse the iniury of occlusal trauma.
Does the lnjury in the Periodontium Produced by
Forces Acting on τeeth contribute in Any Way to
Periodontal Attachment Loss? How Valid ls ttie
Concept of "Co-destructive Forces" in
Periodontitis?
The marginal inflammatory lesion of periodontitis and the
lesion of trauma from occlusion were beΙieved to be Separate
processes. However, it has been hypothesized that the tνvo
processes become co-destructive in the transseptal and alve-
olar crestal fiber region of the marginal periodontium. The
suggestion that the marginaΙ inflammation of periodontitis
could be then spread into the periodontal ligament along fiber
reaΙignment caused by occlusaΙ forces was supported in
animal studies. This concept of periodontal pathogenesis
53

56. Ξ
NoNsURGlcAL THERAPY: scALlNG AND Rooτ PLANING. occLUsAL AND ANτlBloTιc τHΕRAPY
conflicted οritically \Λ/ith the c|assic periodontitis model \Λ/here
marginal inflammation was depicted as following perivascular
connective tissue directly into alveolar bone marrow, and
where the periodontal ligament \Λ/as typically free of inflam-
mation.The projected outcomeof this "co-destructive" process
was the formation of angular bony defects and infrabony
pockets Seen οommonly in periodontitis (Figure 16)'
FIGURE 1 6. A photomicrograph showing an angular orientation of transseptal
fiber apparatus and a corresponding anguιar pattern of interdental bone
loss. According to the co-destructive model, marginal inflammation and
occlusal trauma could have been cofactors in its pathogenesis.
Studies in both animals and humans have not been able to
completely demonstrate the role of occlusal trauma in perio-
dontitis' While it is unclear νvhether potentialΙy destructive
occlusal contacts have any impact on the severity of perio-
dontitis, there is agreement that two of the recognized signs
of occlusal traumatism (eg, mobility and widened PDL
spaces) are associated with greater amounts of attachment
loss, pocket depth, and bone loss.
What Are the Clinical Signs and Symptoms of
occlusal Τraumatism?
The cliniοal signs and symptoms of injury in the periodontal
ligament are commonly:
1. Pain or discomfort around one or more teeth on
percussion, function,and/or parafunction. Pain is one
of the four cardinal signs of inflammation (doΙor/pain,
οalor/heat, rubor/redness, and tumor/swelΙing). Pain
then is a sign of inflammation in the periodontal liga-
ment.
2. Tooth mobility as determined with bidigital manipu-
lation of teeth using the handles of 2 hand instru-
ments. One handle is placed on the buccal surface
and the other is placed on the lingual surface of clin-
ical crowns. Tooth mobility is defined as "visibly
perceptible movement of a tooth away from its normal
position when a light force is applied."
Tooth mobility may be physiologic (ie, horizontal
movement limited to the width of the periodontal liga-
ment), or pathologic (ie, horizontal and/or vertical
movement beyond the expected boundaries of the
periodontal ligament). Mobility occurs when fibers of
the periodontal ligament are injured or destroyed by
inflammation resulting from excessive forces acting
on teeth' lt will also oοcur when the adaptive capacity
of the periodontium has been altered by marginal
inflammation or systemic disease. Mobility is
commonly observed when a tooth has reduced perio-
dontal attachment.
The Miller cΙassification scheme for tooth mobility is
as follows:
- Grade (degree) Ι. The slightest distinguishable
movement in a horizontal direction. Tooth mobility
is classified as physiologic mobility.
- Grade (degree) ll. Movement in a horizontal direο-
tion of a tooth within t mm of its normal position.
- Grade (degree) lll. Movement of a tooth in a hori-
zontal direction greater than 1 mm from its normal
position. Grade lll mobility also includes teeth that
are depressible and/or can be rotated in their
periodontal support.
Fremitus as determined by palpable or visible move-
ment of teeth under verticaΙ (axial) or horizontal
(nonaxial) occlusal forces. Fremitus is detected using
fingertips placed on the crowns of teeth while the
patient occludes. Fremitus is "functional mobility."
Pathologic migration of teeth. Pathologic migration
of teeth usually occurs when teeth have lost their
normal periodontal support due to periodontitis and
subsequently migrate from their normal position in
the dentition in response to occΙusal and nonocclusal
forces (Figure 17).
FIGURE 17. A case of severe chronic periodontitis with secondary
occlusal traumatism. Loss of adiacent teeth and periodontal support
allow teeth to migrate away from forces acting upon them. Posterior
bite collapse and loss of vertical dimension of occlusion are also
signs of advanced secondary occlusal traumatism.
5. Tooth loss
6. Posterior bite collapse. Posterior bite collapse is
the product of tooth loss and pathologic migration.
7. Widened periodontal ligament spaces around
affected teeth in radiographs. Widened periodontal
ligament (PDL) spaces usually indicate that an adap-
tive response has occurred either to excessive force
on a normal periodontium or to normal or excessive
forces on a reduced periodontium. Widened PDL
spaces together \ivith an intact laminadura suggest
that repair occurred following injury (Figure 18).
3.

57. CHAPτER 6
F|GURE 18- A radiograph of mandibuιar molars with severe bone loss.
νιridened periodontal ligament spaces in radiographs are signs of
occlusal traumatism. The retained third molar is probably a contrib-
uting factor to the degree of periodontal attachment loss.
What ls the Basis for Force Control and Occlusal
Therapy?
The essence of occΙusal therapy is to treat the lesion of
trauma from occlusion and to create an environment that will
allow the injured attachment apparatus to repair itself within
the limits imposed by the adaptive capacity of the host. lt is
not a form of therapy for periodontitis. There is some
evidence to suggest that periodontitis patients who receive
periodontal inflammatory disease control therapy along with
occlusal adjustment will display minor (<l mm) gains in
attachment compared to those who did not receive oοcΙusal
adjustment.
Repair to the attachment apparatus will depend directly upon
the effectiveness of force control and indirectly upon the
effectiveness of improvements in the adaptive capaοity
before force control (ie, control of marginal inflammation and
control of diabetes mellitus).
What Are the Components of a Force Control
Treatment Plan for a Periodontal Patient? What
Determines Which Component Is Appropriate in
a Given Case? How Are the Gomponents
Sequenced?
A typiοaΙ force control treatment pΙan for a patient with the
diagnosis of generaΙized moderate chronic periodontitis with
occlusal traumatism would be:
. Re-evaluation of inflammatory disease control. Αfter a
minimum of 4-6 weeks (the time for repair of the dento-
gingival junction), the patient is re-examined and the
results of that examination are compared with those
recorded at the initial examination. This is a critical stage
in treatment as decisions about the working diagnosis
and continuing active therapy are made depending upon
the answers to the foΙlowing questions:
1. Are there any persistent signs and symptoms of
gingival inflammation or debris present?
2.lf so, is there anything shott of periodontaΙ surgery
that can be done to improve the conditions?
ls there any residual tooth mobility/fremitus?
lf the answer to the first and second question is "no" and
the answer to the third question is "yes", the patient's
working diagnosis of generalized moderate chronic perio-
dontitis with occlusal traumatism is supported, and treat-
ment should proceed to the occlusal therapy phase.
Ιf, however, the answer to the first and second question is
"yes", then considerations for improving the patient's oral
hygiene, refining scaling and root planing, instituting
antimicrobial therapy, additional correction of plaque
retentive factors, and discussions concerning progress
made in smoking cessation might be appropriate.
Αssuming that the ansνvers to the first and second ques-
tions are "no" and the answer to the third question is
"yes", the next Step in treatment is to determine \Λ/hat is
responsible for the mobility and fremitus.
o Assessment of parafunctional occlusal habits of compul-
sion.
What ls Meant by Parafunction? ts Bruxism a
Form of Parafunction?
Parafunction is "abnormal function, as in bruxism". Bruxism
(tooth grinding, occlusal neurosis) is "a habit of grinding,
clenching, or clamping the teeth. The force generated may
damage both tooth and attachment apparatus." lt should be
emphasized that bruxism occurs during vertical (clenching)
and horizontal (grinding) nonfunctional movements of the
mandible. lt may occur during sleep (nocturnal bruxism) or
during waking hours (diurnal bruxism). Parafunctional tooth
contacts tend to be repetitive and of greater force and dura-
tion than the more random and 'Tleeting" functional tooth
contacts.
ο Parafunction may have been established during the
dental history. Not all patients are a\,vare of parafunctional
activity, and therefore, an interview with the patient rarely
provides reliable diagnostic information vis-a-vis
parafunction. lt has been estimated that only a few
patients (20%) know they engage in parafunction. Most
patients deny the activity, but when asked to duplicate
jaw movements associated with parafunction, they will
duplicate them easily. Stressful lifestyles, heavy occlusal
wear facets on nonfunctional tooth surfaces, fractured
cusps, tooth mobility, hypercementosis, tenderness and/
or hypertrophy of masticatory muscΙes, and |imited
mandibular opening are frequent "bedfellows" of
parafunction, and their presence in a given case could
have diagnostic ramifications (Figure 19).
3.
-

58. NoNsURGlcAL THERAPY: SOAL|NG AΝD Rooτ PLAN|NG. occLUsAL AND ANτlBloτlc τHΕRAPY
ffir;..,r]r..:,r,L:.,.::,
:::: L:;;. ' ,'.; 1:,
I l:',1,
.:l:',il::,ir'
FIGUFIE 19. A dried specimen of mandibular posterior teeth showing
heavy Wear on supporting and nonsuppofting cusps. τhese wear
facets provide enlarged surface areas for occlusal contact and,
thereby, potentially increase the forces acting on teeth during
parafunction.
. Occlusal analysis. ldeally, the occlusal analysis should
be carried out on an adjustable articulator \Λ/ith the maxil-
lary cast mounted on the hinge axis on an anatomical arti-
culator, and the mandibular cast should be mounted
in centric relation.Alternatively, the analysis may be
performed in the mouth' ln either case' occΙusal contacts
should be recorded along the operator-guided, patient-
generated, movements of the mandible that originate in
centric relation.
How ls Force Control Achieved for a Periodontal
Patient?
Force control in a patient with occlusal traumatism may be
achieved by occlusal adjustment of the natural dentition
(occlusal adjustment), removable appliance therapy (night
guards), removable and fixed provisional splint therapy,
orthodontics, and fixed restorative dentistry. Τhis chapter will
discuss general guidelines for occlusal adjustment and appli-
ance therapy for cases of moderate chronic periodontitis with
occlusal traumatism that can usually be managed effectively
\Λ/ith these two traditional forms of force control. The occlusal
management of advanced periodontitis cases that display
posterior bite collapse, loss of occluding vertiοal dimension,
and skeletal malocclusions that will require the coordinated
efforts of combined periodontal, prosthodontic, and ortho-
dontic providers will not be discussed here.
What Are Occlusal Adlustment and Occlusal
Appliance Therapy?
Occlusal adjustment is the reshaping of occlusal surJaces of
teeth by grinding to create harmonious contact relationships
betνveen upper and lower teeth. This process is also known
as occlusal equilibration or seΙective grinding' The term odon-
toplasty is commonly used to describe the act of ocοlusal
adjustment/oοclusal equilibration/selective grinding. The
guiding principals of occlusal adjustment are the preservation
and refinement of supporting cusp tips in centric ocοlusion
and the elimination of lateral interfering centric and excursive
contacts. Wear facets are also eliminated by vertical grooving
and rounding of edges to reduce the tooth contact surface
area during parafunction.
. Occlusal adiustment. lt is axiomatic that the muscles of
mastication be free of myospasm or other functional
disorders before occlusal adjustment is performed.
Spastic, splinted muscles occur in response to noxious or
injurious tooth contacts and result in neuromuscular
patterns of jaw movement that "avoid" the offending tooth
contact(s). These same οontacts may be the target
contacts of occlusal adjustment, and it is pointless to
adjust an occlusion νvhen target contacts cannot be
recorded. Stressful life-styles or events commonly
provide a psychic background for myospasm (Figure 20).
FIGURE 20. A clinical photograph showing occlusal adiustment of a
centric interference by coronoplasty. Flame shaped or conical high
speed rotary instruments are ideal for the reduction of inclines and
facets.
Pain or tenderness in the masseter, temporalis, or lateral
pterygoid muscles, hypertrophy of the masseter muscles,
limitation in opening the ja\Λ/S, and/or Subconscious resis-
tance to movement of the mandible in hinge-axis and
border movements are signs of myospasm. The applica-
tion of heat to the affected muscles, and the use of an
anterior bite-plane appliance for 1-2 weeks is usually all
that is required to "deprogram" avoidance patterns and
ultimately relieve the myospasm. Patients who are refrac-
tory to this noninvasive therapy may have a more serious
form of myofascial pain dysfunction (MPD) syndrome or
other temporomandibular joint (ΤMJ) disease' Patients
vι/ith refractory pain and dysfunction will require care by a
specialist and should be referred for treatment as soon as
possible.
Detailed methods of occlusal adjustment are presented in
standard periodontics and occlusion textbooks.
Occlusa! appliance therapy.
1. The primary function of appliance therapy in perio-
dontal patients is force control in secondary occlusal
trauma. Αdditional benefits from occlusal appΙiances
in periodontitis patients incΙude splinting of teeth in
the appliance, control of super-eruption, and
anchorage for minor tooth movement. Typically, the
force control appliance will provide fulΙ occlusal
coverage of either the maxillary or mandibular teeth.
The decision over which arch will be chosen for appli-
ance therapy will be affected by Angle's classifica-
tion, the location of teeth that might require splinting,
and the location of teeth that need to be controlled for
super-eruption. Wrought wire clasps and the anterior
Hawley appliance wire are unnecessary unless the
56

59. CHAPTΕR 6
appliance is modified to accomplish anchorage for
orthodontics. Τhe occlusal scheme for full occlusal
force control appliances is maximum οuspal contact
on the flat occlusal surfaces of the guard in centric
relation and all excursions. Because there are no
indentations for cuSp interdigitation, full occΙusaΙ
appliances do not have a centric occlusion. As suοh,
they have been proven io be effeοtive in the long-
term maintenance of muscle "deprogramming." They
are not recommended for initial deprogramming of
splinted muscles of mastication (Figures 21Α and B).
FΙGURE 21Α' A clinical photograph of a fuιl occlusal maxillary appliance
for force control. The appliance is designed to produce a minimal
increase in the vertical dimension of occlusion.
F|GυRE 21B. The appliance Will provide maximum occlusaΙ contact in all
excursiοns. Ιt will also provide intra-arch splinting of teeth during
parafunction,
2. ln patients who have a normal periodontium and
demonstrate heavy occlusal wear of parafunctional
origin, or who have a history of fracturing restorations
or teeth, an occlusal/night guard may be prescribed
aS an ablative shield. Force controΙ may not be aS
much of an issue in these patients as tooth protec-
tion, particularly in cases where teeth have normal
amounts of periodontal support. This appliance
allows the patient io continue engaging in parafunc-
tional aοtivity withoui additional occlusaΙ wear.
lnstead of irreversible tooth \η/ear as a consequence
of parafunction, the appΙianοe is ablated.
3. ln patients who have mild MPD and where muscle
deprogramming is required before occlusal adjust-
ment, an anterior bite plane may be constructed
covering the lingual surfaces of the six maxillary ante-
rior teΘth. A Hawley labial wire is οommonΙy included
in the appliance to stabilize tooth position. A lingual
platform establishes occlusal contact with the six
mandibular anterior teeth, increases the occluding
vertical dimension, and "discΙudes'' all posterior teeth.
The net effect of this appliance is that noxious tooth
contacts are prevented while the patient wears the
appliance. The expected outcome should be the
reduοtion of myospasm in the muscles of mastication
(Figures 22A and 228).
F|GURE 22Α. A clinical photograph of an occlusal appliance with a
Hawley wire. τhis appliance is best suited for short periods of
muscle deprogramming.
F|GURE 22B. τhe anterior bite plane makes contact with ιhe mandibular
anterior teeth only. Poslerior teeth not contained in the appliance are
subiect to supraeruption.
Because anterior bite plane appliances are reasonably
simple to fabricate and usually require less chair time to
adjust than the full occlusal appliances, it is tempting to
use these appliances for longterm force control. One
consequence of this approach may be the extrusion of un-
opposed teeth and unexpected additional occlusal prob-
Ιems. Ιt is recommended ihat anterior bite-plane
appliances be used only for short{erm muscle depro-
gramming.
Force control has been a tradition in the treatment of
periodontitis. lnitially, it was believed that forces acting on
teeth produced gingival recession and attachment loss
and that periodontal therapy was incomplete unless
these forces were eΙiminated or at least οontrolled.
Today, the paradigm is that occlusaι trauma and marginal
57

60. Ξ
NONSURG|CAL τHERAPY: SCAL|ΝG AND RooT PLANING, OCCLUSAL AΝD ANτlBloTlC THERAPY
periodontal diseases are probably distinct clinical entities.
occlusal trauma iS treated !η/ith force control and perio-
dontitis is treated by infection control.
The sequence of treatmΘnt for each is critical. Effeοtive
treatment of marginal periodontal inflammation may
decrease some of the Signs and symptoms of oοc|usal
trauma. ln addition, reactive repositioning (closure of
open contacts) may take place after inflammatory
disease control. There is also evidence that untreated
inflammatory disease may impact negatively on the
repair of occlusaΙ trauma. |n some cases, occlusal
therapy may not be necessary after inflammation control.
ANTIBIOTIC THERAPY
What ls Anti-infective Periodontal Therapy?
Anti-infective theraρy is the use of local and systemic
agents to control the bacterial etiology of the inflamma-
tory periodontal diseases. τhese agents include both
locally and systemically delivered antibiotics and chemo-
therapeutic agents.
When Are Antibiotics lndicated in PerΙodontal
Therapy?
lndications for the use of antibiotics in periodontal therapy
include the following:
ο PeriodontaΙ abscess (see chapter on "Periodontal
Emergencies" on page 105.)
. Aggressive periodontitis
- Juvenile periodontitis
-
Rapidlyprogressiveperiodontitis
-
Prepubertal periodontitis
ο Chronic periodontitis with persistent severe gingival
inflammation
ο Refractory forms of chronic or aggressive periodon-
titis
o Protection vs subacute bacterial endocarditis
. When surgical therapy is contraindicated
ο To control local sites of inflammation
ο As an adjunct to conventional mechanical therapy
ο Subantimicrobial dose of doxycycline to stabilize
collagenase activity
What Antibiotics Are Commonly Used
Systemically in Periodontal Therapy?
Τhe most commonly used antibiotics in periodontal
therapy are:
. Αmoxicillin (with or without οlavulanic acid -
AugmentinΘ)
. Metronidazole
. Ciprofloxacin
o Clindamycin
. Doxycycline
. Azithromycin
What Are Some of the Risks of Using
Systemic Antibiotics in Periodontal Therapy?
There are general and specific risks in the use of antibi-
otics in periodontal therapy. These include:
ο AΙlergic reactions (delayed or immediate hypersen-
sitivity)
o Gastrointestinal problems
ο Development of superinfections by unaffected orga-
nisms
. Development of resistant bacterial strains
How ls the Appropriate Antibiotic Regimen
Chosen?
It is preferable that the bacteria associated with the
inflamed sites have been identified before the selection of
antibiotic therapy. Bacterial identification may be accom-
plished by culturing the bacteria from within the pocket or
by using DNΑ probe identification technology. The
advantage of culturing is that sensitivity of the identified
bacteria to specific antibiotics can also be reported. The
major advantage of DNA probe technology is that viable
bacteria are not needed to identif y the peri-
odontopathogens.
Antibiotics are prescribed without identifying the asso-
ciated microorganisms and the patient is monitored for
for clinical success. The major risks in this approach
are the selection of an antibiotic to which the pathogen
is resistant or the development of a superinfection caused
by an unidentified and unaffected bacterial strain.
What Are the PrincΙpIes of Antibiotic Dosing?
. Employ high doses for a short duration
. Use an oral antibiotic loading dose, especially with
the tetracyclines or \Λ,ith an acute infection
ο Achieve blood levels of the antibiotic at 2-8 times
the minimal inhibitory concenιration
. Use frequent dosing intervals, particularly with anti-
biotics with a relatively short half-life
ο Determine the duration of therapy by the remission
of disease
What Are the Potential Problems With Drug
lnteractions?
Depending on the mechanism of antibiotic action, combi-
nations of antibiotics may have an additive, synergistic, or
antagonistic effect. Static antibiotics used in combination
generally exhibit an additive effect, bacteriocidal antibi-
otics exhibit a synergistic effect, and the combination of
bacteriocidal and bacteriostatic agents exhibit an antago-
nistic effect. Antibiotics may also react \Λ,ith other medica-
tions the patient may be taking or interact with certain
foods (eg, tetracycline chelating with calcium or other
divalent cations). lndividual drug interactions can be
found in the section on specific agents below.

61. cHAPτER 6
What Are Some Gommon Dosing Regimens
for Systemic Antibiotic Use in Periodontal
Therapy?
Arriving at an appropriate antibiotic selection and dosing
regimen is an inexact science. lndividual antibiotics or
combination therapy may be selected depending on
whether or not the infection seems to be οaused by one
bacterial species or is a mixed infection, as most perio-
dontal infections tend to be. ProtocoΙ selection may
depend on the practitioner's knowledge, previous experi-
ence, and perhaps by the most recent advertisement or
sales representative to speak with the practitioner. The
suggested regimens that follow are taken from recom-
mendations of Dr. Thomas Rams, Director of the Oral
Microbiology Testing Service at Τemple University and a
long-time researcher in the field of antibiotic therapy in
the treatment of the periodontal diseases. While there are
other suitable regimens, these recommendations are a
good starting point for those practitioners in need of guid-
ance.
GUlDELlNEs lΝ τHE sELEcTloN oF sYsTΕMlc
ANTlBloτlcs lN PER]oDoNTAL THERAPY
Thomas E. Rams, DDS, MHS
Oral Microbiology Testing Service
Department of Periodontology
Temple University School of Dentistry
Philadelphia, PΑ
1-800-788-OMTS
Possible Antibiotic RΘcommendations for Specific
Microbiological Test Findings
*For
οombinations of anaerobic and facultative perio-
dontal pathogens:
1St choice: Metronidazole + amoxicilΙin or Augmentino
(250 mg each TID for 5-7 days, or metronidazole 500
mg and Αugmentin@ 875 mg each BlD for 5-7 days)
2nd choice: Metronidazole + ciprofloxacin (500 mg each
BID for 5-7 days)
(Note: Combination drug regimens are generally
preferred to single antibiotic administration)
*
F or ActinobacilΙus actinomycetemcomitans:
1st choice: Metronidazole + amoxicillin or AugmentinΘ
(250 mg each TID for 5-7 days, or metronidazole 500
mg and Augmentino 875 mg each BID for 5-7 days)
2nd choice: Ciprofloxacin (adults only) alone or with
metronidazole (500 mg each BID for 5-7 days)
3rd choice: Azithromycin (500 mg/day for 3-5 days)
4th choice: Doxycycline (100 mg BID for 14-21 days)
*For
anaerobic pathogens (Porphyromonas gingivalis,
Prevotella intermedia, Bacteroides forsythus, Fuso-
bacterium species, Peptostreptococcus micros, and
Campylobacter speοies):
1st choice: Metronidazole + amoxicillin or AugmentinΘ
(250 mg each TID for 5-7 days, or metronidazole 500
mg and Augmentino 875 mg BID for 5-7 days)
2nd choice: Augmentin@ (250-500 mg TlD, or 875 mg BID
for 7 days)
3rd choice: Metronidazole (500 mg BID for 7 days)
4th choice: Clindamycin (150 mg TID for 5-7 days)
5th choice: Αzithromyοin (500 mg/day for 3-5 days)
6th choiοe: Doxycycline (100 mg BlD for 14-21 days)
(Note: Some Fusobacterium strains may metabolize
metronidazole and reduce its efficacy; some Peρto-
streptococcus mrbros strains are resistant to tetracy-
clines, metronidazoΙe, and azithromycin; Prevotella
intermedia is often resistant to tetracycline antibi-
otics.)
*For
enteric rods, Pseudomonads, Εnterococci, andlor
Staphylococci.
1st choice: Ciprofloxacin (usually given with metronida-
zole - 500 mg eaοh BlD for 5-7 days)
2nd choice: Variable depending on strain susceptibility
-For
beta-hem olyΙilc Streptococci.
1st choice: Augmentino (250-500 mg TID or 875 mg BID
for 7 days)
2nd choice: Clindamycin (150 mg TID for 5-7 days)
What Are Some Common Reasons for
Antibiotic Failure in Periodontal Therapy?
. lnappropriate choice of antibiotics (the microor-
ganism is not susceptible to the antibiotic of choice)
ο lncorrect / inadequate doses
ο Emergenceof antibiotic-resistant microorganisms
o Too low a blood concentration of the antibiotic
. Slo\ν gro\Λ/th rate of the microorganisms
. lmpaired host defenses
ο Patientnoncompliance
ο Antibiotic antagonism (eg, using bacteriocidal and
bacteriostatic antibiotics togethe0
o lnability of the antibiotic to penetrate to the site of
infection
. Limited vascularity or decreased blood flow
ο Unfavorable local factors
o Failure to eradicate the source of infection
What ls Subantimicrobial Antibiotic Usage?
It has been demonstrated that tetracycline and the tetra-
οycline derivative doxycycline (subantimiοrobial dose of
doxycycline - SDD) can reduce collagenase activity \Λ/hen
used in doses too low to have any antimicrobial effect.
The use of SDD has been shown to reduce the rate and
amount of attachment loss associated with advancing
periodontal disease. SDD is currently used as a 20 mg
dose of doxycycline t\ivice a day. Long-term studies have

62. NoΝsURGlcAL τΗERAPY: scALIΝG AND Rooτ PLANING. occLUsAL AND ANτlBloτlc τHERAPY
been for g-month
durations. There is little data on the manufacturers provide detailed instructions, there is a
effectiveness of SDD therapy for longer periods of time. learning curve to developing an efficient technique for the
use of eaοh product.
What Are the lndications for the Use of
Locally Delivered Antibiotic and Antimicrobial
Therapy? What Therapeutac Mouthrinses Are Available
to Reduce PIaque and Help Control Gingival
o Local site(s) with signs of inflammation that have not lnflammation?
responded to conventional mechanical therapy
rt shourd be remembered that a mouthrinse must not onry
. Local site that has recurrent signs of inflammation at reduce plaque but also have a therapeutic effect.
a maintenance visit Currently, long-term, 6-month studies support only the
use of mouthrinses containing 0.12% chlorhexidine
. Buying time for a so-called hοpeless tooth before gluconate or the "essential oils" (phenolic compounds
extraction thymol, menthol, eucalyptol, methyl salicylate) to reduce
plaque and gingivitis. These mouthrinses are available to
. Resolving marginal inflammation when oral hygiene consumers through a variety of manufacturers and
has reached maximum effectiveness distributors. τhese mouthrinses must be used appropri-
ately, usually a 3O-second rinse twice daily to be effec-
tive. These rinses have an alcohol vehicle ranging from
What Are Some Common LocaI Antibiotic and
17"/o Ιo 26'7%'
Antimicrobial Delivery Systems?
ActisiteΘ - Tetracycline in a nonresorbable
,ethY| What Are other Periodontat Conditions That
-
acetate fiber (1st generation' no longer availabie;
r,,ray nequire Crremoillerapeuiic Treatment?
ArestinΘ - MinocycΙine in a resorbable bead vehicle
. Vesiculobullous diseases
Atridox@ - Doxycycline in a resorbable polylactide gel
-
Benign mucous membrane (cicatriciar) pemphi-
PerioChipΘ - Chlorhexidine in a resorbable gelatin
goid
wafer - Erythema multiforme
-
Lichen planus
How Are These Local Antibiotics Delivered to
* Pemphigus vulgaris
the Site of Choice? ο Viral infections
Each product is delivered in a different manner -
Herpes simplex
depending on the delivery vehicle. Even though the -
Human immunodeficiency virus
60

63. cHAPτER 7
CHAPTER 7: SURGICAL TREATMENT: PRINCIPLES
The treatment of periodontal disease has included some
form of surgery for over 100 years. Early on, periodontal
surgery was performed to remove infected and/or
necrotic bone. By the middle of the 20th Century, thera-
pists vvere more intent on performing periodontal surgery
for pocket elimination or reduction. lndeed, most perio-
dontal surgery performed during the 1950s and 1960s
was resective in nature. The dominant philosophy of the
time \ivas that removal and reshaping of alveolar bone
was essential to assure that the pocket elimination
achieved during surgery would remain stable. ln the
1970s, concepts of bone grafting emerged that chal-
lenged the wisdom of removing bone to maintain shallow
pockets when pocket reduction might be achieved by
graft mediated regeneration of lost periodontal tissues.
Regeneration has become a predictable periodontal
surgical procedure and has eroded the once dominant
role of resective surgery in periodontics.
νvhat Are the Basic Principles of Periodontal
Surgery?
The basic principles of periodontal surgery are no
different than any other form of surgery.
Αbove all, periodontal surgery should do no harm to the
patient. ln addition, the surgery should:
. Be discussed, in alΙ aspects, in advance with the
patient
. Be understood, in all aspects, by the patient and that
understanding should be acknowledged as written
consent
ο Be as atraumatic as possible
. Be conducted in an aseptic environment
o Not exceed the limits of physical tolerance of the
patient in terms of discomfort, blood loss, and stress
. Produce a benefit for the patient
. Be actively monitored postoperatively to assure
uneventful healing
What ls Meant by Periodontal Surgery? What
Are the Categories of Periodontal Surgery?
The term surgery describes that branch of medical
science that is concerned with the treatment of diseases
or injuries by means of manuaΙ or operative methods.
Periodontal surgery is any surgical procedure/operation
used to treat periodontitis or modify the morphoΙogy of
the periodontium. Subcategories of periodontal surgery
based upon expected outcomes incΙude:
. lmplant surgery, defined as operations concerned
with the placement, uncovering, and removal of
dental implants. τhe repair and modification of soft
and hard peri-implant tissue are viewed as implant
surgery.
. Osseous surgery, defined as operations that modify
bone aΙtered by periodontal diseases by either
reshaping or removing alveolar bone. The relation-
ship of the cementoenamel junction to the crest of the
alveolar bone is usually changed by osseous surgery.
o Reconstructive surgery, sometimes called regenera-
tive surgery, defined as operations that restore a
body part to a more normal appearance or funοtion.
. Mucogingival surgery, defined as procedures
designed to correct defects in the morphology or
position of the dentogingival junction. Mucogingival
surgery is also used to augment the dimensions of
the dentogingival junction.
o Re-entry surgery, defined as a second stage opera-
tion performed to improve, enhance, or evaluate the
results obtained from a previously performed proce-
dure.
When ls Periodontal Surgery Necessary?
What Are the Diagnostic and Therapeutic
lndications of Periodontal Surgery? Are There
Any Contraindications to Periodontal
Surgery?
The necessity for periodontal surgery is outlined in the
following three basic goals/objectiyes. Periodontal
surgery wil!:
. Provide access to root surfaces exposed to periodon-
titis for root debridement
ο Provide access to periodontal bony defects for
correοtion by osseous or regenerative procedures
o Provide an opportunity to remove periodontaΙ tissue
infected by periodontal pathogens
The therapeutic indications tor periodontal surgical proce-
dures may be any combination of the following:
ο Allow more efficient and effective Scaling and root
planing
. Reduce or eliminate periodontal pockets
o Remove inflamed periodontaΙ tissue
. Remove gingival overgrowths
ο Create an environment that will Support regeneration
of new attachment or a new attachment apparatus
ο Correct mucogingival deformities that require root
coverage or gingival augmentation
. Create a periodontal environment that will foster
optimal oral hygiene
. lmprove periodontal aesthetics
. Establish a periodontal environment that supports
fixed and removable restorations in health and
comfort
The diagnostic indications of periodontal surgery are:
. Biopsies
. Exploratory fΙap procedures
Periodontal surgery is contraindicafed when:
. The surgery that has been proposed is not in the best
interest of the patient. Recommendations for surgery
61
-

64. sURGlcAL TREATMEΝT: PRlNclPLES
should be based upon the patient's needs and not on
the experience or skill leveΙ of the provider. lf the
provider cannot satisfy those needs, the patient
should be referred to a qualified provider.
There will not be enough time following the surgery to
periodically monitor healing and therapeutiο
outcomes. Postsurgical treatments and evaluations
should ocοur regularly during the first 3 months of
healing.
There are significant health considerations for the
patient.
The patient has a history of cigarette smoking.
Smoking remains the number one environmental risk
factor in periodontitis. lt is also associated \Λ/ith poor
outcomes from periodontal regeneration and dental
implant surgery. The decision to perform periodontal
surgery for a smoker should be made only after the
patient ackno\Λ/ledges the surgical risks on an
informed consent document. Counseling on smoking
cessation is an essential component of initial perio-
dontal therapy.
Following initial therapy, inflammatory disease and
plaque control are inadequate. Surgery should not be
performed in a plaque-infected periodontium!
The periodontitis has been so severe that the sur-
gical risks exceed expected benefits. Surgery to
save hopeless teeth may affect the prognosis of
potentially salvageable teeth. Τooth removal may be
a more reasonable option.
What ls Aseptic Technique? Can Asepsis Be
Achieved in the Oral Cavity?
Asepsis means free from infection or septic material. lt
also means sterile (ie, without life). Αseptic technique
refers to a method/protocol whereby asepsis is achieved
and maintained during a surgical procedure. Rigid
aseptic protocols as practiced in hospital operating rooms
cannot be achieved in periodontics, or for that matter, in
any discipline that involves the oral cavity.
The purpose of an aseptic technique in periodontal
surgery is to prevent the introduction of environmental
bacteria into periodontal surgical !η/ounds. The potential
sourοes of contaminating organisms are the operatory,
the personnel who perform the surgery, the patient, and
the instruments used during the surgery. τo assure that
these potential sources of contamination are controlΙed,
the aseptic teοhnique for periodontal surgery must occur
at 4 levels. They are:
. Preparation of the personnel. lndividuals involved
in periodontal surgical procedures should be trained
in the rationale and the teοhnical aspects of the
aseptic technique. The training should incΙude: Αn
understanding of barrier protection, gowning and
gloving teοhniques, and the discipline of maintaining
sterility of barriers and instruments. Principles of the
aseptic technique should be formally reviewed and
updated at least annually.
lndividuals directly involved in the procedure chair-
side should vvear a clean surgical mask, a clean
surgical cap, a sterile surgical gown, and sterile
surgical gloves. Once gowned and gloved, the
surgeon and the chairside assistant must not lo\,ver
their hands below their \ivaists or contact nonsterile
surfaces (Figure 1). lndividuaΙs who will "circulate" or
assist in the operatory to adjust Mayo stands and
instrument trays, "drop" instruments and supplies,
adjusVregulate power-driven instruments, etc must
Wear a clean οap, mask, and examination gΙoves.
Circulating assistants must also be alert for acci-
dental breaches in aseptic technique anywhere in the
operatory.
F|GUHΕ 1. Aseptic τechnique for surgical Personnel. τhe surgeon and
the assistant must wear a clean mask, a clean hair cover, and sterile
surgical gloves. τhe patient's chest and abdomen are covered with
sterile surgical drapes. Light handles must be covered with sterile
aluminum foil.
. Preparation of the operatory. The dental operatory
must be as clean as any hospital operating room.
Surfaces, including the floor, must be cleaned and
disinfected before and after each procedure. The
antiseptic agent must be used according to the
protocol suggested by the manufacturer and
approved by state and local health agencies.
Surfaces that will be touched by the surgeon or assis-
tant during the surgery (eg, light handles, water
syringes, handpieces, hoses, etc) must be wiped with
antiseptic and wrapped with sterile aluminum foil
before the procedure begins.
The water used to irrigate the wound or cool instru-
ments should be sterile, and dental unit water lines
should be treated regularly \Λ,ith antiseptic agents to
prevent biofilm formation (Figures 1, 2, and 3).
. Preparation of the patienι. τhe patient should be
dressed in loose-fitting, comfortable clothing. When
the patient is seated in the chair, the perioral tissues
should be washed \,vith an antiseptic soap. Once
positioned for the procedure, the patient's head, hair,
and eyes should be wrapped and covered with sterile
drapes. The patient's torso, shoulders, arms, and
hands shouΙd be covered with sterile drapes during
the surgery (Figures 1, 2, and 3).

65. CHAPτER 7
FIGURE 2. Aseptic Technique for the Patient and Operatory. The patient's
hair and eyes are covered with sterile surgical drapes. Air and water
lines must be covered with sterile aluminum foil.
FlGURE 3. Aseptic τechnique for the operatory. Working surtace such as
Mayo stands and bracket tables must be covered with sterile
surgical drapes" Ηand pieces and ultrasonic instruments must be
covered with sterile aluminum foil. τhe water used in high-speed
rotary and ultrasonic instrumentation must be steriΙe as well.
o Preparation of the instruments. All instruments
used in the surgical field must be individually wiped to
remove debris and then ultrasonically cleaned in an
antiseptic solution. They must then be dried, pΙaced
in cassettes, wrapped, and autoclaved.
What ls a Periodontal Flap? What Are the
Technical Features That Are Shared by All
Periodontal Flap Procedures?
A periodontaΙ flap is a Segment of marginal periodontal
tissue that has been surgically separated coronalΙy from
its underlying support and blood supply and attached
apically by a pedicle of supporting vascular connective
tissue. All periodontal flaps have four critical sιages in
common. They are:
lncision of marginal attachment
Elevation by sharp or blunt dissection
Placement or repΙacement
Protection
What Are Partial Thickness and Full Thickness
Periodontal FIaps?
FuΙl thickness periodontaΙ flaps include the surface
mucosa (defined as epithelium, basement membrane,
and connective tissue lamina propria) and the οontiguous
periosteum of the underΙying alveolar bone. FulΙ thick-
ness flaps are usually elevated by blunt dissection using
a periosteal elevator, and alveolar bone is temporarily
exposed during the procedure. ln the process, the blood
supply to bone provided by the periosteum is severed.
νvhile the blood supply is re-established during healing,
infΙammation and associated bone resorption (locaΙized
alveolar osteitis) may produce a permanent deformity in
alveolar bone height and width. Full thickness periodontal
flaps are used for osseous resection and periodontal
regeneration procedures (Figure 4).
FIGURE 4. A Clinical Photograph of a Full-Thickness Mucoperiosteal Flap.
A scalloped internal bevel envelope incision was used and all of the
gingiva was preserued to facilitate wound closure. Alveolar bone is
denuded temporarily. τhe full-thickness periodontal flap provides
optimal access for scaling, root planing, and debridement of perio-
dontal deformities.
A paιtiaΙ thickness f/aρ includes only the mucosa, which
iS separated from the periosteum by Sharp disseοtion.
Alveolar bone is not exposed. Τhe major advantage of a
paιtial thickness flap is that the blood suppΙy to the alve-
olar bone surface is not disturbed, and, the localized
osteitis and bone resorption observed during the healing
of fu|l thickness flaps is minimized. Τhe major disadvan-
tages of paιiial thickness flaps are the technical difficulty
required to perform the procedures successfulΙy and the
high probability of perforation. The vascularity of the
retained periosteum is a frequent source of
intraprocedural bleeding and the limited visibility of perio-
dontal defeοts it produces (Figure 5)'
a
o
a
o

66. sURGlcAL TREATMENT: PRlNοlPLES
FlGURΕ 5. A clinical Photograph of a Partiaι τhickness Mucosal Flap. Α
scalloped internal beveΙ incision was used to separate mucosa trom
underlying periosteum. Alveolar bone remains covered with retained
periosteum. The partial lhickness flap provides adequate access to
root surfaces for scaling and root planing. Partial thickness flaps are
prone to perforation and tears.
A variant of the partial thickness flap is the periosteal
retention procedure. PeriosteaΙ retention is basic to recip-
ient sites for free autogenous sofi-tissue grafts and
vestibular deepening procedures, such as the periosteal
fenestration or the periosteal separation (Figure 6).
FIGURE 6. A Clinical Photograph of a Periosteal Retention Procedure
Used to Prepare a Recipient site for a Free Autogenous Soft-τissue
Graft' τhe incision for the mucosal flap in this case was made at the
mucogingival junction and the remnants of the marginaΙ gingiva
have been removed. lniury to the mental nerve is always a risk
during periosteal retention procedures in the mandibular premolar
region.
What Types of lnitial lncisions Are Made in
Periodontal FIap Surgery? What ls an
Envelope Flap? What ls Crestal Anticipation?
lnitial incisions in periodontal flap surgery are horizontaΙ
internal beyel incisions. The incision line will begin either
in the sulcus, at the gingival margin, or at a submarginal
point in the keratinized gingiva. lnternal bevel incisions
end on the facial surface of the underlying alveolar bone
and are designed to thin the buccal lingual dimensions
of the flap margin. lnternaΙ bevel incisions that end at
the aΙveolar crest are used \η/hen fuΙl gingival retention
is required.
SulcuΙar Incision. The initial incision is a scalloped
incision that is made into, and follows, the gingival
sulcus (Figure 7).
Marginal lncision. Τhe initial incision is a sοalloped
incision at the gingival margin (Figure 7).
Submarginal lncision. Τhe initial incision is made
apical to the gingival margin but sufficientΙy corona| to
the mucogingival junction to preserve gingiva on the
fΙap (Figure 7).
FΙGURΕ 7. A line drawing showing three possible orientations of initial
internal bevel incisions. sulcular inοisions (A) and marginaΙ inci-
sions (B) are used when the zone of keratinized gingiva is narrow
and preservation of gingiva is criticaι. submarginal incisions (c) are
used when the zone of keratinized gingiva is wide and where the flap
must be thinned internally.
FIGURE 8. A clinical photograph showing a partial thickness lateral
pedicΙe flap placed over the mesial buccal root ot a maxillary first
molar. τhe releasing incision was made over interproximal bone to
preserve enough papillary tissue on the flap for suturing and to
minimize surgical trauma to the thin bone over the root prominence
of the second premolar.
b4

67. Access to roots, marginal alveolar bone, and bony
defects can be adequately achieved in most instances
υsing envelope flaps (ie, flaps produced by horizontal
sulcular, marginal, or submarginal incisions). ln some
cases where acοess is difficult to achieve or where the
risk for undue surgical trauma is high, flaps may be
"relaxed" using vertical and/or cutback ("hockey-stick")
releasing incisions. Vertical incisions are made parallel
with the long axis of the teeth in the area^ They must be
placed at line angles of teeth to minimize postsurgical
marginal deformities and through the muοogingival junc-
tion to permit adequate flap "relaxation". The cardinal
principle in planning vertical or cutback releasing inci-
sions' is that the blood supply to the flap margin is
preserved. To do so, the flap should be at least as wide at
its base as it is coronally (see Figure 8).
Crestat anticipation incisions are variants of the submar-
ginal incision and are indicated in areas where the
mucogingival junction is absent and the flap cannot be
repositioned. The best example of this scenario is where
palatal flaps are used for access in osseous surgery.
These inclsions require abundant keratinized gingiva be
present, they are peι'formed to "antiοipate" the position of
ihe future gingival margin in relation to the future crest of
the alveolar bone when apical positioning of the flap is
not possible (Figure 9).
achieved mainly by gains in clinical attachment mediated
by repair.
1. Replaced Flap (RF). The RF is a full-thickness, full
gingival retention mucoperiosteal flap. lt is a "work-horse"
of periodontal surgery as it can be employed in one or
more of the following periodontal applications:
. Access to roots and bony defects in regenerative
surgery procedures
. Αccess to roots in open flap debridement proce-
dures
. Aοοess in diagnostic exploratory procedures
. Access for treatment of periodontal emergencies
RFs are full gingival retention procedures. The initial inci-
sions are always sulcular in origin and include as much
interdental tissue as possible (Figure 10).
FIGURE 9. A clinical photograph shosring a crestal anticipation incision
_ -on
tne palate. The giigii/al tissue ioronal ιo the incision will be
δ.or.i fo, ucc."s ib b,-one and roots. crestal anticipation incisions
a.J ,seα to "anticipate" the apical Position
ot the flap margin at the
aiveoiir οrest wneλ the tιap iiself cannot be aρically positioned'
VVhat Is Meant by Positioned and
Repositioned FIaPs?
Periodontal flaps may be categorized acοording to
whether they will, at the conclusion of the procedure, be
either repositioned back to their presurgical location or
positioned to a nevv, alternative location'
Repositioned ftaps are "open and close" procedures
\Λ/here the coronal fΙap margins, keratinized gingiva, and
the mucogingival junction are returned to the same rela-
tive position on the teeth and bone that they occupied
before flap elevation. Repositioned flaps, as a category'
include replaced flaps, modified Widman flaps' and exοi-
sional new attachment procedures. They all heal by
repair (ie, by a long junctional epithelium and conneοtive
tissue adhesion or attachment) and are considered
pocket reduction procedures. The pocket reduction is
FlGURE 1o. A line drawing showing the initial sulcular incisioΠs.(dotted
lines) for a replaced fιap. Diagonal incision lines that extend across
the iilerproxi'mal spacd from the distal lingual ιine an9les to mesial
facial lin; angles iicrease the chances of primary wound cιosure'
The flaps are raised by blunt dissection from the under-
lying alveolar bone. Conceptually, RF reflection does not
extend apical to the mucogingival iunction, and the RF
οannot be positioned apically, coronally, or laterally. RFs
are "replaced" back to their presurgical location and are
sutured to achieve primary wound closure interdentally.
Repositioning of the RF minimizes postsurgical reces-
sion. RFs are the flap of choice in aesthetically sensitive
regions of the dentition. RFs are indicated for the treat-
ment of suprabony pockets or where periodontal repair is
possible. They are also indicated for aοcess to intraos-
seous defects for periodontal regeneration. ln reality,
many RFs are etevated apical to the mucogingival .iunc-
tion to achieve required access (see previous Figure 4).
Modified Widman Flap (MWF). The MWF is a modifica-
tion of the replaced flap. lt is a full{hickness flap that may
be used in open flap debridement and regenerative perio-
dontal procedures. Unlike the RF, the M\,VF is not a full
gingival retention procedure. Submarginal, scalloped,
2.
65

68. Ξ
SURGICAL TREATMENT: PRINCIPLES
internal bevel horizontal incisions are used to produce
prominent interdental extensions of tissue that ensure
primary flap closure (Figure 11). The MWF is indicated
when access to roots and intraosseous defects for
debridement is needed. Because of its greater opportu-
nities for primary closure that ensures graft retention, the
MWF is also indicated in regenerative procedures.
FIGURE 11. A line drawing showing the initial submarginal incisions
(dotted lines) for a modified νvidman flap. τhe incisions increase the
length of the interproximal tissue extensions. Diagonal incisions
(Figure 10) may also be used in the modified vidman flap design.
Positioned fΙaps are flap procedures where the coronal
margins of the flap are advanced apically, coronally, or
laterally to a ne\Λ/ loοation relative to the site they occu-
pied before the procedure. The category includes apicaιly
positioned flaps, coronaΙly positioned flaps, and laterally
positioned flaps. Like repositioned flaps, most positioned
flaps heal by repair (ie, a new attachment οonsisting of a
long junctional epithelium and connective tissue adhesion
or attachment).
Apically Positioned Flap (APF). The ΑPF is a full-thick-
ness, mucoperiosteaι flap. Like the RF, the APF is a
"work-horse" of periodontal surgery. lt is most commonly
used in conjunction with osseous surgery, and it has few
other applications (Figure 12).
Coronally Positioned Flap (CPF). The CPF is a full-
thickness mucoperiosteal flap that has almost exclusively
been used to restore gingival height and the zone of
attaοhed gingival over isolated areas of gingival reces-
sion. Since it is peformed to correct defects in the
morphology or position of the dental gingival junction, it is
classified as a mucogingival surgical procedure. Briefly,
the surgical principles and wound healing for the CPF are
similar to those of the APF. Sulοular initial incisions and
vertical releasing incisions through the mucogingival
junction are used to mobilize the flap. CPFs are elevated
from bone by blunt dissection and then positioned
coronally to the cementoenamel junction of the affected
tooth. Wound stability at closure, wound contraction
during healing, and local anatomic features will determine
the final amount of root οoverage achieved. ln instances
where there is an inadequate band of gingiva in the tissue
to be coronally placed, a CPF may be performed in 2
stages. ln the first stage, a free autogenous soft tissue
graft is placed to augment the gingiva. Three to six
months later, the second stage CPF is pedormed to
coronally position the nevι/ly augmented gingiva.
Laterally Positioned Flap (LPF). The LPF, also known
as Ιhe pedicle flap, is a positioned flap that is performed
to correct defects in the morphology, position, or amount
of attached gingiva. Positioned and repositioned flaps
are, in reality, pediοle flaps. They are all physically
attached at their apical base by a pediοle of lining
mucosa and an intact blood supply (Figure 13).
1.
2.
3.
FIGURE 13. A clinicat photograph showing a partial thickness pedicle
flap. τwo parallel reιeasing incisions have been made. The base of
the pedicle is as wide as flap margin.
ΑB
F|GUHES
'12Α
and B. A. Line drawing showing a marginal internal bevel
incision (dotted line) to the alveolar crest. B. τhe apical position of
gingival margin to the crest of the bone after osteoplasty (dotted line).
What Are the Anatomic Landmark
Considerations of the Maxilla and Mandible
Before Periodontal Surgery? How Do These
Landmarks Limit the Use of Relaxing
lncisions or Flap Position?
The surgiοal anatomic landmarks of concern in periodon-
ta| Surgery may be grouped into four οategories.

69. CHAPτER 7
They involve:
. Osseous morphology
. Musculotendinous anatomy
ο Vascular anatomy
. Redundant innervation
The osseous landmarks of surgical importance in the
maxilla are the maxilΙary sinuses, the maΙar processes of
the maxillary bone, the pterygoid hamulus, and palatal
tori (Figure 14).
FIGURE 14. A dried human specimen showing the palatal osseous
landmarks of impοrtance in periodontal surgery. τhey are the ptery-
goid hamulus, the palata| torus exostoses, and the greater paΙatine
foramen.
The osseous landmarks in the mandible of surgical
importance are mental and lingual foramina, the mylo-
hyoid and the external oblique ridges, the genial tuber-
cles, and lingual mandibular tori. The lingual undercut in
the mandibular molar area dictates careful full-thickness
flap reflection to avoid penetration into the sublingual
space and possible injury to the lingual nerve and artery
(Figure 15 and Figure 16).
FlGURΕ 15. A dried human specimen showing the mylohyoid ridge and a
lingual mandibular undercut. τhe linqua| nerve runs close to the
mylοhyoid ridge and is at risk durinσsurgery distal to mandibular
second and third molars,
Αlmost a|Ι osseous landmarks have a limiting effect on
the degree of flap reflection, flap positioning, and the use
of relaxing incisions. Τhey indireοtly affect the amount of
surgica| aοcess to teeth and bony defeοts.
FlGURE 16. A dried human specimθn showing the myΙohyoid ridge and
lingual mandibular undercut. lt also shows the attachment of the
buccinator muscle.
The musculotendinous landmarks are the attachment of
the mentalis muscle in the mandible, and the tendon of
the tensor veli palatini (TVP) muscle in the hamular notch
and the attachment of the bucοinator muscle (Figure 17).
Surgery in the maxillary tuberosity and the hamular notοh
also increases opportunities of accidental penetration of
the pterygomandibular space with possible injury to the
superior constrictor muscle and the medial or lateral pter-
ygoid muscles.
The vascular landmarks are the greater palatine artery
and the pterygoid plexus in the maxilΙa and the linguaΙ
artery and mental artery in the mandible. They are in
such proximity to the marginal periodontium to preclude
the pΙacement of relaxing incisions in palatal and mandib-
ular flaps. lf absolutely required for access, vertical inci-
sions within the gingiva only could satisfy that need
without risk of vascular injury. Τhe Ιocation of the mentaΙ
artery rules against verticaΙ and cutbaοk incisions and
lateral positioned full or partial thickness flaps in the
mandibular premolar region (Figure 17). The venous
pterygoid plexus in the pterygomandibular space is
always at risk io injury during loοaΙ anesthesia injeοtions
of the posterior superior alveolar nerve.
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FIGURΕ 17. A companion view ot the specimen in Figure 18 showing the
attachment of the buccinator buccal to mandibular molars. lt also
shows the mental ,oramen located between the apices of the premo-
lars-

70. SURGICAL TREATMENT: PRINCIPLES
The innervation landmarks are the lingual nerve, the long
buccal nerve, the inferior aιveolar nerve, and the mental
nerve in the mandible and the nasopalatine nerve and the
greater palatine nerve in the maxilla. Vertical and relaxing
incisions in the palate or in mandibular posterior facial
flaps increase the opportunity for regional transient or
permanent paraesthesia.
How Are Periodontal Surgery Wounds
Closed? What ls the Role of Suturing? What
Suture Materials Are Best Suited for the
Closure Periodontal Wounds?
All periodontal wounds, except for the gingivectomy,
require a method of closure that will maintain the reposi-
tioning or positioning of flaps during the early phases of
wound healing. Sutures are used to maintain wound
closure and flap position. Other methods of closure
include tissue tacks and the adhesive, cyanoacrylate.
Conceptually, tissue tacks offer an attractive alternative
to sutures, but they have not gained acceptance because
of the trauma they produce at flap margins and to bone.
Cyanoacrylates have potent hemostatic capabilities, and
they are effective in maintaining postoperative tissue
position. On the downside, they are technique sensitive.
They flow easily over tissue before they "set" and are
difficult to contain at νvound edges. Cyanoacrylates have
been known to 'TloW" between flap margins and bone,
which will only abrogate surgical outcomes. lf used care-
lessly in the oropharynx, cyanoacrylates could present
risks to the patient's airway.
Suture materials used in periodontal surgery are either
resorbable or nonresorbable. They may also be made of
braided naturaι fibers or nonbraided monofilament
synthetic fibers. Braided natural fiber sutures (ie, silk and
cotton), tend to absorb wiοk and retain bacteria in the
wound. Suture tracts through tissue νvilΙ develop clinical
signs of inflammation within 3-7 days, which necessitates
their removal at the end of the first postoperative νveek.
Monofilament synthetic fiber sutures will not absorb oral
bacteria and may be kept in the wound site for longer
periods of time. They are generally more expensive than
natural fiber sutures.
The choice of suture material should depend primarily
upon the type of surgery being performed and the require-
ments for the maintenance of extended wound closure
and, secondarily, upon office economics. The cost of the
suture material should not enter into the decision-making
process. For example, one absolute prerequisite for
regenerative periodontal surgery using guided tissue
barrier membranes is that the wound edges maintain
primary edgeto-edge approximation during the initial
weeks of healing. To achieve the objective of optimal
wound closure and, at the same time, minimize the
bacterial contamination of the wound, more expensive
monofilament nonresorbable sutures are clearly prefer-
able over braided sutures.
Sutures should be placed in enough tissue (ie, the base
of interdental papillae) to assure their retention for as
long as intended, and tied with a surgeon's knot. They
also should be tied tightly enough to maintain tissue posi-
tion, but, at the same time, not so tightly that they tear/cut
through the tissue they are intended to stabilize. Sutures
that "pull-out" or untie during healing are of no value to
the surgery. Ties should be planned so that knots will be
accessible for suture removal. Suture removal should not
be a surgical experience for the patient.
What Are the PrincipIes of Periodontal νιround
Closure and Suturing? \Mhat Are lnterrupted,
Figure 8, Sling, and Vertical Mattress
Sutures?
AtΙer wound closure and suturing, the surgeon must
make certain that:
. The wound is clean and the oral cavity has been
irrigated free of debris
. Gentle positive pressure was maintained over the
wound for 3-5 minutes immediately after closure to
control hemostasis
ο A thin fibrin clot has formed betνveen the flap and the
underlying periosteum or bone
. Wound margins are held in their intended position by
sutures and the fibrin clot
o The wound has been covered with a periodontal
dressing, if required
o The patient has been given written and verbal instruc-
tions for postoperative wound care
ο The patient has been given prescriptions for pain and
infection control
ο The patient has been given an appointment to return
for postoperative care in 6-8 days
The interrupted circumferential, the figure 8, the sling,
and the vertiοal mattress sutures are the most popular
suturing techniques in periodontics. Continuous sling
sutures, horizontal mattress sutures, and purse-string
sutures are more difficult to perform and time consuming.
As far as surgical outcomes are conοerned, there may be
little advantage to using complex suturing methods in
most periodontal surgical cases.
The interrupted circumferential suture is the "universal"
suture in periodontal surgery. While they may be used
in almost all periodontal surgeries, they are most appro-
priate for closure of facial and lingual replaced flaps and
modified Widman flaps.
lnterrupted sutures provide the best opportunities for
conneοtive tissue contact betM/een f|aps interproximally,
and, because of this, they are also preferable to figure 8
sutures when closing flaps in edentulous areas (ie, a
distal wedge) (Figures 184, B, and C).
The figure I suture is so called because it looks like an
"8" lying on its side. lt is used most often to close facial
and lingual apically positioned flaps. When tied, the figure
I suture aides in the adaptation of the tips of interdental
papillae to underlying recontoured alveolar bone (Figure
18).
68

71. CHAPτER 7
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/,
FIGURES 184, B, and C. A, lnterrupted circumferential suture. B. Figure 8
suture. C. Vertical mattress suture. lt is used when it is important to
exclude suture material from regenerative periodontal surgery sites.
νιrhen tied, lhis suture aids in the adaptation of interdental papilla to
the underlying alveolar bone.
A verticaΙ mattress Suture may be used when it is impor-
tant to exclude braided natural suture material from
regenerative periodontal surgery sites. The suture mate-
rial is threaded through and over the sudace of each of
the interdental flap papillae (Figure 18). The interpapillary
variation of the vertical mattress suture excludes all
suture material from a regenerative site. The mattress
suture is more technique sensitive than the interrupted
suture, and any perforation of the flap will negate its
purpose (Figure 18).
The sling suture is used primarily to suspend/position a
single facial interdental papilla. lt is usually employed in
cases where a corresponding Ιingual flap may not have
been raised (ie, a laterally or a coronally positioned flap).
The support for the sling suture is derived from either the
lingual of the tooth involved or from an ad.iacent tooth.
What ls the Purpose of a Periodontal
Dressing? Can Periodontal Surgery Be
Successful Without Postsurgical Periodontal
Dressings?
Periodontal dressings were born out of necessity during
the era of reseοtive periodontal Surgery when the gingi-
vectomy and osseous denudation procedures were
popular. These procedures produced "stormy" postopera-
tlve healing. Severe inflammation and pain, hard and soft
tissue necrosis, and bone resorption were οommon' The
period of discomfort was determined by the length of time
needed for inflammatory ceΙls to remove neοrotic tissue.
ln some cases where bone exposure was excessive, this
process took 2-3 weeks to complete. To reduce patient
complainis of postoperative pain, periodontal dressings
of the time were specially formulated to overcome them.
Some contained sedative agents. The most popular, and
most effective, of these agents ννas eugenol. Eugenol
\Λ/as later found to cause its own tissue injury and
necrosis. Commercially available periodontal dressings
currently do not contain eugenol.
Today, there are probably two accepted purposes in peri-
odontal surgery. They:
. Serve as a barrier to protect the periodontal wound
from accidental injury during the critical days of
healing (Figure 19).
. Provide the patient \,vith some degree of comfort
during the acute infΙammation phase of healing and
while epithelialization of the wound takes place
(Figure 20).
F|GURΕ'19. Α clinical photograph of an apically positioned flap posi-
tioned at crest with a continuous sling suture. A delicate fibrin clot
mediates the initiaι union between the flap and underlying tissues
and tooth structure. A periodontaι dressing was placed to protect
the wound from accidental iniury during the first postoperative
week.
FlGURE 20. A clinical photograph of a gingivectomy Wound. τhe exposed
connective tissue will be a source of patient discomfort until epithe-
lial closure is complete. Periodontal dressings were placed to
control patient discomfort during the first and second postoperative
weeks.
Periodontal dressing should not be used to οontrol
bleeding. Hemostasis should be achieved before a
dressing is placed.
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72. SURGICAL TREATMENT: PRINCIPLES
Periodontal dressings have no \η/ell-defined effect on the
proοesses of \Λiound heaΙing or on SUrgical outcomes (ie,
gains of periodontal attachment or reduction in probing
depths).
How Do Periodontal Wounds Heal? How Are
Periodontal Wounds Classified?
The heaΙing of periodontal wounds involves the Same
processes that ocοur in all wounds. Epithelium, ordinary
οonnective tissue, cementum and bone, heal according to
their own tissue specific biologic "rules", which have foun-
dation in tissue embryogenesis. ln the case of wound
healing, surgical injury creates the environment and stim-
ulus for cellular differentiation.
Periodontal wounds are classified according to the envi-
ronment for epithelial closure of the wound.
ο Primary νVound healing occurs when mucosal \Ι/ound
margins are edge to edge and the epithelium has
onΙy a short distanοe to migrate to another \Λ/ound
margin of tooth surface before the \η/ound is sealed.
Primary wound closure occurs folΙowing the closure
of distal wedges and some endodontic access flaps
(Figure 21).
FlGUFlΕ 21. A clinical photograph showing primary closure of an endo-
dοntic access procedure' τhe wound edge of the flap has been
sutured to approximate the wound edge on the attached gingiva.
FΙGURE 22. A clinical photograph showing primary c|osure of a replaced
flap covering a periodontal regenerative procedure. τhe tlap margins
contact tooth structure and the tips ot the facial and lingual inter-
dental papilιae contact each other interproximally.
FIGURΕ 23. A clinical photograph showing a gingivectomy that will heal
by secondary wound healing. Epithelial cells must migrate across
the exposed connective tissue until they contact the tooth or other
migrating epithelial cells.
. Secondary wound healing occurs \η/hen epithelial
cells must migrate several millimeters to close the
wound. The gingivectomy is an example of a wound
that heals by secondary \Λ/ound healing (Figures 22
and 23).
FIGUΗE 24. A clinical photograph showing tertiary wound healing of an
apically positioned flap procedure at the week one postoperative
visil. τhe patient experienced considerable postoperative pain, and
nοrmal epithelial migration will be delayed until it is removed by
resorption and sequestration,
FIGURE 25. A clinical photograph of the removed bony sequestrum four
weeks after surgery.

73. cHAPτER 7
o τertiary \Λ,ound healing occurs \ivhen there iS an
obstacle to epitheIial migration. Τypically, this
obstacle is necrotic tissue created during the surgery.
Epithelial migration and wound closure will be
delayed until the obstacle has been removed
(Figures 24 and 25).
What ls the Sequence of Events in
Periodontal Wound Healing? How May This
Sequence Be Interrupted?
Following surgical injury:
. Epithelium. The epithelium is the first tissue to
respond to injury. Epithelial cells begin to proliferate
at νvound margins at 1-2 days. other epithelial cells
dedifferentiate and migrate onto and across exοori-
ated connective tissue until they either contact each
other or they make contact with a tooth. The migra-
tion takes place at a rate of 0.5 mm per day. The area
to be covered determines duration of migration. For
instance, it may take 10-14 days to cover a gingivec-
tomy wound while a replaced flap may be sealed to
the tooth in 2-4 days. Once the monolayer is formed,
proliferation and differentiation of progeny cells into
mature epitheΙial cells predominates. ln most perio-
dontal wounds, epithelialization and the formation of
a junctional epithelium are complete by the end of the
second week of healing.
ο Gonnective tissue. ln the repair of ordinary gingival
connective tissue, fibroblasts begin to proliferate after
day 2 with evidence of collagen synthesis in the
wound by day 4. The duration of these activities is
determined by the amount of tissue that needs to be
restored. ln the most uncomplicated periodontal
surgery, restoration of gingival connective tissue wiΙl
be complete in 4-6 weeks.
. Alveolar bone. Τhe healing of alveolar bone is
preceded by a period of reactive bone resorption.
Osteoclasts appear in the wound at about day 4 and
display peak osteoclastic activity at day 10. Τhe dura-
tion and severity of the osteitis depends upon the
degree of injury and necrosis of bone. Osteoblasts
begin to appear and proliferate in the wound during
the second week, and they display peak osteoblastic
activity by the end of the third week. Deposition of
bone continues into the second month. Bone remod-
eling and maturation is a feature of the third postoper-
ative month.
. Cementum. Repair of cementum is the "turtle" of
periodontal wound healing. Not only is
οementogenesis delayed in onset; it is also slow to
exert its effect on the overall outcome of periodontal
healing. Proliferating cementoblasts appear adjacent
to root surfaces at the end of month one and proceed
\Λ,ith cementogenesis during the months two and
three. These events are critical to the formation of a
ne!η, attachment apparatus and some forms of new
attaοhment. lt is for this reason that manipuΙation of
the newly healed dentogingival junction should be
delayed at least until the end of the third postopera-
tive month.
ln overview, periodontal wound healing is dominated by
necrosis, inflammation, and resorption in the first week,
proliferation, differentiation, and production in the second
through the sixth week, with maturation and remodeling
from the seventh week through the end of the third
month. Figure 26 details the chronology of events in peri-
odontal wound healing.
Week One Week Two Week Three Week Four
TΑBLE 1. Sμopsis of Bioξical Eγents in the Heιling of Periodontg! Surgicεl Wounds
Εpithelium
Yasculature
Connective
tissue
Bone
Cementum
Migration ( l)--{overage (7}-Maturation (14)*
Ρrοliferation (2p
Junctiοnal epithelium (l4)
Angioblasts (2p
Endothelial budding (7)-Yascularity (14)
Fibroblasts (2 21)
Fibrogenesis (5
Resoφtion(4#l0)t
Deposition (10 / /--------19O)l
Cementoblasts (12 / /-----<9O)
(
) Postoperative day
*
Delayed in the healing of free gingival grafts.
t Delayed in cases where osseous surgery v,as performed.
f Ηealing of the dentogingival junction complete.
The scenario depicted is that οfa hypothetical consιruct based upon scientific data as repοrted in the liιerature. Restorative
procedures should not be performed until after the third postoperative month.
FlGURE 26. A table showin9 the chronology of epitheιiaι, ordinary connective tissue, bone and cementum wound healing events in periodontal surgery.
(Αdapted from Hawley ο and Serio F, "Periodontal ννound heaiing," clark'S cιinical Dentlsιry, Philadelphia, PΑ: JB Lippinοott οo,
'1989,
1:'17.)
71
-

75. cHAPτER 8
CHAPTER 8: SURGICAL τREATMENT: REPAIR' RESΕcTloN,
AND REGENERATION PROCEDURES
Surgical flap proοedures can be divided into two major
categories: Resectiνe and regeneraflve procedures.
Resective procedures are used to gain access to the
roots for οontinued root debridement, recontouring
of bone, and then to position the remaining gingiva api-
οally to reduce the residual pocket depth. Τhe gingivec-
tomy, while not a flap procedure, is a soft tissue resective
procedure to eliminate a suprabony periodontal or pseudo-
pocket. Regenerative surgicaΙ procedures involve flap
reflection, root surface debridement/detoxification, and
then techniques to stimulate the regeneration of lost
periodontal attachment: Bone, cementum, and perio-
dontal ligament.
What Are the Ways That a Periodontal Wound
Can Heal?
The healing of periodontal pockets after therapy may
oοcur in different ways. The four possibiΙities for healing
are defined below.
Repair: Healing of a wound by tissue that does not
fully restore the architecture or the function of the
part.
Reattachment: To attach again. The reunion of
epithelium and connective tissue \lνith the root
surface. Not to be confused with new attachment.
Neι,v attachment: The union of epithelium or connec-
tive tissue with a root surface that has been deprived
of its original attachment apparatus. This new attach-
ment may be epithelial adhesion and/or connective
tissue adaptation or attachment and may inοlude new
cementum.
Regeneration (new attachment apparatus): Repro-
duοtion or reconstitution of a lost or injured part. ln
periodontiοs, this means the formation of new aΙve-
olar bone, periodontal ligament, and cementum on a
root surface that had lost its attachment apparatus
due to periodontal disease.
Scaling and root planing and most surgical flap proce-
dures heal by repair. ln flap surgery, a long junctional
epithelium attachment is formed along the root surface
with the reformation of the supracrestal conneοtive tissue
fibers adjacent to the crest of the alveolar bone. lt is only
by using specialized techniques that a new attaοhment
apparatus may be formed.
What Are the Gingivectomy and Gingivoplasty
Procedures? What Are the lndications for a
Gingivectomy?
The gingivectomy is the excision of a portion of the
gingiva, usually performed to reduce the soft tissue waΙl
of a periodontal pocket. lt is performed using an external
bevel incision which is kept, where possible, entirely
within the band of keratinized gingiva. The gingivectomy
may be performed with a knife, or it may be performed
using electrosurgery or a laser (Figure 1).
FIGURE 1. A clinical photograph of a gingivectomy procedure performed
to correct the preoperative condition seen in Figure 2.
The indications for a gingivectomy are where there are:
. Suprabony pockets coronal to the mucogingival junc-
tion
. No osseous defects that require correction by
osseous surgery or regeneration
. Gingival enlargements secondary to medications,
systemic disease, or the margins and contours of
fixed restorations
. Αdequate zones of keratinized gingiva
. AmpΙe vestibuΙar depths and palatal vaults to permit
instrumentation (Figure 2)
FlGURE 2. A clinical ρhotograph of a case where almost all of the indica-
tions for a gingivectomy exist (ie, suprabony pockets, no intraos-
seous defects, gingivaι enlargement due to medications, adequate
zone of attached gingiva, and ample vestibular depth).
A gingivectomy will produce surgical recession and may
not be the treatment of choice in aesthetically sensitive
regions of the mouth.
Gingivoplasty is the reshaping of the gingiva using
knives, rotary instruments, or electrosurgery. While it is
true that portions of gingiva are excised during the gingi-
voplasty procedure, it is the reshaping, not the excision,
of gingiVa that defines gingivoplasty (Figure 3).
-

76. SURG|CAL TREATMENT: RESECΤ|VE AND REGEΝERAT|VE PROCEDURES
F|GURΕ 3. A clinical photograph of the case in Figure 1 after the gingivec-
tomy was embellished by shaving the wound margins with knives
and creating interdental grooves using rotary instruments. Gingival
bulk has been reduced, and the aesthetics of the case have been
improved.
The gingivectomy and the gingivoplasty should not be
performed in the presence of inadequate inflammatory
disease control.
After satisfying its indications and contraindications, the
gingivectomy is classically performed by:
ο Producing bleeding points on the surface of the
gingiva corresponding to the pocket depth
o Making a 45' angle externaι bevel incision using
sharp Kirkland or Goldman-Fox gingivectomy knives
(Figure 4)
. Beginning the incision on the gingival surface slightly
apical to the bleeding points and ending the initial
incision at the point of gingival attachment to the
tooth
. Using narrow Orban interproximal knives to extend
the initial incision interproximally and to meet any
opposing initial incision
. Removing the excised collar of gingival tissue n fofo
FIGURE 4. A clinical photograph of an initial gingivectomy incision. lt is
made using a Kirkland knife held at a 45" angle with the tooth begin-
ning iust apical to the clinical attachment level and ending at the
attachment level.
Gingivoplasty instruments include coarse rotary diamond
stones, soft tissue nippers, or gingivectomy knives to
smooth, groove, and contour the wound edges (Figure 5).
The procedure is completed using curettes to scale, root
plane, and remove residual tissue tags.
FIGURE 5. A clinical photograph ot a completed gingivectomy showing
the blended Wound margins and vΘrtical interdental grooves made
by gingivoplasty.
Τhe healing of a gingivectomy/gingivoplasty takes place
by secondary wound healing. Beοause of the large area
exposed connective tissue and the fixed rate of epithelial
cell migration, re-epithelialization and the formation of a
new junctional epithelium may take up to 2 \Λ/eeks to
complete. Αnother 2-4 weeks may be necessary to re-
establish the marginal gingiva and gingival sulcus.
What ls Electrosurgery? Is Electrosurgery a
Reasonable Alternative to Knives in
Gingivectomy/Gingivoplasty Procedures?
Εlectrosurgery is the "division of tissues by high
frequency electrical current applied locally with a metal
instrument or needle." ln the process, electrosurgery cuts
and cauterizes. Cutting energy in the form of heat is
produced at the needle tip. The amount of injury
produοed by the heat depends upon:
. How long the electrode maintains static contact vι/ith
tissue
. Ηow current is being applied
. The type of electrode being used
ο The impedance of the tissue
lmpedance is the measure of tissue resistance to the
spread of cutting energy. lt is very low in inflamed gingival
tissue, which makes electrosurgery well suited for gingi-
vectomy/gingivoplasty procedures. lf the electrode is kept
properly tuned and kept in οonstant motion to limit the
lateral spread of heat, soft tissue healing does not appear
to be adversely affected by electrosurgery.
lmpedanοe is very high in mineralized tissues, and elec_
trosurgery should not be used \Λ/here the needle \,νill
contact bone ortooth structure (ie, periodontal flap proce-
dures). Any electrode contact with mineralized tissues
will produce bony necrosis, inflammation, and resorption.
Cementum may also be damaged to the extent that it will
be unable to maintain existing gingival attachment.
Hemostasis is usually better with eΙectrosurgery than with
surgery with a blade. Soft tissue reshaping in gingivec-

77. CHAPτER 8
tomy/gingivoplasty procedures may be done with minimal
bleeding and good visibility. ln addition, periodontal soft
tissue electrosurgery procedures tend to be shorter and
produce less postoperative pain than conventional
surgery. Patient acceptance of electrosurgery is usually
high, but many patients will find the pungent smell objec-
tionable.
VVhat Is an Apically-Positioned Flap (AFP)
With Osseous Surgery? What Are the Goals
and Obiectives of the APF With Osseous
Surgery?
APF with oSSeouS Surgery is a procedure where acοess
to alveolar bone and periodontal intraosseous defects is
gained by APF or crestal anticipation. APF with osseous
surgery is a predictable method of surgical pocket elimi-
nation.
osseous surgery modifies the bony tooth SuppoΙ1 that
has been aΙtered by periodontal disease by either:
ο osteoplasfy (ie, reshaping the alveolar bone without
the removal of supporting alveolar bone)
o Ostectomy (ie, the removal of supporting alveolar
bone)
Supporting alveolar bone is the bone that is directly
involved in tooth support (ie, the alveolar bone proper)
νvhere the principal fibers of the periodontal ligament
attaοh. Frequently, the walls of osseous defects are
composed of supporting bone (Figure 6).
Figure 6: Line drawings showing the removal of supporting alveolar bone
and the restoration of normal bony contours by ostectomy. (Couftesy
of Dr. James Κassouιis)
Nonsupporting bone is alveolar bone not directιy related
to tooth support (ie, bony exostoses, edentulous ridges,
tori, flattened interdental contours and ledges). The walls
of some osseous defects may be composed of nonsup-
porting bone (Figure 7).
Figure 7: Line drawings showing the reduction of a heavy alveolar ridge
by osteoplasty of nonsupporting alveolar bone. (Courtesy of Dr.
James Kassoulis)
Ιhe goaΙs and objectives of osseous Surgery are to
create osseous contours by ostectomy and osteoplasty
that resemble the normal "physiologic" osseous contours
that existed before the onset of periodontitis.
What Are Physiologic Contours? What Are the
Consequences of Periodontitis τhat Are So
Worrisome to the Periodontist and Remedied
by Osseous Surgery? What ls the Rationale
for Osseous Surgery?
The expression, "physiologic contours," refers to the
normal architecture of the soft and the hard tissue
margins of the periodontium. Physiologic contours are
described as parabolic with the most coronal margins
located interproximally and the most apical margins
located over the facial or lingual surfaces of the teeth.
Physiologic contours parallel the cementoenamel .junc-
tion (CEJ). They are more pronounοed in the incisor
regions and become progressively flatter in the premolar
and molar region of the dentition.
Fffit* €x*l.
FlGURΕ 8. A line drawing showing positive bony architecture. The crest
of the alveola. bone, the soft tissue atιachment level (probe), and the
gingival margin follow the cementoenamel iυnclion.
(cour1esy of Dr.
James KassouιiS)
75

78. sURGlcAL TREATMENT: REsEcTlvE AΝD REGEΝERAτlvE PRocEDURΕS
Positive bony architecture is the term used to
describe the normal "physiologic" relationship of inter-
dental and radiοular bone heights. lt is positive bony
architecture that the normal bioΙogic width (sulcus,
junctional epithelium, and connective tissue attach-
ment) and the gingival margin tend to follow in health
(Figure 8).
Νegative bony architecture is the term used to
desοribe any abnormal, nonphysiologic relationship
of interdental and radicular bone heights. Periodon-
titis destroys periodontal attachment and the normal
parallelism bet/een the crest of bone and the CEJ is
Ιost. The bony margins and gingival attachment
levels become irreguΙar and inconsistent /here intra-
osseous defects are formed. Not all intraosseous
defects should be treated by osseous surgery.
β*θB€$ *ι,ι*.
FΙGURΕ 9. A line drawing showing negative bony architeclure. τhe contours of
the aiveolar bone and attachment level (probe) do not follow the cemento-
enamel iunction.
(Courtesy of Dr. James Kassoulis)
. The normal "physiologic" gingival morphology tends
to retain its parabolic gingival margin contours while
bony morphology is changed by periodontitis. The
bulk of gingival tissue is inοapable of adapting to the
sharp, inconsistent bony margins of negative archi-
tecture (Figure 9).
The degree of discrepancy between ihe persistent posi-
tive contours of the gingival margin and the emerging
negative bony contours is measured cliniοally as progres-
sively increasing probing depths (Figures 10 and 11).
F|GURE 10. A cΙinical photograph of a periodontitis case before perio-
dontal surgery. The gingival margin contours do not reflect the 5-7
mm probing depths and negalive bony arοhitecture that exist inter-
proximally.
F|GURΕ 11. A cΙinical photograph of the case shown in Figure'10
following retlection of a full-thickness apically positioned flap and
debridement of osseous defects. τhe generalized pattern of hori-
zontal bone loss and negative bony archilecture was obscured by
the positive contours ot the gingival margin.
The worrisome consequences of periodontitis are the
deepening probing depths that:
. Produce an ecosystem that is conducive to the emer-
gence and gro\Λith of periodontaΙ pathogens
. Αre difficult to efficiently and effeοtively clean, scale
and root plane, and maintain nonsurgically
. Αre associated with the persistence and/or re-emer-
gence of periodontal pathogens after nonsurgiοal and
surgical debridement, and, as a consequence....
ο Αre associated wiih progressive periodontitis
The rationaΙe for osseous Surgery is based upon the
following tenets:
. Deep periodontal pockets are inconsistent with perio-
dontal health
ο The basis for the increased ρocket depths is the
progressively increasing discrepancy between the
position of the gingival margin and the leveΙ of perio-
dontal attachment (see previous Figures 10 and 11).
ο lf ihe underlying negative bony architeοture is elimi-
nated and the positive bony arοhitecture is restored
(Figure 12)
F|GURΕ 1 2. A clinical photograph of lhe case shown in Figures 1 0 and 1 1
after positive bony architecture was restored by osseous surgery.

79. CHAPτER 8
. lf the gingival margins are repositioned to nev/ly
reοontoured bone (Figure
'l3)
FIGURE 13. A clinical photograph of the case shown in Figures 10, 11,
and 12 With the margins of the flap positioned at the aιveolar cresι
using continuous sling sutures.
. The healed dentogingival junction will closely follow
the contours of the recontoured bone
. The new relationship of bone to soft tissue will be
stablΘ
. Shallow pockets will ρersist
. Periodontal health will be restored and more easily
maintained
The dominating influences on postsurgical gingival form
are:
ο The width of the interproximal space
. The morphology of the embrasure
ο The location of the contact poini with respeοt to the
alveolar crest
ln summary, any failure to achieve its goals and objec-
tives (ie, create osseous contours by ostectomy and oste-
oplasty that resemble the normal "physiologic" osseous
contours) wiΙΙ result in discrepancies bet\Λ/een the
gingival margin and the attaοhment leveΙ (ie, periodontal
pockets and progressive disease).
How Are Periodontal Osseous Defects
Classified? Which Defects Are the Best
lndicated for APF and Osseous Surgery, and
Which Defects Are Not lndicated for APF and
Osseous Surgery?
The pattern of bone loss from periodontitis may be either
horizontal (ie, the pattern of interproximal bone loss tends
to parallel the cementoenamel junοtions of adjacent teeth
- see previous Figure 11) or vertical (ie, the pattern of
interproximal bone loss does not parallel the cemento-
enamel junction). Horizontal patterns of bone loss are
usually generalized (ie, they involve multiple teeth in a
segment), and verlical bone loss patterns may be found
around isolated teeth (Figure 14).
FIGURE 14. A clinical photograph of an isolated vertical intraosseous
defecι. τhese defects frequently go unnoticed without the use ot a
periodontal probe.
Periodontal osseous defects are classified acοording to
the number of bony walls present or remaining at the time
of their surgical exposure. The location of the defect with
respect to the tooth will have a lot to do wiih the number
of waΙls. ln order for a defeοt to have a bony wall, it must
be intraosseous (ie, partially or compΙetely within alveolar
bone).
Periodontal osseous defects may be 0 wall, 1 wall, 2 wall,
3 wall, 4 wall, or combination lesions. Common usage
trivial names have been used to describe some defects in
each οlass.
o 0 Wall Defeοts are alveolar dehiscences and fenes-
trationstound on the facial or lingual surfaοes of teeth
where the alveolar housing is typically thin or where
the tooih is abnormally inclined or malpositioned,
They are not seen in radiographs. Fenestrations, in
the presence of marginal periodontitis, may οonveft
to dehiscences (Figures 15 and 23). Osseous
surgery is not a treatment of choice for 0 wall dehis-
cenοeS.
. 1 Wall Defeοts are commonly interproximal oSseoUS
defects where either only the proximal wall is present
(a hemiseptum), or a facial or lingual wall is present
(a ramp) (Figure l6). Shallow 1 wall defects may be
managed suοcessfully using osseous surgery.
FIGURE 15. A dried human specimen showing dehiscences over promi-
nent roots of mandibular anterior teeth. Partiaι thickness flaps
should be considered when planing surgical access to areas where
dehiscences and fenestralions may be present,
77

80. sURGlcAL TREAΤMENT: RΕsEcTlvE AND REGENERAτlvE PRocEDUREs
F|GURΕ 16. A dried human specimen showing a 1 wall hemiseptum defect
on the mesial of a mandibular molar. τhe wall of the defect is formed
by bone attached to the distal of the second premolar.
. 2 Wall Defects \Λ/here the facial and lingual walls are
present, and bone Ιoss has occurred on the proximal
surfaces of adjacent teeth are very common (an inter-
dentaΙ crateη (Figures 17 and 18). 2 wall interprox-
imal defects \,vith either a facial or lingual \Λ/all and a
proximaΙ walΙ are less common. Shallow 2 wall
defects may be managed using osseous surgery.
FIGURE 17. A dried human specimen with shallow 2 wall interdental
craters between maxillary molars. τypically' craters have a buccal
(facial) wall and a lingual wall. Lingual walls are shown.
FIGURE 18. A dried human specimen with the same shallow interdental
craters between maxillary molars in Figure 16. Buccal (facial) walls
are shown,
''
. ..-....Ξ,:-,|.'',.'',,, ' .
' 1
_ ,
:
.
:.;:.-,:.t... :.
F|GURΕ 1 9. A dried human specimen with a 3 wall intrabony detect on the
mesial ot a mandibular molar. τhe 3 walls are the buccal wall, the
proximal (mesial) waΙl, and the lingual wall.
3 Wall Defects occur either interproximally or on the
facial or linguaΙ suι.faces of teeth. lnterproximaΙly, the
3 wall defect has a facial, a lingual, and a proximal
wall and may be caΙled an intrabony defecr. lntrabony
defects are frequently assoοiated with food impaction
(Figure 19). Three waΙl defects may also be found on
the facial and lingual of teeth where there is enough
bone present to support the formation of walls, such
as the lingual or facial of mandibular posterior teeth
and the palatal of alΙ maxiΙlary teeth. These 3 wall
defects are sometimes called wel/s. Periodontal
regeneration, not osseous surgery, is the treatment of
choice for 3 wall defects.
4 Wall Defects are usually present with a facial, a
mesiaΙ, a lingual, and a distal \Λ/all. Because they
sometimes encircle an entire tooth, 4 \Λ/all defects
have been called circumferentiaΙ or moat defects
(Figure 20). Osseous surgery is not the treatment of
choiοe for 4 wall defects.
FIGURE 20. A dried human specimen with a 4 wall well defect on the
buccal of a maxillary second molar. The 4 walls are the distal wall at
the distal buccal line angle, the buccaΙ Wall, the mesial Wall at the
mesial buccal line angle, and the lingual interproximal wall.
. 1, 2, 3, and 4 Wall Defects are also known as combi
nation defecΙs' They are usually found only interprox-
imally, but will be found anywhere there is enough
bone present to form walls in the wake of advanοing
78

81. cHAPτER 8
periodontitis (see 3 wall defects). A combination
defeοi will be more complex (more walls) apically
than coronally (Figure 21). Coronal 1 and 2 waΙl
portions of οombination defects are Sometimes
manageable by osseous surgery. The apical portions
of combination defects are usually candidates for
periodontaΙ regeneration.
Decisions over whether or not to use osseous surgery in
the management of periodontal bony defects should
depend upon:
ο The number of remaining walls
. Τhe depth of the defect
. The width of the defect
o The proximity of the defect to imρortant anatomical
landmarks
. The amount of bone that will be removed to achieve
positive bony architecture
. The predictability of alternate forms of therapy
Segments of the periodontium with generalized horizonial
patterns of bone loss and multiple shallow interproximal
osseous defects with less than 3 walΙs are traditional
indications for osseous Surgery. other indiοations for
osseous Surgery inοlude:
The management of Grade I and early Grade ll furca-
tion invasions (Figures 20 and 23)
The management of bony ledges and interproximal
bone flattened by periodontitis (Figure 22)
The management of exostoses and tori (Figure 24)
Root resections or amputations (Figure 25)
Crown lengthening procedures where osseous
Surgery will be used to remove enough suρporting
bone to support prosthetic treatment ρlans
F|GURE 22. A dried human specimen of a bοny ledge buccal to maxillary
molars. As periodontitis occurs over these teeth, the ledge may
become the mesiaι, buccal, and distal walls of a 3 Wall or a 4 WaΙΙ
osseous defect.
FIGURE 23. A dried human specimen showing horizontal bone loss and
early furcation invasions of maxillary molars. Note the fenestration
on the distal buccal root o, the first molar.
FlGURE 24. A clinical photograph showing the surgical expοsure o,
palatal torus exostoses. These bony protuberances complicate tlap
elevation and positioning of palatal fΙaps and must be removed
during osseous surgery.
4
***bε",
ffi:'
ffi
FIGURΕ 21. A dried human specimen with a combination defect on a
mandibular second premolar. τhe defect has 4 walΙs apically
(lingual, mesial, buccal, and distal) and 1 Wall cοronally (lingual).
φsΨ9
.::*#
-

82. SUBGlcAL TREATMENT: REsEcTtvE AΝD REGENERAτlvE PRocEDURES
FlGURΕ 25. A clinical photograph showing the amputation of the distal
buccal root of a maxillary tirst molar. There was a through and
through furcation invasion from the buccal to the distal. Positive
bony architeοture Will be resιored by osseous surgery after root
removal.
The more \Λ/alls that compose the defeοt (ie, 3 wall inter-
proximal intrabony defects and 4 \η/alι moat defects), the
more likely the defect is contraindicated for osseous
surgery. Defects that conceivably "will hold watel' offer
excellent opportunities for bone graft containment and
periodontal regeneration procedures (see Figures 14, 19,
and 20). Other contraindications for osseous surgery
include:
. Operating in the aesthetic zone where cosmetics will
be adverseΙy affected
. Where the removal of supporting bone during ostec-
tomy will unduly compromise the attachment of teeth
in the operative field
. Where the removal of supporting bone during ostec-
tomy will unduιy compromise the attachment of teeth
at the edge of the operative field
o Where a risk of root caries is considered high
. Cases where patients have experienced problems
contro|Ιing root hypersensitivity
How ls Osseous Surgery Performed? What
lnstruments Are Used in Osseous Surgery?
Αccess to osseous defects for osseous surgery is
performed using an ΑPF. other methods of flap surgery
are Ιess suited because they limit access and do not
permit, in their classic descriptions, the opportunity to
elevate apical to the mucogingival junction. The guide-
lines for using an APF with osseous surgery are that:
. The APF must be full thickness to provide unre-
stricted visibility of osseous defects.
. The incisions must be planned so that an adequate
band of keratinized tissue is retained on the flap.
o The "scaΙloped'' incision line conforms to the
presurgical gingival morphology at the site.
o The initiaΙ inοisions follow, or "antiοipate", the final
bony contours.
o Τhe internal bevel incisions thin, or "filet", the internal
sudace of the flap enough to permit passive adapta-
tion of the flap to the final osseous form.
. Osseous recontouring is performed to eliminate
osseous defects and re-establish positive bony archi-
tecture (Figures 26 and 27).
FΙGUΗE 26. A clinicaI photοgraph showing the shaΙιow 2 and 3 Wall inter-
proximal defects, the buccal ledges, and the flattened interproximal
bone that is typically produced by periodontitis.
FIGURΕ 27. A clinical photograph of the segment shown in Figure 26 after
osseous surgery. The 2 and 3 walι defects, the buccal ledges, and
the tlattened interproximal bone have been eliminated. τhe bone
over the buccaΙ turcation of the tirst molar has been preserved. Note
the vedical interdental groove.
. Flaps are repositioned apically to the crest of the
bone and sutured in place (Figure 28).
FIGURE 28. A clinical photograph o, the flap closure ot the segment of
οsseous surgery shown in Figure 27. τhe facial alveolar οrest was
covered With sofι tissue and secured with continuous sling sutures.
Pressure was applied to stabilize the llap during fibrin clot forma-
tion.

83. cHAPτER 8
What ls a Crown Lengthening Procedure?
What Will Be the Clinical Outcomes if a Crown
Lengthening ls Not Performed?
A crown lengthening (CL) is a preprosthetic surgical
procedure where the principles of osseous surgery are
practiced. lt is "a surgiοaΙ procedure designed to increase
the extent of supragingival tooth structure for restorative
or aesthetic purposes by apically positioning the gingival
margin, removing supporting bone, or both." ln reality, a
typical CL procedure should ideaΙly include osseous
surgery and appropriate apical positioning of the gingival
margin around all teeth in the surgical segment.
Failure to perform a CL wilΙ produce clinical outοomes of
loss of attachment, reverse bony architecture, and
increased probing depths around the restored teeth. τhe
junctional epithelium and the conneοtive tissue attach-
ment collectively occupy a reasonably constant biologic
zone of gingival attachment to a tooth (Figure 29).
FiGURΕ 29. A photomicrograph oΙ a human tooth and a mildΙy inflamed
marginal periodontium. τhe zone of gingival attachment is located
between the crest of the bone and the histologic base of the sulcus
and is occupied by the connective tissue attachment and the iunc-
tional epithelium. τhe sulcus itself iS not shown.
Occasionally, the attachment zone will be invaded by
restorative procedures. lf the impingement is not
rendered permanent by restoration margins placed in the
zone, any injury in the gingival attachment should repair
without deformity. On the other hand, restoration margins
placed in the zone could permanently impinge upon the
attachment. ln this case, the zone of attachment \λ/ill be
re-established apiοal to the restoration margin' using
processes not unlike chronic periodontitis. The most
worrisome clinical outcome is the risk to periodontal
heaιth that will emerge from the increased probing depths
around the restored tooth (Figure 30).
FlGυRE 30. A clinical photograph of osseous deformities produced by a
dental restoration that impinged on the biologic width. τhe
morphology of the osseous crest around the first premolar follows
the crown margin contours. τhere were 5 mm probing depths on the
distal of the restored looth.
lssues of plaque control and force control must be
addressed before CL. lt is also essential that sound deci-
sions be made vis-a-vis the feasibility of the CL proce-
dure and the restorability of the tooth after healing. All CL
procedures result in reduced croνvn to root ratios, and in
the case of teeth that are in secondary occlusal trauma-
tism, force control will be complicated even further by a
CL. Τooth removal and the fabriοation of a fixed or
removable partial denture or tooth removal or the place-
ment of an implant are attractive alternatives to a CL
procedure where aesthetic or periodontal deformities will
be certain outcomes.
CLs may also be accomplished using orthodontics (ie,
forced eruption). ln this instance, the tooth that requires
extension for restorative reasons is orthodontically
extruded, and then the alveolar support that moved
occlusally with the tooth is removed by osseous surgery.
The major advantage to forced eruption is that supporting
bone is not removed from adjaοent teeth. lts disadvan-
tage is that the orthodontic process may require \iveeks to
months before the position of the extruded tooth is stable"
What ls the Biologic ι,vidth and \Mhat Are lts
Dimensions? How Does the Biologic \iVidth
Guide Decision-Making in the Crown
Lengthening Procedure?
CL procedures are based on a thorough knowledge of
the concepts ol the biologic width (BW). Most periodon-
tists wiΙl agree that the biologic width includes the fixed
biologic dimension of gingival attachment (ie, the supra-
crestal connective tissue attachment of the gingival and
the junctional epithelium). Some authors include the
depth of the healthy sulcus in the biologic width as well
(Figure 31).
Ιhe dimension of thedentogingiνal junction (DGJ)' as itis
used in periodontics, is based upon the average of

84. sURGlcAL TREATMENT: REsEcτΙvE AΝD REGENERAτ|VE PRocEDUREs
hundreds of individual measurements. τhe DGJ has
three elements and average of each is:
. The sulcus = 0.69 mm
. The junctional epithelium = 0.97 mm
. The connective tissue attachment = 1.07 mm
The concept of the BW used here includes only the junc-
tional epithelium and the connective tissue attachment.
Τhe dimensional sum of the BW is 2.04 mm. The dimen-
sional sum of the DGJ is 2.73 mm, or, for all practical
purposes, 3.00 mm.
d"ιωcτιn*υ
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co'.')Εeτινε
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FlGURE 3'1. Biologic νidth. Junctional epilheΙium and supracrestal connective
tissue fibers (dentogingival, dentoaΙveolar, circulaf, transseptal) must be
maintained in health.
Concepts of the BW \Λ/ere used aS a decision making
guide to the amount of soft and hard tissue that should be
removed during a CL so that at least 3 mm of tooth
structure would remain above the crest of bone. That
allowed 2 mm above the crΘst of bone for the connective
tissue attachment to the root and the junctional epithe-
lium. The remaining 2 mm provided enough tooth struc-
ture for the margin of the restoration.
\Λ/ith experience, it became apparent that 3 mm of tooth
structure was probably insufficient and at least 5 mm of
supracrestal tooth structure may be required. The 3 mm
target was based on average data, and many BWs are
either greater or /ess than the average. τhe range'for the
sum of the junctional epitheΙium and the connective
tissue attachment is probably more than twice Ιhe 2.o4
mm average dimension.
When it comes to individual patients, averages among
groups of subjects may not apply. Healthy nonperiodon-
titis sites in a given patient usually display uniform BWs,
and the radiographic distance bet\Ι/een the cEJ and the
crest of alveolar bone at healthy sites could be used as a
guideline for determining the BVι/ for individual patients.
The finding that up to 12Υ" ot teeth restored after surgical
CL procedures showed evidence of recession within 6
months suggested that clinicians need to expose >3 mm
of tooth structure during CLs. lndeed, restoration margins
placed <1 mm from the alveolar crest tend to produce
more gingival bleeding, deeper probing depths, and
greater loss of periodontal attachment than restoration
margins placed >2 mm from the crest.
Hoιv ls the Crown Lengthening Performed? ls
the Position of the Relocated Alveolar Crest
Stable Over Time?
The components of a CL are:
. The selection of an appropriate οase for CL (Figure
32)
FIGURE 32. A clinical photograph of a case selected for crown length-
ening. Additional clinicaΙ crown is needed for restoration of the
lateral incisors.
. Α full thickness mucoperiosteal flap
. Removal of supporting and nonsupporting bone
around the tooth in question and adjacent teeth in the
surgiοa| field following the principles of osseous
surgery
o Root planing the exposed root up to a millimeter of
the alveolar οrest
. Αpically positioning the flap margins to the ne\,v level
of the alveolar crest (Figure 33)
FIGURE 33- A clinical photograph of the apically positioned flaps after
crown lengthening. AdditionaΙ increased length of the clinical
crowns is apparent.
lnstrumentation (ie, root planing) to the crest of bone
frequently results in additional bone resorption to provide
space for a new biologic width. To prevent this un\ivanted
and unpΙanned for loss of tooth support and to minimize
recession following CLs, it is suggested that a 1 mm zone
of periodontal attachment fibers be preserved coronal to
the alveolar crest.
82

85. CHAPτER 8
The properly planned and executed CL that conforms to
the principles of osseous surgery and respects the
concepts of the biologic width will result in stable restora-
tion and periodontal tissue relationships (Figure 34).
F|GURE 34. A clinical ρhotograph of the healed and restored case
How Does Osseous Surgery Heal? Does the
Application of Hand and Rotary lnstruments
to Bone Delay the Healing of an APF With
Osseous Surgery?
ln general, osseous surgery heals according to the basic
prinοipΙes of periodontal wound healing. lrregularities and
delays in healing events will depend upon the extent of
osseous manipulation and the duration of the procedure.
The healing of bone following osseous surgery occurs in
two phases.
. Phase one begins aΙ day 4 with the appearance of
osteoclasts in the marro\,v and periodontal ligament. lt
reaches a peak during the second week of healing
and ends early in the third postoperative week. The
outcome of this reactive bone resorption is an overall
loss of crestal alveolar bone. The amount of resorp-
tion will range from several millimeters to something
less than a millimeter.
. Phase two begins during the second postoperative
week with the initial deposition of osteoid by osteo-
blasts. The measurable events of phase two (ie, the
recovery of most of the bone lost in phase one) are
οomplete by the end of the third month' Evidence of
bone maturation and remodeling can be seen in
osseous surgery wounds for over 18 months.
Postoperative wound care of ΑPF and osseous surgery
wounds should include weekly postoperative visits
through the end of the sixth week of healing. Τhe effec-
tiveness of plaque control by the patient must be moni-
tored closely, and professional supragingival
debridement should be pedormed weekly. During the first
month, the patient should avoid harsh foods, such as
shellfish, popcorn, peanuts, and pretzels that might
displace the flap from the underlying bone.
PERIoDoNτAL REGENERATIoN
τhe ultimate goal for any dental therapy would be to
restore that which has been damaged or destroyed by
disease to its original form. Periodontal regenerative
therapy is the only procedure in dentistry that restores
both histologically and functionally identiοal tissue to that
which has been lost. Significant progress has been made
to ensure predictable results when applied to the appro-
priate clinical situations.
ls it Possible to Regenerate Lost Attachment
Apparatus on a Previously Diseased Root
Surface?
Many studies and case reports have demonstrated new
alveolar bone growth in areas of previous periodontal
disease' Clinical or radiographiο evidence of new bone
growth alone does not indicate \Λ/hether or not the attach-
ment apparatus has been regenerated. For many years,
the ability to stimulate the formation of new attachment
apparatus on a previously diseased root surface had yet
to be ansvι/ered. Τhe regeneration of true new histologic
attachment apparatus was shown by Bowers, et al, in
several studies entitled "Histologic Evaluation of New
Attachment in Humans." ln these studies, the most apical
extent of radicular οalοulus in a periodontal defect was
marked by making a notch with a 1/4 round bur. The
roots νvere then submerged by being covered with the
gingival flap with the osseous defects left unfilΙed or
treated with demineralized freeze-dried bone. After a 6-
month healing period, the roots and surrounding hard
and soft tissues were surgically removed for histologic
anaΙysis. Consistent formation of bone, ne/ cementum,
and periodontal ligament was shown coronal to the notch.
The average amount of new attachment apparatus
formed νvas approximately 2 mm, the amount depending
on the treatment utilized.
What CellTypes Are lnvolved in Regeneration
of the Periodontium?
Pluripotential progenitor celΙs from the periodontal liga-
ment and bone are responsible for regeneration of the
attachment apparatus. These cells differentiate into oste-
obΙasts, cementoblasts, and fibroblasts to form new peri-
odontal tissues. lt has been shown that junctional
epithelial cells and cells from the gingival connective
tissues do not contribute to regeneration. lt is preferable
that these cells be excluded from the healing surgical site
to allow complete regeneration to occur. Regeneration is
limited by the ability of these pluripotential cells and the
vasculature to proliferate into a defect or furcation area.
What ls Meant by the Terms Osteoconduction,
Osteoinduction, and Osteogenesis?
Osteoconduction. The creation of a site suitable for
bone growth. The graft material acts as a trellis or
scaffold around and through which new bone will
form. ln regeneration, this includes the use of various
bone fill materials that act as a trellis or template to

86. sURGlcAL TREATMΕNT: BEsEcτlvE AND REGΕNΕRAT|VE PROOEDUREs
assist in ne\Λ/ bone formation. Τhe graft material itself
does not have any properties that actuaΙly stimulate
ne\Λ/ bone formation'
Osteoinduction. The direct stimulation of nevιl bone
formation. This inductive process may be achieved
by a bone-grafting material containing substances
such as bone morphogenetiο proteins or other growth
factors (platelet-derived gro\,vth factor, insulin-like
growth factor, transforming growth factor B).
Osteogenesis: The development or formation of
bone, usually by the grafting of bone forming cells
from one site to another.
What ls "Bone Fill" in Periodontal Therapy?
Bone fill is the clinical restoration of bone tissue in a
treated periodontal defect. Bone fill does not address the
presence or absence of histologic evidence of a new
connective tissue attachment or the formation of a new
periodontal ligament. Clinically, bone fill may be demon-
strated as increased bone in a defect on surgical re-entry
or radiographic radiopacity in an area that previously
demonstrated a periodontal defect.
What ls Guided Tissue Regeneration?
Guided tissue regeneration is a procedure that blocks the
repopulation of the root surface by long junctional epithe-
lium and gingival connective tissue to allow cells from the
periodontal ligament and bone to repopulate the perio-
dontal defect. This physical blockade may be aοcom-
plished using nonresorbable barriers such as expanded
polytetrafluoroethylene (ePTFE) or resorbable
membranes and barriers such as Type 1 bovine collagen,
calcium sulfate, or polylactic acid (Figures 35Α and B).
FlGURΕ 35A. Expanded Polytetrafluoroethylene Membrane (ePτFE).
Nonresorbable ePτFE membranes come in several shapes for
different anatomic locations. (Couιlesy of Dr. Paul A. Posen)
FlGURE 35B. Expanded Polytetrafluoroethylene Membrane (ePτFE). An
ePτFE membrane is in place durin9 a regenerative procedure for the
furcation of the molar. (Courtesy of Dr. Paul A. Rosen)
What Are the lndications for Periodontal
Regeneration Procedures?
Case seiection and proper technique are critical to the
success of regenerative therapy. Currently, regenerative
procedures are applicabΙe and predictable under a
certain set of circumstances:
. The patient exhibits exemplary plaque control both
before and after regenerative therapy.
o The patient does not smoke.
. There is occlusal stability of the teeth at the regenera-
tive site.
. Osseous defects are vertical in nature, with the more
walls of bone remaining increasing the likelihood of
regenerative success (if the osseous defect will hold
\Λ/ater, regenerative therapy is a viable treatment
option). The probabiΙity of success is as follows:
three-wall defects > two-wall defects > one-wall
defects, and class l furcas > class ll furcas \Λ/ith areas
of horizontal bone loss and class lll or class lV furca-
tion involvement offering no chance of practical
regenerative success.
What Are the Contraindications for
Periodontal Regeneration Procedures?
There are general and specific contraindications for
regenerative therapy. Flap surgery of any kind is contra-
indicated in patients who do not exhibit excellent plaque
οontrol. Performing surgery in a plaque-infected dentition
will result in further attachment loss. Patients with an
unstable medical condition are also poor surgical risks. lt
has been sho\η/n that smoking results in poorer treatment
outcomes with both surgical and nonsurgical therapy.
Osseous defects must have the appropriate topography
(numbers of walls, furcation involvement) and depth for
regenerative therapy to be effective.
What Are the Expected Clinical and
Radiographic Results from Periodontal
Regeneration Procedures?
Decreased probe depth, increased tooth stability, and
closure of furcations are the expected clinical outcomes
84

87. CHAPTER 8
of regenerative therapy. Radiographically, there should
be evidence of increased bone density (radiopacity) in
previously detected vertical or furcation defects. Regen-
erated defects heal at markedly different rates in different
individuals. Final radiographic healing may continue up to
2 years after the surgical procedure (Figures 36, 37, and
38).
FlGUΒE 36A. Badiographic Evidence of Bone Fill. τhis patient had a 10
mm defect on the distal of the molar.
FIGURE 368. Radiographic Evidence of Bone Fill. Seven months after
guided tissue regeneration with a DFDBA graft, significant osseous
healing is visible. τhe increase in radiodensity in this area continued
for another year. clinically, the probing in ιhis area was reduced to 3
mm.
FlGURE 37Α- Demineralized Freeze-Dried Bone Allograft (DFDBA) Withouι
GτR. Preoperative radiograph shows severe bone loss on the distal
of lhe maxillary right second premolar. A vertical defect is also
visible on the distal of the canine.
FΙGURE 37B. Demineralized Freeze-Dried Bone Allograft (DFDBA) without
GTR. Afιer flap reflection, the extent of the defects is apparent.
FlGUΒE 37ο. Demineralized Freezθ-Dried Bone Allo9raft (DFDBA) without
GTR. The defects have been fil|ed wilh rehydrated DFDBA. Εxcess
graft material was removed be{ore flap closure.
FlGURΕ 37D. Demineralized Freeze-Dried Bone Allografι (DFDBA) without
GτR. one year after surgery, the patient shows exemplary plaque
control and optimaι gingival health' Probings on the distal of the
second premolar decreased trom 10 mm to 4 mm.
85
-

88. SURGlcAL TREATMENT: REsEcτιvE AND REGΕNΕRAτ|VE PROOEDURES
FIGURE 37E. Demineralized Freeze-Dried Bone Allograft (DFDBA) without
GTR- τhere is radiographic evidence of substantiaι bone fill on the
distal of the second premolar and the distal of the canine.
F|GURES 38A and B. Guided τissue Regeneratiοn and DFDBA Graft. A
and B' τhis 32_year-old patient had one periodontal defect on the
mesial of ιhe lateral incisor. (case courtesy of Dr' Paut A' Rosen)
FiGURE 38c. Guided τissue Regeneration and DFDBA oraft. A 2-wall
defect was present on the mesiotacial aspect of the lateral incisor.
(case courtesy of Dr' Pauι A. Rosen)
FιGURE 38D. Guided Tissue Regeneration and DFDBA Graft. An ePτFE
membrane was placed over a DFDBAgtaf1- (οase courtesy ot Dr. Paul
A. Rosen)
FlGURE 38Ε. Guided τissue Regene.ation and DFDBA Graft.
Significant bone was regenerated and the tissue returned to a
state of health. (Case courtesy of Dr. Paul A. Rosen)
86

89. CΗAPτER 8
FIGURE 38F. Guided Tissue Regeneration and DFDBA Graft.
significant bone was regenerated and the ιissue returned to a
state of health. (case couΙtesy of Dr' Pauι A' Rosen)
What Materials May Be Utilized in Periodontal
Regeneration Procedures?
Bone graft materials:
Autograft: Α graft from one part of an individual
to another part of that same individual. Autografts
include iliac crest marro\Λ/, osseous οoagulum,
harvested bone from a healing extraction site,
bone swaging, and bone shavings from various
sources.
lliac crest marro!ν grafts have sho/n to have the
highest osteogenic potential. Unfortunately, there
is high morbidity with this material as procuring
iliac crest marro\η/ is expensive and painful, and
these grafts have been shovvn to cause signifi-
cant root resorption over time.
Osseous coagulum is bone that is harvested wiih
a slow speed at about 25-30,000 rpm. Τhe bone
is then mixed with blood. Bone may be harvested
from extraction sites that are 6-12 weeks old.
Bone swaging is the creation of a "greenstick"
fracture to move bone into a defect without sepa-
rating the grafted bone from its base. Bone shav-
ings may be collected from exostoses,
edentulous ridges, or the lingual bone of the
mandible.
Allograft: Α graft between genetically dissimilar
members of the same species. Freeze-dried
bone alΙograft and demineraΙized freeze-dried
bone allografi (DFDBA) are the two major types
of allografts. DFDBA contributes to bone gro/th
by osteoinduction as the bone morphogenetic
proteins are exposed by the demineralization
process. Properly procured and prepared allo-
graft materials are nonantigenic and do not
transfer infeοtious agents to the recipient. Τhese
graft materials should be obtained from licensed,
accredited tissue banks that can ensure these
conditions of procurement and preparation
(Figures 394 and B).
FlGURE 39Α. Demineralized Freeze-Dried Bone Aιlograft. DFDBA material
as it is received from the tissue bank.
FlGURΕ 39B. Demineralized Freeze-Dried Bone Allo9raft. DFDBA material
in a Dappen dish awaiting rehydration with sterile saline.
Alloplast: Α Synthetic or inert foreign graft. There
are many alΙoplast graft materials, some resorb-
able, and Some nonresorbable. Αmong alloplast
materials are "bioactive" silica based glasses,
nonresorbable hydroxyapatite, calcium
carbonate, and others.
Xenograft: A graft taken from a donor of a
different species. Various preparations have
been used over the years. Currently, bovine
xenograft materials, and porcine xenograft
enameΙ matrix proteins are being used.

90. sURGlcAL TBEATMENT: REsEcτlvE AND REGENERAτlvE PROOEDUREs
Guided tissue regeneration membranes:
Nonresorbable. Expanded polytetrafluoro-
ethylene (ePTFE). The majority of GTR clinical
studies have been done using this mem-
brane. The major disadvantage to any non-
resorbable membrane is the need for a second
procedure to retrieve the membrane several
weeks after the initial surgery.
Resorbable. There are several resorbable
membranes from which to choose. Some are
Type I collagen based and others are made of
poΙymers that are metabolized to carbon dioxide
and water.
Collagen-based membranes: Type I
coΙlagen
Polymer-based membranes: Polylactic acid
others: Calcium sulfate, pιaster of Paris
Root conditioners:
Citric acid, tetracycline, and EDTΑ (ethylene
diamine tetra-acetic acid) are chelating agents
that have been advocated as root conditioners.
These substances remove the smear layer and
endotoxin from root surfaces that have been
scaled and root planed, dissolve microscopic
pieces of calculus, and expose collagen tufts in
the dentinal surface that can unite with the flap
when replaced. Tetracycline also has an antimi-
crobial effect. The evidence for improved regen-
erative results is somewhat equivocal, and the
use of root conditioners is by clinician's prefer-
ence at this time.
Growth factors:
Bone morphogenetic proteins (BMP). The
BMPs are proteins found in bone and are respon-
sible for the stimulation of bone gro\Λ/th. Pure
BMPs may be manufactured using recombinant
DNA technology.
Platelet-derived gro\Λrth factor (PDGF). PDGF
is obtained from thΘ patient's own platelets and
mixed with the bone graft material. This is a rela-
tively new technology that shows promise in
improving the regenerative result.
Other growth factors. Other factors such as
insulin_Ιike growth factor and transforming growth
factor B are being investigated for use in regener-
ative therapy.
What Are the Techniques Used in
Regenerative Therapy?
Τhe overarching approach to regenerative therapy is to
eliminate or control any negative influences on the
healing of both soft tissue and bone to the greatest
degree possible. The basic technique of successful
regenerative surgical therapy is as follows. There may be
variations due to specific clinical conditions or the prefer-
ence of the practitioner.
Gase selection. The patient should have exemplary
plaque control and not smoke. Periodontal osseous
lesions to receive regenerative therapy should be 2-
or 3-wall vertiοaΙ defects at least 3 mm deep. Molars
with CΙass l and ll furcation involvement are also
amenabΙe to regenerative therapy.
Plaque control. The better the patient's plaque
contro|, the greater the chanοes of suοcess. Surgery
in a plaque infected dentition leads to additional
attachment loss.
Marginal inflammatory control. lnflammation of the
gingival margin must be controlled presurgically to
maximize gingival health for the surgical procedure.
FΙap reflection and suturing are more predictable
when accomplished in healthy marginal tissue and
intraoperative bleeding is reduced. Of course, deep
inflammation may still be present, necessitating the
surgical procedure in the first place.
Aseptic technique. The chance for infection from
sources other than the patient's mouth must be mini-
mized. Aseptic teοhnique includes the use of sterile
drapes for the patient and equipment and strict
adherenοe to the sterile zone once the operator and
assistant don sterile gloves. Sterile water or saline
must be applied when a high-speed handpiece is
used for bony recontouring. Tap water is by no
means sterile.
FIap design and surgica! technique. Flaps must be
designed and incisions made to maximize the reten-
tion of the interdental papillae, minimize trauma to the
flap, and allow for coronal positioning of the flap if
desired. Envelope replaced flaps are often used in
regenerative therapy. Vertical incisions may be used
as long as there are no anatomic or aesthetic contra-
indications to their use.
Debridement" Soft tissue debridement of the
osseous defect must be complete. This allows for
inspection of the defect itself and exposure of any
residual radicular calculus that is then removed by
scaling and root planing.
Scaling and root planing. All visible and detectable
calculus must be removed as thoroughly as possible.
Microscopic calculus may be removed by root condi-
tioning.
lntramarrour penetration. lntramarrow penetration is
the creation of small holes with the corticated
osseous walls of a periodontal defect. lt is thought
that by penetrating the calcified walls of the osseous
defeοt, cells involved in repopulating the defect may
migrate from the marro\iv spaces more readily.
Root preparation. The use of citric acid, tetracycline,
or ethylene diamine tetra-acetic acid (EDTA) to
detoxify the root surface, remove the smear Ιayer,
decalcify minute pieces of residual calculus, and
expose collagen tufts in the dentinal surface has
been advocated.
88

91. CHAPτER 8
Graft placement. The graft material should be
placed within the confines of the osseous defect to
ensure maximum success. Graft material placed
outside the defect may contribute to increased bone
growth, but results are less predictable.
Guided tissue regeneration. The membrane used
should be pΙaced over the osseous defect, being well
adapted to the root surface and extending at least 2
mm past the edges of the defect. The membrane may
be resorbable or nonresorbable as described above.
The membrane aids in graft containment as well as
serving as a barrier to unwanted cell migration and
growth.
Wound closure. Primary closure should be achieved
if at all possibΙe. Bone graft materials, when used
alone, must be completely covered by the flap to
ensure that the material remains in the osseous
defect. Membranes must be covered to minimize
plaque accumulation on the membrane surfaces and
to allow for the dissolution of resorbable membranes.
Flaps are generally closed using vertical mattress
sutures and monofilament suture material such as
nylon suture.
Wound adaptation. The flaps must be well adapted
to the underlying bone and around the roots of the
teeth. The thickness of the blood clot under the flap
must be minimized by placing gentle pressure on the
flap for several minutes. Flap/wound stability is crit-
ical to regenerative success. A periodontal dressing
may be used to aid in flap stability and wound protec-
tion.
Postoperative care. Standard postsurgical instruc-
tions apply to regenerative surgical procedures as
well. Pain and swelling must be minimized so ice and
the use of nonsteroidal anti-inflammatory drugs is
recommended. There is some evidence to suggest
that a postoperative course of antibiotics (tetracy-
cline, doxycycline, or penicillin) may be of some
advantage. Smoking is to be strongly discouraged.
'The
patient should not use mechanical means of
plaque control in the area. An antimicrobial
mouthrinse is a useful plaque control adjunct. The
patient should not use interproximal plaque control
measures untiΙ the membrane has been removed or
is resorbed. Nonresorbable membranes are removed
6-9 \η/eeks after surgery unless evidence of infection
necessitates earlier removal.
What ls Guided Bone Regeneration?
Guided bone regeneration (GBR) is the application of the
principles of guided tissue regeneration to enhancing the
osseous topography of the edentulous ridge. Bone graft
materials and barrier membranes may be used to create
a space within the bony compartment of the ridge into
which new bone will form. GBR may be used either
before or in con.iunction with endosseous implant place-
ment.
What ls Distraction Osteogenesis?
Distraction osteogenesis is a technique whereby bone is
split, mechanically separated in an incremental fashion,
with new bone forming betu/een the separated bony
segments. The underlying biological principle is that of
osseous healing by tension-stress. As the new reparative
callus forms on either bone edge, the bone segments are
slowly moved apart placing the callus under tension. After
the desired amount of bone length is achieved, the
distraction is halted and the bone allowed to mature.
Distraction osteogenesis has applications in cranio-
mandibular orthopedics and in remodeling atrophic alve-
olar ridges, either to improve contour or provide room for
endosseous implant placement.
-

92. Ξ

93. CHAPTER 9
GHAPTER 9: SURGIOAL TREATMENT: PERloDoNΤAL PLAsTlc
SURGERY
Aesthetics are a primary focus of dental care today. Αs
patients live longer and have the means by which to
change their appearanοe, more and more patients are
taking advantage of the recent advances in aesthetic
treatments. Aesthetic dentistry is not only related to
proper color matching of composite resin or porcelain
restorations but to the entire presentation of the orofacial
complex. Color and contour of the soft tissues. and the
soft tissue relationship to restorations are important
οomponents of aesthetic dentistry.
What ls Periodontal Plastic Surgery?
Periodontal plastic surgery involves surgical techniques
that alter the shape of the gingiva or edentulous alveolar
ridge. These techniques relate to morphological changes,
not necessarily functional changes. Traditional muco-
gingival procedures are also considered to be periodontal
plastic surgical procedures. Functional or support
changes must be accomplished using either guided bone
regeneration or distraction osteogenesis.
What Types of SofVHard Tissue Defects May
Be Treated with Periodontal Plastic Surgery
Techniques?
Periodontal plastic surgery procedures may be used to
augment the zone of attached gingiva, correct isolated or
adjacent areas of gingivaΙ recession, correct excessive
gingival display (the "gummy smile"), to move or eliminate
an aberrant frenum, and to augment the morphoΙogy of a
resorbed edentulous ridge prior to the pιacement of a
fixed prosthesis.
How ls the Patient's Aesthetic Presentation
Evaluated?
The patient's aesthetiο presentation includes not just the
characteristics of the teeth but also the soft tissues
(gingival margins and edentulous ridges), lips, and
overall facial appearance.
The evaluation must staft with an analysis of the patient's
desires and a history of any aesthetic change. ln some
cases, the patient has a clear idea of what features are to
be improved. ln other instances, the patient may not be
aware of aesthetic problems, or may be self-conscious
about the aesthetic presentation. The patient who hides
or stifΙes a smile when something humorous is said may
have an unrecognized aesthetic need. lt is important that,
\ivhatever the need, the request is reasonable and may be
accompΙished by the praοtitioner. lt may be necessary to
refer the patient to a practitioner /ith more expertise in
aesthetic approaches to dentistry.
Τhe face is then examined for symmetry of shape and
movement, the relationship of the interpuρillary line to the
midsagittal plane, and the proportions of the various
facial features. The rule of fifths - the breaking up of the
face into 5 equal vertical sections - can help in pinpointing
disproportionate features. The overall shape of the face
and contours of the cheeks are important. The visual
inclinations of the maxillary anterior teeth, particularly the
frontal visual profile of the canine, should parallel the
frontal visual contour of the cheeks. Recent work by Dr.
Stephen Marquardt has attempted to quantify the
aesthetically pleasing face using calculations based on
The Golden Proportion. The so-called Phi Mask has been
derived from the Golden Ratio of 1.618:1.0:0.618. The
closer the faοial features fit the mask, the more pleasing
the faοe is to the eye. Further information may be
obtained at W\iv\Λ/.beautyanalysis.com.
The lips are examined in repose and in a full smile. lt is
important for the patient to produce a spontaneous smile
thereby maximizing the extent of the exhibition of the
teeth and intraoral soft tissues. A patient with a high lip
line will present a Signifiοant challenge particularly if fixed
restorations are planned for the maxillary anterior
aesthetic zone (Figure 1). The lateral extent of tooth visi-
bility is also determined (Figure 2).
F|GURE 1. τhe High smile Line. This patient's high smile line makes any
periodontal or restorative therapy a challenge to maintain a pleasing
aesthetic presentation.
F|GURE 2. τhe Broad smile. τhis patient shows the mesial of the maxil-
lary first molar when she smiles. Metal restorations in the molar area
may not be acceptable to some patients with this broad a smile,
The features of the gingiva should be studied for contours
of the gingival margins, width of keratinized tissue, eΧces-
sive gingival display, any inflammation, open embrasures
(the dreaded black triangles), recession, discolorations,
and edentulous ridge defects in the aesthetic zone.
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94. Ξ
SURG|CAL TREATMΕNT: PERloDoNTAL PLASTIC SURGERY
Tooth characteristics and position should be noted. The
relative visual widths of the maxillary central incisor-
maxiΙlary lateral incisor and the maxillary οanine shou|d
also approach the Golden Proportion of 1.618:1.0 (laterai
incisoQ: 0.618 (visual width when viewed from the front,
not the actual width of the canine (Figure 3). Root prox-
imity may be important in developing interdental papilΙae
and proper interproximal restorative οontours (Figure 4)'
F|GURΕ 3. τhe Goιden Proportion. τhe appearance of these teeth is
arranged in the Golden Proportion, 1.618:1.0:0.618.
FιGURE 4c- Root Proximity. After aesthetic crown lengthening, more
appropriate crown contours and increased embrasure space were
possible in these provisionaι reslorations.
How ls Gingival Recession Classified?
Τhere are tio maior classifiοation systems for gingival
recession.
The SulΙivan and Atkins Classification of recession is a
descriptive system first presented in 1968. lt was thought
at the time that it u/as often not possible to achieve
complete soft tissue coverage for the denuded root
surface. Τhe classification system described the type of
recession and expected amount of root coverage utilizing
the free gingival graft procedure. Deep, wide defects
were thought not to be able to be covered, although
almost complete coverage was possible with narrow
defects. The four classes of reοession are:
Shallow, narrow
Deep, narrow
Shallow, wide
Deep, wide
Miller presented a system of classifying recession based
both on the apical extent of the recession and the adja-
cent interproximal bone height. Τhe system also predicts
the amount of root οoverage possible. With no interprox-
imal bone loss, most roots may be covered with new soft
tissue to the cementoenamel junction.
Miller Classification System (Figure 5):
FlGURE 4Α. Root Proximity. τhe contours of the maxillary anterior
crowns are too straight due to the proximity ot the adjacent roots.
There is nοt enough embrasure space tor the interdental papillae'
FIGURE 48. Root Proximity. The surgical appearance of the closeness of
the roots.
FlGURE 5A. Miller Recession cΙassitication. class lrecession
Class l. Recession coronal to the mucogingival junc-
tion with no interproximal bone loss. 100% rool
coverage to the cementoenamel junction is ρossible.

95. cHAPτER 9
FIGURE 58. Miller Recession Classitication. Class ll recession
Class ll. Recession apical to the mucogingival junc-
tion with no adjacent interproximal bone loss. 100%
root coverage to the CEJ is possible.
FlGURΕ 5c. Miιler Recession classification. class lll recession
Class lll. Recession apicaΙ to the mucogingival junc-
tion /ith mild to moderate adjacent interproximal
bone loss. Some root coverage is possible, based on
the level of the interproximal bone.
FlGURΕ 5D. MiΙler Recession classification. class lv recession
Class lV. Severe recession with accompanying
severe bone loss. No root coverage can be expected.
How Are Alveolar Ridge Defects Classified?
Αβproximately 95Y" of maxillary anterior edentulous
ridges exhibit resorption to some degree. lt is often a
challenge to fabricate an aesthetically pleasing restora-
tion in the face of this ridge deformity. ln addition, once
teeth are removed, ridge contours are generaΙly smooth
with root eminences obΙiterated. GingivaΙ margins and
interdentaΙ papilla are also absent when pontics are fabri-
cated. li then becomes difficult to provide a pontic that
appears to be emerging from the soft tissue rather than
sitting on the ridge. Ridge defects may be classified as
follows:
Seibert Classification (Figure 6).
F|GURE 6Α. seibert classification of Bidge Defects. class l facio-palatal
defect
Class l. Bucco-IinguaΙ defect-ridge height is intact but
there is a concavity on the facial surface of the ridge.
May be best treated with a submucosal connective
tissue graft
*.1::j+ :##r,_i;.*?:::
+.; i:. 'i:::iΞffi;ii:: .
.: :i 1.*.
FΙGURE 6B. seibert classirication ot Ridge Defects. Predominantly
vertical defect
cΙass ll. Αpicoronal defect. Ridge height is lost by the
facial ridge contour is intact. This is the last common
ridge defect.
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96. Ξ
sURGlcAL TREATMENT: PERloDoNτAL PLAsτlc SURGERY
F|GURE 6ο. seibert classification of Ridge Defects. combination defΦt
class l]l. Combination of a class l and οlass ll defect'
This may be treated wth a single procedure or may
require multiple procedures depending on the
severity of the initial defect.
What ls Excessive Gingival Display?
Excessive gingival display, also referred to as altered
passive eruption, delayed passive eruption, or the
"gummy smile," is a condition where a significant amount
of gingiva is visible in the maxillary aesthetic zone when
an individual smiles (Figure 7). This may occur when the
gingival margin has not migrated to the vicinity of the
cementoenamel junction (CEJ) after eruption of the tooth
(altered passive eruption) or be related to skeletal anom-
alies.
F|GURE 7. Altered Passive Eruption. τhe gingival margins on the maxil-
lary central incisors are 5 mm coronal to the cementΦnamel iunc-
tion in this 27 year old patient.
Excessive gingival display may be caused by:
. Failure of the gingiva to migrate apically along the
crown of thΘ tooth after active tooth eruption is
completed.
o Facial crestal alveolar bone located adiacent to the
CEJ thereby preventing apical migration of the
gingiva.
. Vertical maxillary excess \Λ/here the gingival margin is
at the proper location but the maxilla is enlarged in
the superioιinferior dimension'
. Upper lip incompetence where the upper lip does not
cover the teeth or gingiva.
How ls Altered (Delayed) Passive Eruption
Classified? What Corrective Procedures Are
Applicable to Each Classification?
Type 1. There is excessive gingiva present. ln Type
1A, the gingival margin is coronal to the cemento-
enamel junction (CEJ) and the tip of the probe can
penetrate to the CEJ. The crest of the alveolar bone
is apical to the CEJ. This may be corrected using a
gingivectomy procedure. ln Type 1B, Ιhere is exces-
sive gingiva but the probe cannot penetrate to the
CEJ. ln this case, the crest of the alveoΙar bone on
the facial of the tooth is most likely at the level of the
CEJ. This must be οorreοted with an apically posi-
tioned flap, perhaps with local gingivectomy and with
ostectomy/osteoplasty as neοessary to create 1-2
mm of exposed root structure for the biologic width.
Type 2. The width of the gingiva is in the normal
range. ln Type 2A, the crest of the alveolar bone is 1-
2 mm apical to the CEJ. ln Type 2B' Ιhe crest of the
bone is at the Ievel of the CEJ. ln either case, an
apically positioned flap with or without osseous
recontouring is indicated. Τhere is not enough gingiva
present to allow for a gingivectomy.
lf a gingivectomy is performed in either Type 18 or
28, the tissue will grow back in a matter of months
and the procedure will be for naught. Skeletal abnor-
malities (verticaΙ maxillary excess) cannot be
corrected by periodontal surgical procedures.
What Types of Procedures Are Available in
Periodontal Plastic Surgical Therapy?
There are various approaches to periodontal plastic
surgery techniques. Grafts may be autogenous, allograft,
alloplast, or xenograft in nature. Ridges may be
augmented \Λ/ith οonnective tissue only, or with bone or
bone substitutes with or without connective tissue
grafting. The foοus of this chapter will be on the use of
autogenous connective tissue harvested from the palate
to achieve the desired aesthetic result. Details of each
surgical procedure may be found in standard periodontics
texts or surgical atlases listed in the Reference Section.
Free ginglval graft (Figure 8)
Lateral pedicle graft (flap) (Figure 9)
Submucosal connective tissue graft (Figure 10)
lnterpositional connective tissue graft
Onlay connective tissue graft (Figure 11)
Double papillae connective tissue graft (Figure 12)
Ovate pontic seat preparation (Figure 13)
CoronalΙy-positioned flap
Allograft (Αllodermo) use for root coverage or ridge
augmentation
Gingivectomy (Figure 14)
Aesthetic crown lengthening (Figure 15)
Frenectomy (Figure 16)

97. cHAPτER 9
What Materials Are Available for Periodontal
Plastic Surgical Procedures?
There are a variety of materials available for periodontal
plastic surgery proοedures.
. Αutogenous gingiva, connective tissue and/or bone
ο Allograft connectiνe tissue substitutes (Allodermo) or
bone grafting materials
o Xenograft bone fill materials
. Membranes used in guided tissue regeneration have
been used to increase the zone of attached gingiva
and for guided bone regeneration
What Are the Aesthetic Problems and
Potential Solutions Most Often Encountered
in Aesthetic Periodontal Therapy?
Surgical Problems and Treatment Options
What ls a Free Gingival Graft?
A free gingival graft (Figure 8) is the grafting of a piece of
gingiva that has been οompletely detached from the
donor area to the recipient site. \Λ/hile originally intended
to increase the zone of attached gingiva, the free gingival
graft may provide root coverage in the appropriate situa-
tion. Difficulty in getting complete root coverage lies in the
fact that an avascular graft is placed over a root surface
also devoid of a blood supply. For the first 30 hours, the
free gingival graft survives by plasmatic circulation, the
oozing of nutrients from the cut blood vessels of the
recipient site into the graft. At day 2 the blood supply
begins to re-establish itself and continues to reorganize
for the next 28 days. Creeping attaοhment, the coronal
migration of the free gingival margin after a free gingival
graft, may ocοur when there is coronal interproximal bone
and the original dentogingival junction and free gingival
margin are removed when the reοipient site for the graft is
prepared (Figures BE, F, and G). This procedure is used
to increase the zone of attached gingiva with the
possibiιity of gaining root οoverage as well.
F|GURE 8A. Free Gingival Graft. τhis patient has no keratinized tissue on
the facial surfaces of the mandibular central incisors.
F|GURΕ 8B. Free Gingival Graft. τhe graft recipient site is prepared using
split thickness dissection.
FIGURE 8C. Free Gingival Graft. The graft was haruested from the palate
and plaοed at the recipient site.
Problem Solution(s)
Gingival recΘSsion and/or
Inadequate zone of attached gingiva
Free gingival gratt (Figure 8)
Submucosal connective tissue graft (Figure
10)
Lateral ρedicle
graft (Figure 9)
AllodermΘ graft
Continuous connective tissue gratt
coronally positioned Ιlaρ
lnadequate zone of attached gingiva
without recession
Free gingival graft (Figure 8)
AllodermΘ graft
Prevention of ridge resorption Socket preservation procedures
RetΘniion of natural teeth or roots
Resorption of the edentulous ridge SUbmuοosal connective tissue gratt (Figure
10)
Onlay connective tissue graft (Figure 1 1)
Particulate bone graft
Guided bone regeneration
Distraction osteogenesis
Submucosaι connective t Ssue graft (Figure
10)
Combination Drocedures (Fioure
1 7)
Abetranl
Excessiγe gingival display
Altered passive eruption
Gingiveοtomy (FigUre 14)
Aesthetic crown lengthening (Figure 15)
ot'hοοnathie sllrnοru
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98. Ξ
sURGlcAL TREATMENT: PEΒloDoΝτAL PLAsτlc sURGERY
F|GURΕ 8D. Free Gingival Graft. Finaι heaιing. The zone of attached
gingiva was increased and 2 mm of root coverage was accomplished
on the right central incisor.
F|GURE 8Ε. Free Gingival Graft. Preoperative view of a free gingival graft
site.
FlGURE 8G. Free Gingival Graft. τhe root of the right central incisor was
eventually covered with gingiva due to creeping attachment.
What ls a Lateral Pedicle Graft?
Α lateral pedicle graft (Figure 9) iS the transposition of
gingiva from one site to an adjacent area of recession or
minimal attached gingiva while leaving the bΙood supply
of the donor connected at the base of the graft. lncreased
root οoverage compared to a free gingival graft may be
expected. Τhe donor site must have a sufficient amount
of gingiva to be moved. lt is possible to get a slight
amount of recession at the donor site. This technique is
used to obtain root coverage and increase the zone of
attached gingiva.
FiGURE 9Α. Lateral Pedicle Fιap. Tttis patient had severe reοession on
both the maxiιlary and mandibuΙar canines.
FlGURΕ 98. Lateral Pedicle Flap. τhe lateral pedicle graft in pιace on the
mandibular left canine- τhe denuded area by the donor site wilI heal
by granulation and maturalion.
FlGURE 8F. Free Gingival Graft. τhree weeks after the graft was placed.
96

99. CHAPTER 9
FIGURE 9C. Lateral Pedicle Flap. Complete root coverage was obtained.
What ls a Submucosal Connective Tissue
Graft?
Α submucosal connective tissue graft (Figure 10) is one
where connective tissue devoid of surJace epithelium is
either compΙetely or partialΙy submerged under a par1ial
thiοkness flap or ρlaced in a prepared pouch. This graft
may be used to augment a deficient ridge, usually a
Seibert Class I or Class Ill defect. The submucosal
connective tissue graft may also be used to cover a
denuded tooth root.
FlGURΕ 1 0Α. submucosal connective Tissue Graft. τhis patient presents
with a Seibert Class I ridge defect.
FIGURE 10B. submucosal connective Tissue Graft. τhe 4 mm depth ot
the defect strained this procedure to the limit due to the inelasιicity
of the gingiva.
F|GURE 10c. submucosal connective Tissue Graft. τhe graft is in place.
Notice the smalΙ vertical lear in the pouch. τhis healed without
complication.
F|GURE 1 0D. submucosal connective τissue Graft. The facial contour of
the ridge was completely restored with one graft procedure.
FlGURE 10E. submucosal connecιive τissue Graft' τhis patient
presented with a Class I ridge defect and recession on the maxillary
left lateral incisor.
97
-

100. Ξ
sURGΙcAL TREATMENT: PERloDoNτAL PLAsτlc sURGERY
FlGURΕ 10F. submueosaΙ connective τissue Graft. τWo submucosal
grafts are in place, one to correct the ridge defect and ιhe second to
cover the root.
FIGURE 10G. Submucοsal connective τissue Graft. Final healing shows
accomplishment οf both goals. τhe maxilιary left central incisor is
an ovate pontic.
What ls an lnterpositional Connective Tissue
Graft?
Τhis procedure is simiΙar to the submuοosal connective
iissue graft when used for an edentuΙous ridge. With the
interpositional graft, the donor tissue is usually quite thick
So that the reοipient site may not be comp|etely closed.
The donor tissue is placed between the facial tissue and
alveolar bone, \i'fith the coronal aspect of the graft
exposed. This technique is used to increase the height
and width of an edentulous ridge.
What ls an Onlay Connective Tissue Graft?
The onlay connective tissue graft (Figure 11) is essen-
tially a large free gingival graft. The donor tissue is
completely severed from its blood supply and plaοed on
the edentulous ridge that has been denuded of its epithe-
lium. This graft may be used for Seibert Class ll ridge
defects to increase ridge height and for Class lll defects.
li may also be used to improve the facial contours of an
edentulous ridge. When ρlaced, it is imperative that the
onlay connective tissue graft has intimate contact with a
bleeding recipient site surface.
F|GURE 1 1 A. onlay connective τissue Graft. This patient lost significant
ridge dimension after exlraction of the maxillary anterior teeth. She
insisted on not have any type of removable appliance.
FlGURE 11B. onΙay connective Tissue Graft. τhe recipient site is
prepared by epithelial denudation to receive the 9raft.
98
FlGURE 11c. onlay connective τissue Gratt. τhe onlay 9raft was
harvested from the palate and placed with intimate adaptation to the
recipient site.

101. CHAPτER 9
FlGURΕ 11D. onlay οonnective τissue Graft. The final fixed prosthesis
was placed using ovate pontics.
What Is a Double Papilla Connective Tissue
Graft?
The doubΙe papilla connective tissue graft (Figure
'|2)
is
basically a double papilla graft wiih donor conneciive
tissue placed beneath the released tissue. This technique
may be used to increase the blood supply over the
midsection of an exposed tooth root.
FlGURE 12A. Double Papilla connective Tissue Graft. τhis patient had
ιrauma to the facial 9ingiva subsequent to an endodontic perfora-
tion.
FlGUFlΕ
'12ο.
Double Papilla connective τissue Graft. τhe final result Was
acceptable ιo ιhe patient.
What ls an Ovate Pontic?
The ovate, or egg shaped pontic, is used as the preferred
pontic design once an edentulous ridge has been
augmented. The tissue surface of the pontic is completeΙy
convex and has passive but intimate contact with the
properly prepared ridge. The advantages of the ovate
pontic are that a gingival margin and interdental papilla
may be sculpted from the restored ridge, giving the pontic
the appearance of a natural tooth as it emerges from the
soft tissue. The convex tissue surface of the pontic may
be easily οleaned with dental floss, dental tape, or yarn.
The ovate pontic seat is prepared (Figure 13) by anes-
thetizing the patient in the vestibule, taking care not to
distend the shape of the ridge. A large coarse diamond is
used to prepare the ovate pontic seat. This area should
be about 1.5 to 2.0 mm deep vvith development of
gingival margins and interdental papillae. The pontiο
should have intimate but passive contact with the under-
lying ridge surfaοe. The advantage of using connective
tissue for ridge augmentation is that there is a sufficient
thickness of tissue to develop the pontic seat. There must
be approximately 2 mm of soft tissue covering bone or
grafted bone substitute in heaΙth. When a conneοtive
tissue graft is utilized, there is sufficient room to deveΙop
this site without worry of involving the underlying bone.
FiGURE 1 3Α. ovate Pontic seat Preparation. Pretreatment view showing
an attempt at gingival colored porcelain.
FlGURE 12B. Double Papilla connective τissue Graft' τhe connective
tissue graft is ρlaced under the lifted interdental ρapilla.
99
-

102. Ξ
sUΒGlcAL TΒEATMENT: PEBloDONTAL PLASτ|c sURGERY
FlGURE 138. ovate Pontic seat Preparation. An examplθ of the coarse
round diamond used to prepare the depression and define the
gingival margins and interdental papilla.
F|GURΕ 13c. ovate Pontic seat Preparation- τhe pontic seat prepared
and ready for the provisional restoration.
What ls a Coronally Positioned Flap?
A οoronally positioned flap is, as the name suggests, the
coronal placement of an elevated flap. Τhis procedure
may be used to cover an area of recession or to cover a
connective tissue graft that has been placed on a root
suιJace. There must be interproximaΙ bone of sufficient
height to support this flap in its new coronal position. The
extent of οoronal posiiioning may be limited by the depth
of the vestibule, as this depth will be shallower with this
procedure.
What ls a Gingivectomy?
A gingivectomy (Figure 14) is the surgical removal of
excess gingiva down to the base of the sulcus. Τhis is
aοcomplished using an external bevel incision. Τhere
must be a sufficient amount of attaοhed gingiva
remaining after the procedure for this technique to be
used. A gingiveοtomy is the procedure of choice with
Type 1A excessive gingival display. Gingivoplasty
reshapes the gingival contours without removing any of
the soft tissue pocket wall.
F|GURE 14A. Gingivectomy for Excessive Gingival Display. τhis patient
presented with Type 1A altered passive eruption.
FIGUΗE 148. Gingivectomy for Excessive Gingival Display. A gingivec-
tomy Was pertormed because there was sufΙicient gingiva and the
cΕJ was reached preoperatively.
FlGURΕ 1 3D' ovate Pontic seat Preparation. τhe provisional restoration
with ovate pontic for the patient shown in Α.
100

103. cΗAPTER 9
F|GURE 14ο. Gingivectomy for Excessive Gingival Display. Final healing
after ιhe palient received composite veneers on the maxillary inci-
sors.
What ls Aesthetic Crown Lengthening?
Aesthetic cro\η/n |engthening (Figure 15) is an apically
positioned flap with or without osseous recontouring
(resective surgery) to improve the aesthetic presentation.
ln many cases, routine resective surgery to treat perio-
dontitis will detract from a pleasing appearance in the
aesthetic zone. With excessive gingival display, this type
of procedure may be of great benefit to the patient.
FlGURE 15Α. Aesthetic crown Lengthening for Excessive Gingival
Display. τhis 25 year old lemale presented With τype 2B allered
passive eruptiοn.
FlGURE 15c. Aesthetic crown Lengthening for Εxcessive Gingival
Display. Bone is removed to aΙΙow room for ιhe biologic width and to
be able to apically position lhe gingival flap.
FIGURE 15D. Αesthetic crown Lengthening for Excessive Gingival
Display. τhe flap is placed With the gingival margins at the cΕJ of
each tooth.
FlGUΒΕ 15E' Aesthetic crown Lengthening ,or Excessive Gingival
Display. The compΙete contours of the crowns of the teeth are now
visible-
FΙGURE 15B. Aesthetic crown Lengιhening ,or Εxcessive Gingival
Display. After flap reflection, the crestal bone is seen aι the cEJ.
101
-

104. sURGlcAL TREATMENT: PEΒloDONτAL PLAsTΙc sURGERγ
FlGURE 15F. Aesthetiο crown Lengthening for Excessive Gingival
Display. τhis 28 year old male presented With a complex set of
aesthetic probΙems.
FlGURΕ
'15G.
Aestheiic οrown Lengthening for Εxcessive Gingival
Display. The maxillary right segmenl underwent aesthetic crown
lengthening to level the gingival margins.
FlGURE
'15Η.
Aesthetic crown Lengιhening tor Excessive Gingival
Display. There was a dramatic improvemeηt in the patient's appear-
ance when the provisional restorations were placed.
What ls a Frenectomy?
Α freneοtomy (Figure 16) is the Surgical removal of a
frenum. Often, the maxillary labial frenum must be
removed and the interdentaΙ papilla recontoured after the
orthodontic closure of a midline diastema. Αt times,
misplaced frenula may cause diffiοulties in the retention
of removable prostheses. Α lingual frenum may be
removed to relieve ankyΙogΙossia.
F|GURE 16A. Frenectomy. τhe patient disliked the appearance of the
maxiΙlary labial frenum.
FlGU RE 1 6B. Frenectomy. τhe frenectomy was accomplished using sharp
disseclion. A CO2 laser could be used for this procedure.
F|GURE
'16ο.
Frenectomy. τhe frenum was completely removed from the
facial. A small piece of frenum was left on the palate to help close
the diastema.
102

105. CHAPTER 9
FlGURE 1 6D. Frenectomy. τhe diastema Was closed With composite resin.
Orthodontic therapy was not an option in this case.
What ls a Socket (Ridge) Preservation?
Socket preservation, better described as ridge preserva-
tion, iS the maintenanοe of the dimensions of the alveolar
ridge after the removal of a tooth. This is particularly
important in the aesthetic zone where ridge resorption
should be minimized. Socket preservation may be
accomplished by keeping the facial plate of bone intact
and placing a bone fill material in the socket. There may
be some sΙight resorption even with these measures.
Shallow Seibert ridge defects are much easier to rectify
than deep ridge concavities.
Ηow ls the Patient Treatment Planned for
Aesthetic Periodontal Therapy?
Treatment of the aesthetic patient usually requires a
multidisciplinary approach. ln many cases, the perio-
dontal plastic surgical procedures are done in conjunction
with, or in advance of, restorative dentistry. ln situations
where excessive gingival display, recession, or a lack of
attached gingiva is ihe problem, the periodontal plastic
surgery procedures may stand alone.
ln compΙex cases, the patient must be advised that the
addition of aesthetic surgery to the treatment plan will
increase the effort, expense, and time for treatment
compΙetion. The patient should also be reminded from
time to time, that alΙ of the bother will be weΙl worth it in
the final outcome. As with other plastic surgical proce-
dures, the desired result may not be obtained or be
possible with one approach. Combination procedures
(Figure 17) may be necessary to achieve complete reso-
Ιution of the aesthetic challenge.
F|GURES 17A and B. combination τherapy. This patient has resective
periodontal surgery after the placement of the crowns in the maxiF
lary arch.
F|GURΕ 17c' combination Therapy. τhe right centraι incisor was
removed and a submucosal connective ιissue graft placed.

106. SURG|CAL TREATMEΝT: PERloDONTAL PLAST|C SURGERY
FlGURΕ
'17D.
combination Therapy. An onlay grafι was the second stage
procedure performed.
F|GURE 17E. combination Therapy. τhe ovate pontic seats Were
prΘpared.
FIGURE 17F. Combination Therapy. Four years after the completion of
therapy the aesthetic zone remained stable.

107. CHAPτER 10
OΗAPTER 10: PERIODONTAL EMERGENOIES
Periodontal emergencies are a part of the everyday prac-
tice of dentistry. The clinician must be able to assess the
emergent condition rapidly and accurately in order to
provide relief for the patient. Effective management of
periodontal emergencies aids in both the patient's phys-
iοal and psychological well-being and may contribute to
personal satisfaction for the treating clinician.
Clinical manifestations and general treatment regimens
will be presented in this chapter. Detailed information
about therapeutic agents may be found in Chapter 6.
νvhat Are the Common Periodontal
Emergencies?
o Acuteherpeticgingivostomatitis
o Necrotizing ulcerativegingivitis
. Periodontal abscess
ο Pericoronitis
o Differentiation of the endodontic from periodontal
abscess and the combined endodontic-periodontal
abscess (lesion)
How ls the Diagnosis of the Emergency
Condition Determined?
One of the most difficult yet rewarding challenges in
dentistry is arriving at an accurate diagnosis and
rendering appropriate treatment for the emergency
patient. Τhis patient presents with an acute prob|em and
is seeking immediate relief. At this time, all dental proce-
dures should be focused on identifying and rectifying the
problem at hand. Proper treatment of the emergency may
provide the practitioner with a lifelong patient.
A diagnosis may be determined by first obtaining a
complete history of the problem from the patient and
completing a targeted clinical and radiographic examina-
tion. Questioning the patient regarding the signs and
symptoms of the problem may lead to the diagnosis.
ο ls the problem acute or chronic?
ls there pain?
ls the pain sharp, dull, or throbbing? (Periodontal
pain is usually dull or throbbing.)
ls the pain intermittent or chronic?
Does anything in particular cause the pain (cold,
sweets)?
Did the pain awaken the patient from a sound
sleep? (A yes ansνver, the problem is usually endo-
dontic in nature.)
ls the pain relieved/made worse by cold? (Pain
relieved by cold, think endodontics.)
Does heat make the pain worse? (Yes, think endo-
dontics.)
Does the tooth in question feel longer (now biting
on that tooth first)? (Yes, think endodontics.)
ls the tooth sensitive to biting or percussion?
ls the tooth mobile?
Has there been any swelling? (Localized by gingival
margin, generally periodontal; more diffuse or cellu-
lites, generally endodontic in nature.)
lf so, when, what kind (indurated or fluctuant),
where, and for how long?
Has there been any drainage from the swelling or
bad taste?
ls there a fistula present? Can the fistula be traced
radiographically with a piece of gutta percha?
Are there any ulcers or other oral lesions present?
How long have they been present?
Does the patient feel sick or fatigued?
ls the patient febrile?
Ηas this happened before?
ls it getting worse?
What are the radiographic findings?
ls the pulp vital?
What is the periodontal probing pattern? (lsolated
deep probings, probably endodontic; broad probing
pattern more likely a periodontal problem.)
Are there any systemic problems (ie, diabetes
mellitus Type 1 or Tyρe 2' smoking)?
Has the patient been eating popcorn or nuts? (lf
yes, possibly a periodontal abscess due to food
impaction.)
once the ans\Λ/ers to these questions have been obtained,
the diagnosis is often evident. Occasionally, there is still
some question and further tests, such as a biopsy of some
suspicious tissue, may be in order.
What Are the Signs and Symptoms of a Gingival/
Periodontal Abscess?
A gingival abscess is a supeι'ficial, painful, rapidly expanding
purulent inflammatory lesion found in the supedicial gingival
tissues. A periodontal abscess (Figure t) is localized purulent
infΙammation deeper in the periodontal tissues. Both lesions
may be marked by pain, fluctuant swelling, and collection of
purulence. The pain generally does not awaken the patient
from a sound sleep. The periodontal abscess may have rapid
destruction of alveolar bone. Teeth may be sensitive to
percussion, mobile, and may have extruded or shifted posi-
tion in the alveolar housing. A gingival abscess may occur in
a patient who has no chronic periodontal disease. The most
Ιikely cause is the lodging of a foreign object or other irritant,
usually food (popcorn hull, etc)' in the gingival tissues. Α
periodontal abscess may be οaused by the entrapment of a
foreign object, loose calculus after scaling and root planing,
or by superficial healing of the gingival tissues \Λ/ith active
infection deeper in the pocket.
105
-

108. Ξ
PΕRloDoNτAL EMERGENclEs
FlGURE 1. Periodontal Abscess. τhis patient has multiple periodontal
abscesses as noted by the extreme erythema and edema at the gingival
margins of the maxillary right canine and maxiΙlary right central incisor.
What ls the Treatment for a Gingival/Periodontal
Abscess?
Primary treatment for an abscess is to establish drainage to
relieve pressure and rid the area of pus' Local infiΙtration
anesthesia with amide anesthetics may be ineffective due to
the acidic nature of the purulence. Regional or block anes-
thesia techniques may be neοessary. Drainage may be
achieved through the pocket itself using a periodontal curette
or may require an external incision to establish drainage.
Once drainage has been established and any foreign mate-
rial removed from the area, the absοess is rinsed thoroughly
to remove any remaining debris. occlusaΙ adjustment may be
necessary if the tooth in question has extruded in the socket.
As an acute periodontal absοess may have a greater poten-
tial for healing and repair than a chronic abscess, flap surgery
may be accomplished to remove any granulomatous tissue
and stimulate regeneration of lost periodontal tissues. lf the
abscess is an acute exacerbation of a chronic condition and
there has been extensive attachment loss, removal of the
tooth in question may be the best treatment option. Antibi-
otics are generally not indicated unless there is some
systemic involvement such as fever or lymphadenopathy.
What Are the Signs and Symptoms of
Pericoronitis?
Pericoronitis (Figure 2) is an infΙammatory Ιesion generally
associated \Ιvith erupting mandibular third molars. lt is caused
by an accumulation of bacteria and food debris trapped under
the operculum, the flap of gingiva partially covering an
erupting tooth. This may be exacerbated by impact of the
opposing tooth during closing of the mouth. Pericoronitis may
be marked by pain, possibly radiating to the ear or throat,
swelling, fever, lymphadenopathy, mobility of the tooth,
partial or complete trismus, and general malaise. Αt worst, an
untreated or poorly managed case of pericoronitis of a
mandibular third molar may develop into a peritonsillar
abscess or Ludwig's angina.
FιGURE 2. Pericoronitis. τhe tissue around this mesioanguιar impacted
mandibular right third molar has diffuse sweιling and iS tender to the
touch. τhis patient also has submandibular ιymphadenopathy.
How ls Pericoronitis Treated?
There are several approaches to the treatment of pericoro-
nitis. After anesthesia, the underside of the operculum flap
may be irrigated with a syringe or ultrasonic instrument to
remove any debris. lt may be neοessary to perform some
oοcΙusal adjustment on the opposing tooth or to remove it to
eliminate that source of trauma. Antibiotics, usually penicillin,
are indicated if there are systemic signs and symptoms.
Αppropriate analgesics are indicated aS vι/ell. The tooth in
question should not be removed at this stage because of the
danger of spreading the infection into adjacent anatomic
spaοes. once the acute phase of the infection has subsided,
final disposition of the affected tooth may be determined.
What Are the Signs and Symptoms of Acute
Ηerpetic Gingivostomatitis?
Acute herpetic gingivostomatitis is caused by herpes
simplex virus (HSV) type 1. lt is characterized by small
ulcers with elevated margins that may be disbursed
throughout the mouth on both attached and unattached
mucosa (Figure 3). These lesions may be quite painful, inter-
fering with eating and drinking. Systemic signs and symp-
toms, such as fever and malaise, are also present. The course
of the disease generalΙy lasts from 7-10 days.
FlGURE 3. Herpetic Gingivostomatitis. τhese uιcerative lesions are found on
both attached and moveable tissue and are quite painful.

109. CHAPτER 10
What ls the Treatment for Acute Herpetic
Gingivostomatitis?
Τhere is a two-pronged approach to the treatment of acute
herpetic Aingivostomatitis. First, antiviral agents, such as
acyclovir, may be used topically and/or systemically to control
the infection. ln addition, palliative therapy to relieve pain
must be initiated to allow the patient to eat and drink. Dehy-
dration is a threat, particularly in infants and small children.
Once the acute phase of the disease has passed, about one
third of these patients will have recurrent herpes infections.
These recurrent infections may be managed with the antiviral
medications. There is some evidence to suggest that the
amino acid, lysine, may play a role in prevention or attenua-
tion of herpetic outbreaks by disrupting viral replication.
\Mhat Are the Signs and Symptoms of Necrotizing
Ulcerative Gingivitis (NUG)?
The patient with NUG presents for treatment because of pain.
This disease is characterized by gingival and oral pain that
may be severe, fetid oris (bad breath), necrosis of the
gingival papilla that appear to be punched out, pseudomem-
brane formation at the tips of the papillae, and spontaneous
gingival bleeding (Figure 4). Systemic signs and symptoms
include fever, lymphadenopathy on the affected side, loss of
appetite, and malaise. Stress, fatigue, smoking, poor oral
hygiene, and an impaired immune system may all contribute
to the development of NUG. NUG must be differentiated from
acute gingivitis, primary herpetic gingivostomatitis, the
vesiculobullous diseases, leukemia, and the secondary stage
of syphilis.
FlGURE 4. Necrotizing υΙcerative Gingivitis. τhis patient presents with
extremely painful gingiva, foul smelling breath, spontaneous gingival
bleeding, and necrosis of the interdental papilιa. The patient was also
febrile and had sUbmandibuιar ιymphadenopathy.
What ls the Treatment for Necrotizing Ulcerative
Gingivitis?
Necrotizing ulcerative gingivitis is treated in a stepwise
fashion to control the baοterial infection, manage the acute
symptoms, and eliminate the predisposing factors. At the first
visit, as much debris, plaque, and calculus should be
removed as gently as possible, either with hand or powered
instrumentation. The patient should be instructed in plaque
οontrol using a neνv toothbrush. Chemotherapeutic
mouthrinses (chlorhexidine, phenoliο compounds) may be
helpful although could be uncomfoι1able at first due to their
alcohol content. Αntibiotics, such as penicillin, are indicated if
there is systemic involvement. Patients should refrain from
smoking until the acute phase subsides although this may
increase the patient's stress. Α bland diet should be recom-
mended along with drinking plenty of Water. τhe patient
should return 24 hours after the first appointment to continue
the debridement of the area and to polish the teeth. The
patient should return for a third visit one to t\Λ/o days later. By
this time, the acute phase should have subsided. lf signs and
symptoms persist, other systemic diseases must be ruled
out. Send for a medical evaluation if necessary.
Hoι,v ls an Endodontic Abscess/Lesion
Differentiated From a Periodontal Abscess/
Lesion?
Endodontic and periodontal emergencies are sometimes diffi-
cult to distinguish. The patient presents with pain that is
sometimes severe. Other signs and symptoms may be vague
making a rapid diagnosis of the problem difficult. lt is impor-
tant to arrive at the correct diagnosis as the sequence of
treatment is different for each type of lesion. ln general, there
are several patterns that help the practitioner differentiate
between these t\ι/o lesions.
Pain. Both lesions may cause pain. The pain of an endo-
dontic lesion may be sharp, have an intermittent nature
with each succeeding bout of pain being more intense, be
of more rapid onset, and awaken the patient from a
sound sleep. The pain of a periodontal abscess is gener-
ally more diffuse and can be described as a "throbbing"
type of pain. Periodontal pain, except in the case of NUG,
generally does not awaken the patient from a sound
sleep. Teeth in both instances may be sensitive to
percussion.
Probing depths. An endodontic abscess may drain
through the gingival sulcus. ln general, probe depths will
be shallow until the drainage area is reached upon which
there wilΙ be a sudden deepening of the pocket. ln other
cases, the abscess may create a fistula somewhere in
the soft tissue. Using a size 30 gutta percha cone placed
into the fistula and then exposing a radiograph will often
lead directly to the pathologiο tooth apex. Periodontal
lesions generally have a wider area of deep pockets.
Although it is possible to have a narroνν, deep pocket,
such as a pocket associated with a cervical enamel
projection of a mandibular first molar, this is less common
than with an endodontic lesion.
Pulp vitality. This may be problematic in multirooted
teeth. The pulp tissue in one canal may be necrotic with
vital tissue elsewhere in the root canal system.
Endo-perio problems may be classified as primary pulpal
disease, primary pulpal disease with secondary periodontal
disease, primary periodontal disease, primary periodontal
disease with secondary pulpal disease, or combined pulpal
and periodontal disease. Pulpal disease can contribute to the
initiation or progression of periodontal disease by communi-
cation through lateraΙ οanals, dentinal tubules, the apical
foramen, tooth οraοks or fractures, and periodontal disease
may contribute to pulpal disease through the same pathways.
107
-

110. Ξ
PERloDoNτAL EMERGΕNclEs
How Are Endodontic-Periodontal Problems
Treated?
ln an emergency situation, it is important to address the
problem that is causing pain and/or swelling for the patient. ln
a chronic situation, if the determination has been made that
the lesion is primarily of pulpal origin but there is some perio-
dontal involvement, the pulp is treated first and then the
periodontal condition is re-evaluated 2-3 months after the
completion of endodontic therapy. At that tame, any residual
periodontal defect may be treated. ln the presence of both a
chronic endodontic and periodontal lesion, both lesions must
be treated in order to achieve comριete healing.
'
l
108

111. CHAPτER 11
CHAPTER 11: CONSIDERATIONS lN IMPLANT DENTISTRY
The placement and restoration of endosseous dental
implants has become a predictable part of dental treatment.
While many patients have had missing teeth, or even an
entire dentition restored with implant supported dentistry,
implant dentistry is not a panacea. lt is important to
remember that most implant patients are dental failures and
that the clinician should identify the causes of the patient's
tooth loss. ιf a patient lost teeth due to periodontal disease, it
is probable that there will be plaque-induced peri-implant
disease if the etiology cannot be οontrolled. lmplant
supported prosthesΘs may also be jeopardized by inappro-
priate occΙusa| forces that are directed onto the restorations
or the implants themselves. Proper maintenance is as impor-
tant as the proper placement and restoration of implants.
What Are the Biomechanics of Modern lmplants?
Although there are many varieties of implants available, most
implants are either threaded Screνv or press-fit endosseous
root-form implants (Figure 1). lmplants are made of titanium
or titanium alloy with a highly polished collar at the top or
coronal end of the implant fixture. The surface of the implant
has been roughened to increase the surface area of contact
bet\iveen the implant and the bone. The implant surfaοe may
be blasted or coated with a titanium plasma spray or hydroxy-
apatite.
F|GUΒΕ 1. Root-form endosseous implants usually have a threaded screw
design (left) or a ρress-fit design (right). τhe implant is placed in a
prepared osteotomy site of a slightly smaller diameter that the diameter of
the implant.
The coronal aspect of all implants has a highly polished collar
trom 1-4 mm wide. This collar may be kept relatively plaque-
free with the appropriate home care devices and titanium-
friendly instruments. lmplants should never be cleaned with
metaltipped ultrasonic deviοes.
There is a permucosal attachment of the gingiva to the coΙlar
of the implant. Histologically, the gingiva attaches to the
implant collar by a hemidesmosomal attachment from the
junctional epithe|ium celΙs. This is the only soft tissue attach-
ment that protects the underlying bone. Connective tissue
fibers cannot insert into the body of the implant. As such, this
soft tissue attachment is more fragile and may be more
susοeptible to trauma' once this attachment is compromised,
the bone-implant interface may be reached. Connective
tissue fibers adjacent to the implant suface are oriented
parallel to the implant surface.
Current thinking suggests that there should be a band of
attached gingiva surrounding the implant collar. This denser
tissue can better protect the fragile permucosal epithelial
attachment than thinner alveolar mucosa can. lt is preferable
that this keratinized tissue be present either before implant
placement or uncovering.
What Are the Clinical and Radiographic Signs of
a HΘalthy and AiIing or FaiIing lmplant?
Muοh as /ith a tooth with a healthy periodontium, a healthy
implant will be surrounded by gingiva that is firm and pink
with no evidence of erythema, edema, or suppuration. Radio-
graphically, bone will approximate the implant surface from
the area of the most coronal thread to the apex of the implant
fixture (Figures 2A and B). The implant will be nonmoveable
when gently pushed upon with tvvo instruments.
F|GURE 2A. τhese radiographs show the appearance of impΙants in healthy
bone. τhreaded Screw type implant.
FIGURΕ 28. These radiographs show the appearance of implants in healthy
bone. Press-fit type implant, Note the dense bone extending to the
coronal aspect of each implant.
-

112. coΝslDERAτloNs lΝ lMPLANT DENτ|SτRY
lmplants may be jeopardized from two directions. Plaque-
induced inflammation caused by the same bacteria that
cause chronic periodontitis may be responsible for the initia-
tion and progression of peri-implantitis. τhiS process begins
around the implant collar. As long as the implant is still stable,
this type of problem may be treated using surgical
approaches similar to those used to treat periodontitis. A retro-
grade implantitis may be caused by microfracture of bone
surrounding the implant due to an overload of occlusal forces
on the implant. This problem may be manifest by a radiolu-
cency at the apeΧ of the implant. This is an irreversible
process.
An ailing or failing implant may exhibit any number of signs of
inflammation. Ιncreased probing depth in the peri-impΙant
sulcus, soft tissue erythema, or suppuration either from the
sulcus or a draining fistula οan denote an ailing implant
fixture. Bone loss will occur around the body of the implant.
Any mobility of the fixture in the osseous housing is defined
as a failing implant that must be removed. Radiographic
signs of an ailing implant include bone Ιoss at the collar, an
inοrease in the number of threads no longer in bone, or a
radiolucency at the apex of the implant (Figure 3A and B).
FlGURE 3Α. Radiographic and cιinical appearance of two ailing impιants. τhere
are radiolucencies around the body of each of these implants.
FιGURE 3B. Badiographic and clinical appearance of two ailing implants. υpon
flap reflection, the extent of the bone destruction can be seen. τhese
implants were rescued using regenerative techniques similar to those
used around natural teeth.
What ls the Protoοol for Implant Maintenance?
The sulcus around an implant must be examined with a
plastic periodontal probe (Figure 4) as a metal probe may
mar the implant surface. Gentle probing forοe must be used
in order not to completely penetrate the junctional epithelium.
ln the presence of inflammation, the probe tip may approxi-
mate the surface of the bone. Some authors suggest that an
impΙant sulοus should not be probed unless there is some
evidenοe of pathology. Unfortunately, inοreased probing
depth and bleeding upon gentle probing, the t\Λ/o most
obvious clinical signs of inflammation and destruction, cannot
be ascertained without probing.
F|GURE 4. τhis is an example of a plastic probe that may be used around an
implant. Gentle probing force must be used to avoid complete penetration
of the permucosal seal.
The maintenance appointment for implant patients is in many
ways similar to that for other dental patients with some
notable exceptions. only plastiο, graphite, or titanium instru-
ments should be used on implant surfaces (Figure 5). Stan-
dard stainless steel scalers and curettes will scratch the
implant surface. Although the metal tips of ultrasonic scaΙers
will damage the implant surface, the use of a sonic scaler
\,νith plastic inserts is safe. An ultrasonic scaler may be used
on the surface of an ailing or failing implant during a surgical
rescue procedure in order to help detoxify the implant
surface.
FiGURE 5. τhese instruments are examples of plastic curettes that should be
used when cleaning ιhe implant collars. steel-tipped instruments should
never be used for implant cleaning.

113. CHAPTER 11
Several protocols have been developed for the implant main-
tenance appointment. All protocols have essentially the same
components.
Clinical and Radiographic Examination
Remove superstructure (if possible): Removal of a
screw-retained prosthesis will facilitate cleaning.
Removal of the restoration will also allow the clinician
to differentiate between a loose restoration and a
loose implant.
EvaΙuate tissue for tone, coΙor, consistency, size, and
texture.
Check for mobility: Α mobile implant is a failed
implant.
Probe implant sulcus depth: This should be done with
a plastic periodontal probe and gentle force.
Evaluate plaque for quantity and location.
Evaluate calculus for quantity and location.
Radiograph implant area: There may be bone loss to
the first thread during the first year. Αfter this, bone
loss shouΙd be negligible from year to year.
Record cliniοal and radiographic findings.
lmplant Maintenance Treatment Procedures
. Home care instructions emphasizing missed plaque:
Have the ρatient demonstrate these new procedures.
Behavioral modification may be necessary if the
patient is reverting to poor habits that caused tooth
loss in the first place. Powered toothbrushes may
be more effective than manual brushes in working
around implants (Figure 6). An end-tufted brush may
also be used for hard to reach areas (Figure 7).
FIGURE 6. Powered toothbrushes may be used for effective home care around
implants. τhere are many designs of powered brushes avai|able. lt is
important to ensure that the head of the brush can contact the implant
surfaεe'
:ri::::,],:r:::t,t.. ..:.. t:.., : :::..
:!::.: ::
_:a]]
.::'--a
1 :,.τjl:a'ι:a a||.1...a :.
FIGURE 7. An end-tuft brush can be used to clean hard-to-reach areas for
implant and superstruoture maintenance.
Specially designed floss provides effective yet safe plaque
removal from implant surfaces (Figure 8). lnterproximal
brushes with nylon coated wires, soft foam inserts, or
brushes without a wire core οan also be used (Figure 9).
Chlorhexidine gluconate may be used adjunctively to
οontroΙ plaque.
FlGURE 8. γιride-diameter floss is an important component of implant mainte-
nance.
FIGURE 9. lnterproximal devices may be used to remove plaque and to deliver
antimicrobial agents to the interproximaι sufaces of implants during
home care procedures.
-

114. coNs|DERAτtoNs lN |MPLANτ DENTISτRY
. Remove supra- and subgingival plaque from the ο Clean any remaining natural teeth
implant surface: Plastic, graphite or titanium curettes
^--:__ ^_i ^^^^i+λ,i+ι, ^^A..^l
may be used. '
caries and sensitivity control
ο Remove supragingival plaque and stain: Use a '
Establish recaΙl interval
rubber οup and fine paste. Beware of heat buildup'as
Proper maintenance is the key to implant surviνal. While the
the titanium implant will conduct heat to the inte-
prinlipμs ire the same as with natural teeth, care must be
;
grated osseous surface'
taken to use instruments that are both effective and safe for
. Clean superstructure
the implant surface'
112

115. ;
APPENDIX TABLΕ oF coNτENTS
Medical Considerations in the Periodontal Patient " 114
Calcium Channel Blockers and Gingival Hyperplasia
. '.
. . .. " 115
Dental Drug lnteractions: Update on Drug Combinations Requiring Special Considerations ........... 116
occupational Exposure to Bιoodborne Pathogens (Universal Precautions). . . . '
121
Predominant Cultivable Microorganisms of the Oral Cavity ' "
124
Reference Values for Adults '. " " 125
DentifriceProducts " "128
Oral Rinse Products. ... " " 133
PrescriptionWriting " '134
Abbreviations Commonly Used in Medical Orders ..
' '.. " ' 1U
SafeWritingPractices.
.......'.136
lnsurance Coding for the Periodontal Patient
r Selected Readings - General. "' " "
141
SelectedReadings-Specific. " " ""142
:
1

116. Ξ
AΡPEΝDlx
MEDICAL CONSIDERATIONS IN THE PERIODONTAL PATIENT
American Society of Anesthesiologists (ASA)
Physical Status Classification System
The Αmerican Society of Anesthesiologists has developed a
patient classification system to categorize surgery patients
based on their medical condition. General precautions are
presented based on these medical findings.
ASA Class l: Class I patients are normal, healthy
nonsmokers who are not under the care of a physician
and do not take prescribed medications. Medical consul-
tations are not required before surgery and there is no
need to modify the surgical plan because of medical
concerns.
ASA Class ll: Class ll patients have mild systemic
dΙsease, are Class l patients νvith some dental anxiety'
and are generally older than Class I patients. Controlled
systemic diseases include diabetes, seizure disorders, or
hypertension. Pregnant patients are also categorized as
Class ll. Such patients have medical conditions that
either require alterations in patient management during
surgery (eg, SBE antibiotic prophylaxis is necessary), or
they may have lifestyle conditions that potentially could
affect the outcome of periodontaΙ surgery (eg' smoking,
stress, or alcohol consumption). A consultation with the
patient's physician is recommended with Class ll
patients.
ASA Class lll: Class lll patients require a medical
consultation and recommendations from a physician
before any periodontal surgery. Patients in this category
have serious, potentially life-threatening medical condi-
tions (eg, poorly controlled diabetes, epilepsy, hyperten-
sion, ischemic heart disease, or a recent myocardial
infarction). Their physiοal activity is limited, but patients
are not completely incapacitated. Elective surgical proce-
dures may not be in the best interest of these patients.
Commonly, health considerations in Class lll patients
require that the procedure be modified (eg, shorter dura-
tion, no vasoconstrictors in the local anesthetic, or stress
management).
ASA Class lV: Class lV patients have major, life-threat-
ening health conditions (eg, severe cardiovascular
disease, uncontrolled diabetes or hypertension, unstable
angina pectoris, or unstable seizure disorders). Their
physical activity is extremely limited. Any elective perio-
dontal surgery is contraindicated and emergency surgery
should only be performed in a hospital environment
where medical life support systems are readily available.
ASA Class V: Class V patients are moribund and are not
surgical candidates. These patients are hospitalized and
usually in the end-stages of disease. Any periodontal
procedures rendered to Class V patients should be
limited to procedures to οontrol infection and relieve pain.

117. CALCIUM CHANNEL BLOCKERS AND GINGIVAL HYPERPLASIA
Druq FDA Aooroval Cases Cited in Liteiature
Amlodioine (NorvascΘ) 1 992 3
BeDridil (Vascοr@) 1 993 0
Diltiazem (cardizemΘ, DiιacorΦ) 1 982 >20
Felodioine (PlendilΘ) 1 992
lsradioine (DvnacircΦ) 1 991
Nicardiοine (cardene@) 1989 0
Nifedioine (Adalat@. ProcardiaΘ) 1942 >120
Nimodipine (NιmotopΘ) r989 0
Nisoldipine (Sulaρ) I 99s ο
l.linincl fBavnress@\ 1
VeraoamΙl (calan@. lSootinΘ, verelan@) 1 982 7
lNot
yet approved for use in the United States.
SOME GENERAL OBSERVATIONS OF CCB-INDUCED GH
Calcium channel blockers (CCBs) are νveΙl known to cause control subjects Were inοluded. lt νvas found that 6.3% of
gingival enlargement. ln the early 199Os, it was thought that subjects taking nifedipine \Λ/ere seen to have significant over-
tniJctass of drugs caused a true hyperplasia of the gingiva. gro\Mth, which was significantly greater than the overgrowth
Current thinking is that the term "hyperplasia" is inappropriate seen with the other two drug groups or the control group. The
since the drug-induced effect results in an increase in extra-
prevalence of gingival overgrou/th induced by amlodipine or
cellular tissue volume rather than an increase in the number
diltiazem νvas not significantly different compared to the
of οells.l Most of the reported cases of CCB-induced gingival
c9n]19] sΨue Τhis study concluded that the prevalence of
enlargement have involved patients >50 years of age"taiing
significant gingival overgrowth related to CCBs was low'
ccBs for postmyocardiat infarction syndrome,
"ngin"
;rir, l'jil iil".t
were 3 times as likelv as females to develop
essential hypertension, and Raynaud's syndrome. iiii"αipi"J
significant overgro\Λ/th'
(Procardia@) is associated with the highest
"'TP9Ι :] ln a second study by Jorgensen,g a large group of patients
reported cases in the literature, followed by diltiazem
irκinδirloαipinqwasstrδiedinordertodeterminetheprev-
(Cardizemo).2 Depending on the CCB in question, gingival
,δnJ" ot, what he called,
,,gingival
hyperplasia,,. out oi lso
enlargement has appeared any time betνveen 1-24 months
dentate patients who volunteered to undergo a screening
after daily dosing. Discontinuance of the CCB usually results
examinaiion, mild hyperplasia was found in 5 patients (9.3%).
in compιete disappearance or marked regression of symp- This was significantiy less than rates reported for patients
toms, with symptoms reappearing upon remedication. The taking nifedipine and not significantly different from rates
time required after drug discontinuance for marked regres- reported in control groups of cardiac patients not taking
sion of enlargement has been 1 week. Complete disappear- CCBs. Jorgensen concluded that amlodipine, at a dose of 5
ance of all symptoms usually takes 2 months. lf gingivectomy mg daily, did not induce gingival hyperplasia.
is peι{ormed and the drug retained or resumed, the gingival
enlargement can recur. Only when the CCB is discontinued There have been reports of verapamil-induced gingival
or a switch to a non-CCB occurs, will the gingivectomy enlargement in the literature with at least 7 cases listed in the
usually be successful. one study of Nishikawa
"t
ai. snoreδ review by this author.2 The prevaΙence of verapamil-induced
that if nifedipine could not be discontinued, gingivaΙ enlarge-
enlargement, however' has not been investigated.
ment did not recur after gingivectomy when extensive plaque
control \ivas carried out. lf the CCB is changed to another
class of cardiovascular drug, the enlargement will probably Footnotes
regress and disappear. A switch to another CCB, however,
will probably result in οontinued gingival enlargement. For 1. Desai P and Silver J_G, "Drug-lnduοed Gingival Enlargements," J can Dent ASSΦ,
example, Giustiniani et al,a reportei disappearance of symp-
199Θ' 64(4):263-8'
toms within 15 days after discontinuance of verapamil, with 2. !νynn FlL, "Update on calcium channel Blocker-lnduced Gingival Ηyperplasia,''
recurrence of symptoms after resumption with diltiazem. One
Gen Dent' 1995' 43(3\:218'20' 222'
case report described a nonsurgical management of a patient
3. Nishikawa s, Τada H, Hamasaki A, et al,
,.Nifedipine-lnduced
Gingival Hypetr
presenting with nifedipine-induced gingival overgrowth.' plasia: Α clinical and ιn Vitro sιυdy,'' J Periodonfol, 1991, 62(1):30-5.
Establishment and maintenance of a considerably improved
standard of plaque control led to οomplete resolution of the '
u'BτHilbfiλ::,l"iι"J',l.i?,''''?'f,"!b!;il'o,ξ'Τ,'!?,$,'r;?Ιt'Φ'"'ic Gingivitis
overgro\ivth without recurrence, even though the medication
dosgwas inοreased. The reader is referred to the review of
5 οianttr
lJ,;"i+i""',:i,!,:;';3χ:i'ir:i::l'rxr};{.iow1h:.Remission
Following
1 99 t6 for descriptive clinical and histological f indings of CCB-
induced gingival enlargement. Α more recent review has 6.\Λ/ynn.RL,'calciumchannel BlockersandGingival Hyperplasia,''GenDent,1991,
been author2ed by Silverstein et al, and published in 1997.7
3e(4):240-3'
τνvo reports described the prevalence of amlodipine
(Norvasc@)-induced gingival overgro\Λ/th. The study by EΙlis et
al,8 examined a sample of patients taking 1 of 3 CCBs who
were drawn from a community-based population in north-
eastern England. out of 911 patients, 442ν'tere taking nifedi-
pine, 181 amlodipine, and 186 diltiazem. ln addition, 102
7. Silverstein LH, Garnick JJ, Szikman M, et al, "Medication-lnduced Gingival
Enlargement: A Clinical Review," Gen Dent, 1997, 45(4):371 -6.
8. Ellis Js, Seymour RA, Steele JG, et al, "Prevalenοe oΙ Gingival overgroMh
lnduced by Calcium Channel Blockers: A Community-Based Study," J Peri
odontol, 1999, 70(1):63-7.
9. Jorgensen MG, "Prevalence of Amlodipine-Related Gingival Hyperplasia, J Perι
odontol, 1997, 68(7):676-8.
Ξ

118. APPENDIX
DENTAL DRUG INTERACTIONS: UPDATE ON DRUG COMBINATIONS
REQUIRING SPECTAL CONSIDERATIONS
This update disοussion includes 16 drug interaction mono-
graphs describing clinically important drug combinations
requiring special considerations in dental praοtice. The
actions which have resulted from these combinations range
from life-threatening adverse effects to attenuation of the
therapeutic effects of the interacting drug. The monographs
are organized acοording to the four major groups of drugs
used in dentistry: Antibiotics, nonsteroidal anti-inflammatory
drugs (including aspirin), epinephrine (vasoconstrictors), and
narcotic analgesics. Αn additional monograph on Valiumo
and alcohol is included.
ANτIBloTlcs
_ oRAL coNTRAcEPTIvEs
Description of the lnteraction
Case reports suggest that antibiotics used in dentistry can
reduce the effectiveness of oral contraceptives resulting in
breakthrough ovulation and unplanned pregnancies.
Mechanism
Εstrogens, which are components of oral contraceptives, are
activated in the intestine by bacteria and reabsorbed into the
blood stream as active compounds to inhibit ovulation. Αntibi-
otics reduce the bacteria population in the intestine, which
may result in less activated estrogen available to inhibit
ovulation.
Background Reports
Tetracyclines: one report described a \Λ/oman on an
estrogen-type oral contraceptive who became pregnant after
a S-day course of tetracycline.1 Αlso, several cases of unin-
tended pregnancy and menstrual irregularities have been
reported following concurrent use of tetracyclines and oral
contraceptives.2'3
Penicillins: Ampicillin has been shoνvn to reduce estrogen
levels in νvomen not taking oral contraceptives and there are
reports of unplanned pregnancies in women taking ampicillin
with oral contraceptives.a's Concomitant use of penicillin with
estrogen-containing oral οontraceptives decreased the effi-
cacy of the contraceptive and increased the incidence of
breakthrough bleeding.6,7 Since amoxicillin is closely related
to other penicillins, it may also interact with oral contracep-
tives.
Cephalosporins: Cephalexin (Keflexo) has been reported to
interact with oral contraceptives resulting in an unplanned
pregnancy.s
Erythromycins: Unlike ampicillin and tetracyclines, erythro-
mycins have been implicated in only a few cases of oral
contraceptive failure over the last 15 years and it is question-
able whether erythromycin was the cause of those reported
failures.
Management
lf antibiotics are prescribed to oral contraceptive users, it is
suggested that the patients be advised to use additional
methods of birth control during both 7- to 1O-day dosing, and
the two-dose prophylaxis regimens. Any additional method of
birth control should be continued through the remaining oral
contraceptive cycle.
1. Bacon JF and Shenfield GM, "Pregnancy Αttributable to lnteraction Between
Tetracycline and oral contraceptiνes,'' Br Med J,1980' 280(6210):293.
2- orme ML, 'τhe cliniοal Pharmacology of oral contraceptive stθroids," Br J
cιin PharmacoΙ, 1982' 14'.31.
3. Back DJ, Grimmer SF, orme ML, et aι, "Evaluation of οommittee on safety of
Medicines Yellow card Reρorts on oral contraceptive-Drug lnteraοtions
\,νith Αnticonvulsants and Antibiotics,'' Br J clin Pharmacol' 1988'
25(5):527-32.
4. Trybuchowski H, "Effect ot Αmpicillin on the Urinary output of steroidal
Hormones in Pregnant and Nonpregnant ννomen,'' clin chim Acta, 1973'
45:9-18.
5. Αldercreutz H, Martin F, Lehtinen τ, et al, "Effect of Amρicillin Administration on
Plasma conjugated and Unconjugated Εstrogen and Progesterone
Levels in Pregnancy,'' Am J obstet Gynecoι,1977,128(3\|266'71.
6. Proudfit c\Λ/, "concurrent oraI contraceptive and Antibiotic τherapy''' JAMA'
1981, 246t2076.
7. True RJ, "lnteractions Between Antibiotics and oral contraceptives," J/MΑ,
1982, 247(1O)t14Oa.
8. Bainton R, "lnteraction Between Antibiotic τherapy and contraceρtive Medica-
lion,'' olal Surg oraι Med oraΙ Pathol, 1986, 61(5):453-5.
TETRACYCLINES - ANTACIDS (Containing
Divalent or τrivaIent Ions)
Description of the lnteraction
Concomitant therapy with a tetracycline and an antacid
containing aluminum, calcium, or magnesium can reduce
Serum concentration and the efficacy of the tetraοycline.
Mechanism
Aluminum, calcium, and magnesium ions can combine with
the tetracycline molecule in the gastrointestinal tract to form a
larger ionized molecule unable to be absorbed into the blood
stream.
Background
τhe interaction between tetracyclines and antacids
containing aluminum, calcium, and magnesium is well docu-
mented. Foods and dairy products containing calcium \Λ/ill
also impair the absorption of tetracyclines. Some reports
suggest that doxycycline and minocycline are minimally
affected by antacids and dairy products.l'2
Management
Tetracyclines should be given as far apart as possible from
antacids and dairy products.
1. \Λ/elling PG, Koch PΑ, Lau cc' et al, "Bioavailability of Tetracycline and Doxy-
cycline in Fasted and NonΙasted subjects,'' Antimicrob Agents
chΘmothe r, 1 97 7' 1 1 (3):462-9.
2. 'Anti-lnfective Drug lnteractions," Drug ιnteractions and υpdates, Hansten PD
and Horn JR, eds, Malvern, PA: Lea and Febiger.
TETRACYCLINE - PENICILLIN
Description of the lnteraction
Simultaneous tetracycline-penicillin therapy may impair the
efficacy of penicillin.
Mechanism
Penicillin kills bacteria by inhibiting cell wall synthesis. Tetra-
cycline inhibits protein synthesis in bacteria and this action
has been sho\Λ/n to antagonize the cell \ΙvaΙl inhibiting the
effect of penicillin.
Background
Most of the manufacturers' product information contains
warnings against using tetracyclines and penicillins together.
116

119. APPENDIX
Management
Tetracycline-penicilΙin combination should never be used to
treat oral infections. For penicillin t\η/o-dose prophylaxis' it
would be prudent not to give to patients taking tetracycline.
Reappoint if possibΙe.
ΕRYTHRoMYCIN - PENIcILLIN
Description of the lnteraction
Simultaneous erythromycin-penicillin therapy may impair the
efficacy of penicillin.
Mechanism
Penicillin kills bacteria by inhibiting cell wall synthesis. Eryth-
romycin inhibits protein synthesis in bacteria and this action
may antagonize the cell wall inhibiting the effect of penicillin.
Background
τhis interaction has not been sufficiently documented in clin-
ical studies.
Management
Erythromycin-penicillin combination should not be used to
treat oral infeοtions. For penicillin two-dose prophylaxis, it
would be prudent not to give to patients taking erythromycin.
Reappoint if possible.
ERYτHRoMYCIN - τHEoPΗYLL|NE
Description of the lnteraction
Erythromycins interact ιΛ/ith theophylline' a bronchodilator, to
result in symptoms suggestive of a relative overdose of theo-
phylline. Resulting symptoms \ivere nausea, vomiting, and
seizures.
Mechanism
A recent study showed that erythromycin forms οomplexes
with a specific enzyme that metabolizes theophylline and that
this complex may explain the impairment of theophylΙine
metabolic inactivation resulting in symptoms of theophylline
overdose.l
Background
An erythromycin regimen of 5- to 20-day daily dosing in theo-
phylline patients caused increased blood leveΙs, a longer half-
life, and decreased urinary clearance of the theophylline.2 A
more reοent review indicated that many patients did not
experience any interactions betνveen the t\Λ/o drugs with 8 out
of 22 studies reporting no change in theophylΙine kinetics
after erythromycin dosing.3 The interactions which have
occurred have included all formulations of erythromycin.
There have been no reported interactions between erythro-
mycin and theophylline when using the prophylaxis dosing
schedule.
Management
Patients taking theophylline and who may be at increased
risk for theophylline toxicity should be given erythromycin
νvith caution and on|y if there is absolutely no alternative to
erythromycin. τhese patients should be monitored closely.
1.Delaforge M and Sartori Ε, "ln Vivo Effects oΙ Erythromycin, oleandomycin,
and EΦhralosamine Deriνatives on Hepatic ομochrome P-50,'' Biochem
Phamacol, 1990, 40(2):223-8.
cummins LH, et al, "ΕMhromycin's Effect on τheophylIine Bιood Levels.
Correspondence," Pediatrics, 1977, 59i1 44-5.
Ludden TM, "Pharmacokinetic lnteractions of the Macrolide Antibiotics," C/n
Pharmacokιnet' 1 985' 10(1 ):63-79.
ERYTΗROMYOIN - OARBAMAZEPINE (TegretoIo)
Description of the lnteraction
Erythromycin has interacted with carbamazepine (Tegretolo),
an antiepileptic, to cause increased blood Ιevels resulting in
carbamazepine toxicity.l Symptoms were drowsiness, dizzi-
ness, nausea, headache, and blurred vision.
Mechanism
Τhis interaction is suggestive of an inhibition of the hepatic
metaboΙizing enzymes by erythromycin which normally
convert carbamazepine to inactive products.
Background
The increased blood levels of carbamazepine have occurred
within 1 day of concomitant erythromycin therapy.l This effect
has not been reported with the t\Λ,o-dose erythromycin,
prophylaxis regimen.
Management
Patients taking carbamazepine and who may be at increased
risk for carbamazepine toxicity should be given erythromycin
with caution and only if there is absolutely no alternative to
erythromycin. These patients should be monitored closely.
1. Ludden TM, "Pharmacokinetic lnteractions oΙ the Macrolide Antibiotics," c/ln
Phamacokinet, 1985, 10(1):63.
ERYTHROMYOIN - TRIAZOLAM (Ηalciono)
Description of the lnteraοtion
Erythromycin has interacted with triazolam (Halciono), a
hypnotic type antianxiety agent, to cause increased blood
levels resulting in triazolam toxicity. Resulting effects were
psychomotor impairment and memory dysfunction.
Mechanism
This interaction is suggestive of an inhibition of the hepatic
metabolizing enzymes by erythromycin which normally
convert triazolam to inactive products.
Background
Erythromycin has caused significant increases in triazolam
blood concentrations within 3 days after 333 mg erythromycin
base 3 times/day and triazolam 0.5 mg daily.l
Management
Patients taking triazolam should be given erythromycin with
caution and only if there is absolutely no alternative to eryth-
romycin. These patients should be closely monitored.
1. Philιips JP, 'Α Pharmacokinetic Drug lnteraction Between Erythromycin and
τriazolam," J cιin Psychopharmacol, 1986, 6(5):297-9-
2.
117
Ξ

120. APPEΝDlx
IBUPROFEN (Motrino, Advil@, Nuprino) - ORAL
ANτIOOAGULANTS (Coumarins)
Description of the lnteraction
Bleeding may ocοur when ibuprofen is administered to
patients taking coumarin-type anticoaguΙants.
Mechanism
lnhibition of prostaglandins by ibuprofen results in decreased
platelet aggregation and interference with blood clotting,
resuΙting in an enhancement of the anticoagulant effect of
coumarins.
Background
Product information on ibuprofen in the 1995 edition of the
Physicians' Desk Reference (PDR) states that Motrino
inhibits platelet aggregation, but the effeοt is quantitatively
less and of shorter duration than aspirin. lt goes on to state
that bleeding has been reported when Motrino \Λ/as adminis-
tered to patients on coumarin-type anticoagulants and the
clinician should use caution in these circumstances. Addi-
tional product information on naproxen, diflunisal, and flurbi-
profen is listed in the same edition of the PDR. lt advises
caution when using naproxen with coumarins since interac-
tions have been seen with other NSAIDS of this class; it
states that diflunisal, when given with warfarin, resulted in
prolongation of prothrombin time; and it states that serious
clinical bleeding has been reported in patients taking flurbi-
profen together \Λ/ith coumarins. Product information for
warfarin (Coumadino) in the 1995 PDR states that ibuprofen,
naproxen, and diflunisal may be responsible for increased
prothrombin time response of the ιλ,arfarin. Flurbiprofen was
not mentioned.
Management
It is suggested that ibuprofen (Motrino, Advilo, Nuprino) and
other dental NSAIDS such as naproxen (Naprosyno),
naproxen sodium (Anaproxo, Aleveo), diflunisal (Dolobido),
flurbiprofen (ANSAιDΘ), and ketorolac (Τoradolo oral), be
used νvith caution (if at all) in patients taking coumarin-type
anticoagulants. Use of other analgesics is preferred.
IBUPROFEN (Motrino, Advi]@, Nuprino) - LlτHIUM
Description of the ]nteΙaction
Concurrent administration of ibuprofen with lithium produces
symptoms of lithium toxicity including nausea, vomiting,
slurred speech, and mental confusion.
Mechanism
Prostaglandins stimulate renal lithium tubular secretion.
NSAIDS inhibit prostaglandin-induced renal secretion of
lithium, which increases lithium plasma levels and produces
symptoms of lithium toxicity.
Background
Lithium is used for the treatment of acute mania and to
prevent recurrent episodes of bipolar (manic-depressive)
illness. The therapeutic lithium plasma concentration is
extremely narrovv (0.8-1.2 mEq/L) and drugs that cause
lithium plasma levels to go outside this narrow therapeutiο
range will result in lithium toxicity. Of the four NSAIDS used in
dentistry (ibuprofen, naproxen, diflunisal, and flurbiprofen)
the former t\ivo have been well documented to interact \ivith
lithium. ln 1980, Ragheb et al, reported that a patient taking
2400 mg ibuprofen daily experienced nausea and drowsiness
while stabilized on lithium.1 τhe lithium plasma leveΙ
increased from 0.8-1.0 mEq/L. Subsequently, in a study of 11
healthy volunteers, Kristoff et al, observed that 400 mg of
ibuprofen 4 times/day combined with 450 mg of lithium
οarbonate every
'12
hours, increased lithium plasma levels
within several days.2 Decreased ability to concentrate, light-
headedness, and fatigue resulted from this interaction.
Ragheb reported that concomitant administration of lithium
and ibuprofen (1.8 g/day) in nine patients with bipolar- or
schizoid-type disorders resulted in significant increases
(average 34%) in lithium plasma concentrations as well as
decreases in lithium clearance.3 lndividual variations were
observed, with increases in lithium levels ranging from 12/o
to 66% within 6 days of concomitant administration of
ibuprofen. ln this study, tremors occurred in three patients as
a result of this interaction. Ragheb reported that patients
older than 50 years νvere more susceptible to lithium toxicity.
The 1993 edition of the Physician's Desk Reference (PDR)
(in the monograph for Motrino) warns that concomitant use of
ibuprofen and lithium citrate or carbonate may elevate lithium
plasma leveΙs and reduce renal lithium clearance.
ln a 1986 study by Ragheb and Powell, concomitant adminis-
tration of naproxen and lithium resulted in individual varia-
tions in plasma lithium Ιevels (from increases of 0% to 42"λ.a
ln that study, lithium renal clearance decreased in patients
who were taking daily doses of lithium (900 mg) and
naproxen (750 mg) for 6 days. The monograph for Naprosyno
in the 1993 PDR cautions that conοomitant use of naproxen
and lithium could increase lithium plasma concentrations.
lnteractions bet\Λ/een difIunisal (DoΙobido1 and lithium, and
flurbiprofen (AnsaidΘ) and lithium have not been reported.
Nor is any potential interaction between these tνvo NSAIDS
and lithium mentioned in the PDR, lnterestingly, aspirin has
been shown to affect plasma lithium levels in healthy
subjects.s Lack of documentation about diflunisal and flurbi-
profen does not mean these agents are safe to use in
conjunction with lithium. NSA|Ds should be used \Λ/ith caution
by dental patients who are taking lithium. Substitution of
NSAIDS with acetaminophen preparations may be warranted.
Management
Extreme caution is necessary in administering NSAIDS to
lithium patients; use of analgesics other than NSAIDS is
preferred.
1. Ragheb M, Ban τA, Buchanan D, et ai, "lnteraction of lndomethacin and
lbuprofen \Λ/ith Lithium in Manic Patients Under a Steady-State Lithium
Leνel,'' J cιin Psychiatry, 1980, 41(1 1):397-8.
2_ Kristofi cA, Hayes PE, Barr \Λ/H, et al, "Effect of lbuprofen on Lithium Plasma
and Red Blood ceΙl concentrations,'' clin Pharm,1986' 5(1):51-5.
3. Ragheb M,'lbuρrofen can lncrease serum Lithium Level in Lithium-τreated
Patients," J C/n Psychiatry, 1 987, 48(4):161 -3.
4. Ragheb M and Powell AL' "Lithium lnteraction \Λ/ith sulindac and Naproxen,'' J
cιin Psychophamacol,'1986, 6(3):1 50-4.
5. Reimann l\Λ/, Diener U, and Frolich Jc, "lndomethacin But Not Αspirin
lncreases Plasma Lithium lon Levels," Arch Gen Psychiatry, 1983,
40(3):283-6.

121. APPENDIX
ASPIRIN - ORAL ANTICOAGULANTS (Coumarins)
Description of the lnteraction
Aspirin increases the risk of bleeding in patients taking oral
anticoagulants.
Mechanism
Small doses of aspirin inhibit platelet function. Larger doses
(>3 g/day) elicit a hypoprothrombinemic effect. Aspirin may
also displace oral anticoagulants from plasma protein-binding
sites. These actions of aspirin alΙ contribute to increase the
risk of bleeding in patients taking oral anticoagulants.
Background
There is much documentation in the literature confirming this
interaction. One study using over 500 patients showed that
exοessive bleeding \,vas about 3 times more common with
warfarin (Coumadino) plus aspirin (500 mg/day) than with
warfarin alone.1 Αnother study showed enhanced hypopro-
thrombinemia in warfarin patients during the first few days of
aspirin therapy (1 glday).2 There are other reports describing
bleeding episodes due to concurrent therapy with aspirin and
oral anticoagulants.3'a
Management
Patients receiving oral anticoagulants should avoid aspirin
and aspirin-containing products.
1. chesebro JH, Fuster v, Elveback LR, et al, "Τrial of combined Warfarin
Therapy Plus Dipyridamole or Aspirin τherapy in Prosthetic Heart Valve
Replacement: Danger of Aspirin compared ννith Dipyridamole," Αm J
cardioι, 1 983' 51 (9):1 537-41.
2. Donaldson DR, Sreeharan N, crow MJ, et al, "Assessment of the lnteraοtion of
Warfarin \Λ/ith Αspirin and Dipyridamole," τhromb Haemost, 1982,
47(1):77.
3. Starr KJ and Petrie JC, "Drug lnteractions in Patients on Long-Term Oral
Αnticoagulant and Antihypertensive Αdrenergic Neuron-Blocking Drugs,"
Br Med J,1972, 4(833):133-5.
4. Udall JA, "Drug lnterference \Λ/ith Warfarin τherapy,'' cιin Med' 1970' 77:20.
ASPIRIN - PROBENECID (Benemido)
Description of the lnteraction
Aspirin inhibits the uricosuric action of probenecid.
Mechanism
Unknown
Background
The inhibition of probenecid-induced uricosuria by aspirin is
dose-dependent. Doses of aspirin of 1 g or less do not
appear to affect probenecid uricosuria. Larger doses,
however, appear to considerably inhibit uricosuria.
Conversely, probenecid appears to inhibit uricosuria following
large doses of aspirin. Aspirin does not interfere with the
actions of probenecid to inhibit the renal elimination of peni-
cillins.
Management
It appears prudent to use a nonsalicylate-type analgesic (ie,
acetaminophen or NSAID) in patients receiving probenecid
as a uricosuriο agent (treatment of gouty arthritis).
EPlNEPHRINE (Vasoconstrictor) - τRIcYcLlc
ANτIDEPREssANTs
Description of the lnteraction
Use of epinephrine as a vasoconstrictor in local anesthetic
in.lections may cause a hypertensive interaction in patients
taking tricyclic antidepressants.
Mechanism
Τricyclic antidepressants cause increases of norepinephrine
in synaptic areas in the centra! nervous system and
periphery. Epinephrine may add to the effects of norepineph-
rine resulting in vasoconstriction and transient hypertension.
Background
There is adequate information in the literature to confirm a
hypertensive interaοtion between epinephrine, norepineph-
rine, and levonordefrin with TCΑs. An l'V' infusion of
epinephrine to healthy subjects reοeiving imipramine resulted
in two- to fourfold increases in the pressor response to
epinephrine.l,2 Also cardiac dysrhythmias M/ere reported.
Αlthough these effeοts \Λ/ere seen with l.V. infusions, these
reports suggested that caution should certainly be exercised
if epinephrine is administered by other routes. l.V. infusions
of norepinephrine to healthy subjects receiving imipramine
resulted in a four- to eightfold increase in the pressor
response to norepinephrine,l'2 and a later study showed a
twofold increase in pressor response to norepinephrine.3
other tricyclics were associated \Λ/ith a threefold increase in
pressor response to norepinephrine.4 This increased pressor
response was probably due to tricyclic antidepressant-
induced inhibition of norepinephrine reuptake. Similar effects
have been reported with levonordefrin.s
Management
The use of epinephrine in patients taking tricyclic type antide-
pressants is potentially dangerous. Use minimum amounts of
vasoconstrictor νvith caution in patients on tricyclic antide-
pressants.
1. Boakes AJ, Laurence DR, Teoh PC, et al, "lnteractions Between Sympathomi-
metic Amines and Αntidepressant Agents in Μan,'' Br Med J' 1973'
1 (849):31 1 -5.
2. Svedmyr N, "The lnfΙuenοe of a τricyclic Antidepressive Agent (Protriptyline) on
Some of thΘ circulatory Effects of Noradrenaline and Αdrenaline in Man,"
ιlfe sc,, 1968' 7(1):77-84.
3. Larochelle P, Hamθt P, and Enjalbert M, "Response to Tyramine and Norepi-
nephrine Αfter lmipramine and τrazodone,'' cιin Pharmacoι τher,1979,
26(1\:24-30.
4. Mitchell JR, cavanaugh JH, Arias L, et al, "Guanethidine and ReIated Αgents.
lll. Antagonism by Drugs μ/hich lnhibit the Norepinephrine PUmp in Man,''
J cιin ιnvest, 1970, 49(8):1596-604.
5. Jastak JT and Yagiela JΑ,'γasoconstrictors and Local Αnesthesia: Α Review
and Rationale tor υSe,'' J Am Dent Assoc,1983, 107(4):623-30.
EPINEPHRINE (Vasoconstrictor) - MONOAMINE
oxIDASE INHIB!τoRs
Description of the lnteraction
Use of epinephrine as a vasoconstriοtor in local anesthetic
injections may cause a hypertensive interaction in patients
taking monoamine oxidase inhibitors.
Mechanism
Drugs which inhibit monoamine oxidase cause increases in
the concentration of endogenous norepinephrine, serotonin,
and dopamine in storage sites throughout the central nervous
system. Epinephrine may add to the effects of norepinephrine
resulting in vasoconstriction and transient hypertension.
-

122. APPENDIX
Background
One study reported on four healthy subjects taking MAOIs
and given l.V. epinephrine. There \Λ,as no significant effect on
heart rate or blood pressure.1 τhis same Study also Sho\Λ/ed a
lack of interaction with norepinephrine and MAOls. Never-
theless, it is advisable that vasoconstrictors be used with
caution in these patients. Hansten and Horn2 report that
MΑols may slightly increase the pressor response to norepi-
nephrine and epinephrine, an action \Ιvhich appeared to be
due to receptor sensitivity by the MAOI.
Management
There is a potential for unexpected increases in blood pres-
sure when using epinephrine vasoconstrictor in patients
taking monoamine oxidase inhibitors. Use vasoconstrictor
with caution in these patients.
1. Boakes ΑJ, Laurence DR, Teoh Pc, et al, "lnteraοtions Between symρathomi-
metic Amines and Αntidepressant Agents in Μan,'' Br Med J, 1973'
1 (849):31 1 -5.
2. Ηansten PD and Ηorn JFi, eds, "Monoamine oxidase lnhibitor lnteractions,"
Drug lnteractions and υpdates, Malvern, PA: Lea and Febiger, 1 990, 387-
8.
NARcoTIc ANALGEslcS - cIMETIDINΕ
(Tagameto)
Description of the lnteraction
Cimetidine may increase the adverse effects of narcotic anal-
gesics.
Mechanism
The hepatic metabolism of narcotic analgesics to inactive
products may be inhibited by cimetidine. The central nervous
system effects of narcotic analgesics and cimetidine may be
additive.
Background
One study reported that cimetidine, when given to patients
taking meperidine (Demerol@), reduced the rate of renal
excretion of the narcotic, resulting in increased sedation and
an increase in respiratory depression.l Additional studies
sho\Λ,ed that cimetidine may inhibit the liver metabolism of
meperidine and fentanyl, another narοotic analgesic, thus
exacerbating the sedative effects of both of these
narcotics.2'3
Management
Αlthough the side effects of cimetidine on codeine, hydroco-
done, and oxycodone are unkno\Λ,n, it iS advised to use
caution in prescribing these narcotic analgesics in dental
patients taking cimetidine. Ranitidine (Zantaco) is probably
less likely to interact with narcotic analgesics.
1. Guay DR, Meatherall Rο, chalmers JL, et al, "cimetidine Αlters Pethidine
Disposition in Μan,'' Br J clin Pharmacol, 1984, 18(6):907-14.
2. Knodell RG, Holtzman JL, Crankshaw DL, et al, "Drug Metabolism by Rat and
Human Hepatic Microsomes
jn
Responsθ to lnteraοtion \Λ/ith H2-Reοeptor
Antagonists," Gastroenterology, 1982, 82(1):84-8.
3. Lee HR, et al, "Effect of Histamine H2-Fleceρtors on Fentanyl Metabolism,"
P h arm acologist, 1982, 24:1 45 -
BΕNzoDlAzEPlNEs
_ Diazepam (VaIiumo1 -
ALCOHOL
Description of the lnteraction
Αlcohol may enhance the adverse psychomotor effects of
benzodiazepines such as Valium@. Combined use may result
in dangerous inebriation, ataxia, and respiratory depression.
Mechanism
Αlcohol and benzodiazepines have additive central nervous
system depressant activity. AΙso, alοohol may inοrease the
gastrointestinal absorption of diazepaml,2 leading to symp-
toms of diazepam overdose.
Background
There is much documentation in the literature to confirm the
serious interaction bet\Λ/een alcohol and benzodiazepines.
Many controlled studies have shown that benzodiazepines,
suοh as diazepam, enhance the detrimental effects of alcohol
on simulated driving, reaction times, and other psychomotor
skills.3-6
Management
Patients receiving benzodiazepines, such as diazepam
(ValiumΘ), should be warned against consuming any alcohol
until the benzodiazepine is cleared from the body. This is
usually 48-72 hours after the last dose. This interaction has
been unpredictable and significant CNS depression and
ataxia have occurred with only a single dose of diazepam (5
mg) along with a moderate amount of alcohol.
1. Hayes SL, Pablo G, Radomski Τ, et al, "Εthanol and oral Diazepam Absorp-
lion," N Εngι J Med,1977, 296(4)-186-9.
2. Macleod sM, Giles HG, Parzalek G, et al, "Diazeρam Actions and Plasma
concenιrations Following Ethanol lngestion," Εur J cιin Phamacoι,1977,
1 1 (5):345-9.
3. Linnoila M and Hakkinen s, "Effects of Diazepam and οodeine, Alone and in
combination \Λ/ith Alcohol, on Simulated Driνing,'' clin Pharmacol τher,
1974,15(4):368-73.
4. Linnoila M, "Εffects of Diuepam, chlordiαepoxide, Thioriduine, Haloperidol,
Fluρenthixole, and Alcohol on Psychomotor SkillS Related to Driνing,'' Ann
Med Εxp Bioι Fenn' 1973, 51(3):125-32.
5. Linnoila M, "Drug lnteraction on Psychomotor Skills Fielated to Driving: Diaz-
epam and Alcohol,'' Εur J cιιn Pharmacoι,1973, 5:186.
6. Morland J, setekleiv J, Haffner JF, et al, "οombined Εffects of Diazepam and
Ethanol on Psychomotor Funοtions,'' Acta Pharmacoι τoxicoι, 1975'
34(1 ):5-1 5.

123. APPENDIX
OCCUPATIONAL EXPOSURE TO BLOODBORNE PATHOGENS
(uNrvERsAL PRECAUTIONS)
ovERvIEι'v AND REGULAτoRY
CONSIDERATIONS
Every healthοare employee, from nurse to housekeeper, has
some (albeit small) risk of exposure to HIV and other viral
agents such as hepatitis B and Jakob-Creutzfeldt agent. The
incidence of ΗlV-1 transmission associated \ivith a percuta-
neous exposure to blood from an HIV-1 infected patient is
approximately o.3"λ per exposure.1 ln 1989, it was estimated
that 12,000 United States healthcare workers acquired hepa-
titis B annually.2 An understanding of the appropriate proce-
dures, responsibilities, and risks inherent in the collection
and handling of patient specimens is necessary for safe prac-
tice and is required by Occupational Safety and Health
Administration (OSHA) regulations.
The occupational Safety and Health Αdministration
published its "Final Rule on Occupational Exposure to Blood-
borne Pathogens" in the Federal Register on December 6,
1991. OSHA has chosen to follow the Center for Disease
Control (CDC) definition of universal precautions. The Final
Rule provides full legal forοe to universal preοautions and
requires employers and employees to treat blood and certain
body fluids as if they were infectious. The Final Rule
mandates that hea|thcare workers must avoid parenteraι
contact and must avoid splattering blood or other potentially
infectious material on their skin, hair, eyes, mouth, mucous
membranes, or on their personal οlothing. Hazard abatement
strategies must be used to protect the workers. Such plans
typically include, but are not limited to, the following:
. safe handling of sharp items ("sharps") and disposal of
such into puncture-resistant containers
. gloves required for employees handling items soiled with
blood or equipment contaminated by blood or other body
fluids
o provisions of protective οlothing when more extensive
contact with blood or body fluids may be anticipated (eg,
surgery, autopsy, or deliveries)
. resuscitation equipment to reduce necessity for mouth to
mouth resuscitation
ο restriction of HlV- or hepatitis B-exposed employees to
noninvasive procedures
oSHΑ has specifically defined the following terms: occupa-
tional exposure means reasonably anticipated skin, eye
mucous membrane, or parenteral contact with blood or other
potentially infectious materials that may result from the
performance of an employee's duties. Other potentially
infectious materials are human body fluids including
semen, vaginal seοretions, cerebrospinal fluid, synovial fluid'
pleural fluid, pericardial fluid, peritoneal fluid, amniotic fluid,
saliva in dental procedures, and body fluids that are visibly
contaminated with blood, and all body fluids in situations
where it is difficult or impossible to differentiate between body
fluids; any unfixed tissue or organ (other than intact skin)
from a human (living or dead); and HIV-containing cell or
tissue cultures, organ cultures, and HIV- or HBV-containing
culture medium or other solutions, and blood, organs, or
other tissues from experimental animals infected with HIV or
ΗBV. Αn exposure incident involves specific eye, mouth,
other mucous membrane, nonintact skin, or parenteral
contact with blood or other potentially infectious materials
that results from the performance of an employee's duties.3 lt
is important to understand that some exposures may go
unrecognized despite the strictest precautions.
A written Exposure Control Plan is required. Εmployers must
provide copies of the plan to employees and to OSHA upon
request. CompΙiance with oSHΑ rules may be accomplished
by the following methods.
ο Universal precautions (UPs) means that all human
blood and certain body fluids are treated as if known to
be infectious for ΗlV, HBV, and other bloodborne patho-
gens. UPs do not apply to feces, nasal secretions, saliva,
sputum, s\iveat, tears, urine, or vomitus unless they
contain visible blood.
. Engineering controls (ECs) are physical devices which
reduce or remove hazards from the workplace by elimi-
nating or minimizing hazards or by isolating the νvorker
from exposure. Engineering control deviοes include
sharps disposal containers, self-resheathing syringes,
etc.
o Work practice controls (ιlvPCs) are practices and
procedures that reduce the likelihood of exposure to
hazards by altering the way in which a task is performed.
Specific examples are the prohibition of two-handed
recapping of needles, prohibition of storing food along-
side potentially contaminated material, discouragement
of pipetting fluids by mouth, encouraging handwashing
after removal of gloves, safe handling of contaminated
sharps, and appropriate use of sharps containers.
. Personal protective equipment (PPE) is specialized
clothing or equipment worn to provide protection from
occupational exposure. PPE includes gloves, gowns,
laboratory coats (the type and characteristics will depend
upon the task and degree of exposure anticipated), face
shields or masks, and eye protection. Surgical caps or
hoods and/or shoe covers or boots are required in
instances in which gross contamination can reasonably
be anticipated (eg, autopsies, orthopedic surgery). lf PPE
is penetrated by blood or any contaminated material, the
item must be removed immediately or as soon as
feasible. The employer must provide and launder or
dispose of all PPE at no cost to the employee. Gloves
must be worn when there is a reasonable anticipation of
hand contact with potentially infectious material, including
a patient's mucous membranes or nonintact skin. Dispos-
able gloves must be changed as soon as possible after
they become torn or punctured. Hands must be washed
after gloves are removed. OSHA has revised the PPE
standards, effective July 5, 1994, to include the require-
ment that thΘ employer ceι1ify in writing that it has
conducted a hazard assessment of the workplace to
determine whether hazards are present that will necessi-
tate the use of PPE. Also, verification that the employee
has received and understood the PPE training is
required.a
Housekeeping protocols: oSΗΑ requires that alΙ bins,
cans, and similar receptacles, intended for reuse which have
a reasonabΙe likelihood for becoming contaminated, be
inspected and decontaminated immediately or as soon as
feasible upon visible contamination and on a regularly sched-
uled basis. Broken glass that may be contaminated must not
be picked up directly with the hands. Mechanical means (eg,
brush, dust pan, tongs, or forceps) must be used. Broken
glass must be plaοed in a proper sharps container.
Employers are responsible for teaching appropriate clean-up
procedures for the work area and personal protective equip-
ment. A 1:10 dilution of household bleach is a popular and
effective disinfectant. lt is prudent for employers to maintain
signatures or initials of employees who have been properly
educated. lf one does not have written proof of education of
-

124. APPENDIX
occUPAτIoNAL ExPosURE τo BLooDBoRNE PAτHOGENS (UNIVERSAL PRECAUTIONS) (Continued)
universal precautions teaching, then by OSHA standards,
such education never happened.
Pre-exposure and postexposure protocols: oSHΑ's Final
Rule includes the provision that employees, who are exposed
to contamination, be offered the hepatitis B vaccine at no cost
to the employee. Employees may decline; however, a decli-
nation form must be signed.. τhe empΙoyee must be offered
free vaccine if he/she changes his/her mind. Vaccination to
prevent the transmission of hepatitis B in the healthοare
setting is widely regarded as sound practice.s ln the event of
exposure, a confidential medical evaluation and follow-up
must be offered at no cost to the employee. Follow-up must
include collection and testing of blood from the source indi-
vidual for HBV and HlV if permitted by state Ιaw if a blood
sample is available. lf a postexposure specimen must be
specially drawn, the individual's consent is usually required.
Some states may not require consent for testing of patient
blood after accidental exposure. One must refer to state and/
or local guidelines for proper guidance.
The employee follow-up must also include appropriate
postexposure prophylaxis, counseling, and evaluation of
reported illnesses. The employee has the right to decline
baseline blood collection and/or testing. lf the employee gives
consent for the collection but not the testing, the sample must
be preserved for 90 days in the event that the employee
changes his/her mind \η/ithin that time. Confidentiality related
to blood testing must be ensured. The employer does not
have the right to know the results of the testing of either
the source individual or the exposed employee.
MANAGEMENT OF OCCUPATIONAL EXPOSURE
To Htv lΝ THE \,lvoRKPLAcE6
.l
. Likelihood of transmission of HIV-1 from occupational
exposure is O.2o/" per parenteral exposure (eg, needle-
stick) to blood from HIV infected patients.
2. Factors that increase risk for occupationaΙ transmission
include advanced stages of ΗlV in source patient, hol|ow
bore needle puncture, a poor state of health,or inexperi-
ence of the healthcare worker (HCW).
3. lmmediate actions an exposed healthcare worker should
take include aggressive first aid at the puncture site (eg,
scrubbing site \λ/ith povidone-iodine solution for 10
minutes) or at mucus membrane site (eg, saline irrigation
of eye for 15 minutes). Then immediate reporting to the
hospital's occupational medical service. The authors indi-
cate that there is no direct evidence for the efficacy of
their recommendations. Other institutions suggest
rigorous scrubbing \ivith soap.
4. After first aid is initiated, the healthcare worker should
report exposure to a supervisor and to the institution's
occupational medical service for evaluation.
5. Occupational medicine should perform a thorough inves-
tigation including identifying the HIV and hepatitis B
status of the source, type of exposure, volume of inoc-
ulum, timing of exposure, extent of injury, appropriate-
ness of first aid, as well as psyοhologicaΙ status of the
healthcare worker. ΗlV serologies should be performed
on the healthcare worker. HIV risk counseling should
begin at this point.
6. All parenteral exposures should be treated equally until
they can be evaluated by the occupational medicine
service, who wilΙ then determine the actual risk of expo-
sure. Follow_up οounseling sessions may be necessary.
7. Although the data are not clear, antiviral prophylaxis may
be offered to healthcare workers who are parenterally or
mucous membrane exposed. lf used, antiretroviral
prophylaxis should be initiated within 1-2 hours aftΘr
exposure.
8. Counseling regarding risk of exposure, antiviral prophy-
laxis, plans for follow-up, exposure prevention, sexual
activity, and providing emotional support and response to
concerns are necessary to support the exposed health-
care worker. Follow-up should consist of periodic sero-
logic evaluation and blood chemistries and counts if
antiretroviral prophylaxis is initiated. Additional informa-
tion should be provided to healthcare workers who are
pregnant or planning to become pregnant.
HAzARDoUs coMMUNIcAτloN
Communiοation regarding the dangers of bloodborne infec-
tions through the use of labels, signs, information, and
education is required. Storage locations (eg, refrigerators and
freezers, \Λ/aste containers) that are used to store, dispose of,
transport, or ship blood or other potentially infectious mate-
rials require labels. The label background must be red or
bright orange with the biohazard design and the word
biohazard in a contrasting color. The Ιabel must be part of the
container or affixed to the container by permanent means.
Eduοation provided by a qualified and knowledgeable
instructor is mandated. The sessions for employees must
include:
. accessible copies of the regulation
. general epidemiology of bloodborne diseases
ο modes of bloodborne pathogen transmission
. an explanation of the exposure control plan and a means
to obtain copies of the written plan
. an explanation of the tasks and activities that may involve
exposure
. the use of exposure prevention methods and their limita-
tions (eg, engineering controls, work practices, personal
protective equipment)
. information on the types, proper use, location, removal,
handling, decontamination, and disposal of personal
protective equipment)
. an explanation of the basis for selection of personal
proteοtive equipment
ο information on the HBV vaccine, including information on
its effiοacy, safety, and method of administration and the
benefits of being vaccinated (ie, the employee must
understand that the vaccine and vaccination will be
offered free of charge)
. information on the appropriate actions to take and
persons to contaοt in an emergency involving exposure to
blood or other potentially infectious materials
. an explanation of the procedure to follow if an exposure
incident occurs, including the method of reporting the
incident
. information on the postexposure evaΙuation and follow-up
that the employer is required to provide for the employee
following an exposure incident
. an explanation of the signs, labels, and color coding
. an interactive question-and-answer period
RECORD KEEPING
The OSHA Final Rule requires that the employer maintain
both education and medical records. The medical records
must be kept confidential and be maintained for the duration
of employment plus 30 years. They must contain a copy of
the employee's HBV vaccination status and postexposure
incident information. Education records must be maintained
for 3 years from the date the program was given.

125. APPEΝDlx
OSHA has the authority to conduct inspections ι/vithout
notice. Penalties for cited violation may be assessed as
follows.
Serious violations. ln this situation, there is a
substantial probability of death or serious physical
harm, and the employer kneνv, or should have known,
of the hazard. A violation of this type carries a
mandatory penalty of up to $7000 for each violation.
Other-than-serious violations. The violation is unlikely
to result in death or serious physical harm. Τhis type of
violation carries a discretionary penalty of up to $7000 for
each violation.
Willful violations. These are violations committed know-
ingly or intentionally by the employer and have penalties
of up to $70,000 per violation with a minimum of $5000
per violation. lf an employee dies as a result of a wiΙlful
violation, the responsible party, if convicted, may receive
a personal fine of up to $250,000 and/or a 6-month iail
term. Α corporation may be fined $500,000.
Large fines frequently follow visits to laboratories, physicians'
offices, and healthcare facilities by OSHA Compliance Safety
and Health Offices (CSHOS). Regulations are vigorously
enforced. Α working knowledge of the final rule and imple-
mentation of appropriate policies and practices is imperative
for all those involved in the collection and analysis of medical
specimens.
Effectiveness of universal precautions in averting exposure to
potentially infectious materials has been documented.T
Compliance with appropriate rules, procedures, and policies,
including reporting exposure incidents, is a matter of personal
professionalism and prudent self-preservation.
Footnotes
1. Henderson DK, Fahey BJ, Willy M, et al, "Risk Ιor occupational τransmission of
Human lmmunodeficiency Virus Tyρe 1 (HlV-1) Associated \Λ/ith cliniοal Expo-
sures. A Prospective ΕValuation," Ann ιntern Med' 1990' 113(10):740-6.
2. Niu MT and Margolis Ηs, "Moving lnto a New Era of Government Regulation:
Provisions Ιor Heρatitis B Vaccine in the Workplace, cιin Lab Manage Rev,
1 989, 3:336-40.
3. Bruning LM, τhe Bloodborne Pathogens Final Rule
-
Understanding the Regula-
Ιion,'' AoRN Journaι' 1993' 57(2':439-40-
4. "Rules and Regulations," Federal Register,1994, 59(66):16360-3.
5. sοhaffner W, Gardner P, and Gross PΑ, "Hepatitis B lmmunization strategies:
Εxρanding the Target," Ann ιntern Med, 1993, 1 18(4):308-9.
6. Fahey BJ, Beekmann SE, Schmitt JM, el al' "Managing occupalional Exρosures
to HιV-1 in the Healthcare ννorkplace," ιnfect control HoSp Εpidemioι' 1993'
14(7):405-12.
7. \Λ/ong ES, stoιka JL, chinchil|i VM' et aι, iAre Universal Precautions Etfective in
Reducing the Number of Occupational Exposures Among Healthcare
ννorkers?'' JAMA' 199'l' 265(9):1 123-8.
References
Buehler J\Λ/ and Ward JW, 'Α New Definition for AlDs Surueillance,'' Ann ιntern Med'
1993, 1 18(5):390-2-
Brown Jμ/ and Blackwell H, "complying \Λ/ith the NeW oSHA Regs, Part
'1: Teaching
Your Staff About BiosaΙety," MLo' 1992' 24(4)24-8. Part 2: "saΙety Protocols
No Lab can lgnore,"
'1992,
24(5'|27-9. Part 3: "οompiling Employee safety
Records τhat \Λ/ill Satisfy oSHA," 1992, 24(6):45-8.
Department of Labor, occupationaI safety and HΘalth Administration, "occupational
Exposure to Bioodborne Pathogens; Final Rule (29 CFR Part 1910.1030),
'' Federaι Register' December 6,
'l99'1,
64004-182.
Gold J\Λ/, "Hlv-1 lnfection: Diagnosis and Management," Med clin North Am, 1992,
76(1
):1
-18.
"Hepatitis B Virus: A comprehensive Strategy for Eliminating τransmission in lhe
United states τhrough Universal childhood Vaccination," Recommendations of
the lmmunization Practices Advisory committee (Ac'P)' MMWR Morb Moιtaι
wkΙy Rep' 1991' 40(RR-13):1-25.
"Mortality Attributable to HlV lnfection/ΑlDs
-
United sΙates'', MMWH Morb Mor1aι
Wkly Rep, 1991, 40(3):41-4.
National Committee for Clinical Laboratory Standards, "Protection of Laboratory
\Λ/orkers From lnfectious Disease Transmitted by Blood' Body Fluids, and
Tissue,'' NccLS Document M29-T, Villanova, PΑ: NCCLS' 1989' 9(1).
"ΝosocomiaI Transmission of Hepatitis B Virus Αssociated \Λ/ith a sρring-Loaded
Fingerstick Device
-
california," MMWR Morb Mortaι wkιy Eeρ' 1990,
39(35):610-3.
Polish LB, Shapiro CN, Bauer F, et al, "Nosocomial Transmission of Hepatitis B Virus
Associated With the Use oΙ a spring-Loaded Fingerstick Deνice,'' N Εngl J
Med, 1 992, 326(1 1 t:721
-5.
"Recommendations for Preventing τransmission of Human lmmunodeficiency Virus
and Hepatitis B virus to Patienιs During Exposure-Prone lnvasive Procedures,"
MMWR Morb Mortal wkιy Reρ' 1991, 40(RR-8):1-9.
"Update: Acquired lmmunodefiοiency Syndrome
-
United Sιates," MMWR Morb
Mofial wkly Reρ, 1992' 41 (26):463-8.
"Update: τransmission of ΗlV lnfection During an lnvasive Dental Procedure
-
Florida,'' MMWR Morb Mortal wkιy Reρ' 1991' 40(2)j21-7' 33.
"Update: Universal Precautions Ιor Prevention oΙ Transmission of Human lmmuno-
deficiency virus, Hepatitis B Virus, and other Bloodborne Pathogens in Ηealth-
care settings,'' MMWR Morb Moltaι wkly Rep' '1988' 37(24):377-82' 387-8'
123

126. PREDOMINANT CULTIVABLE MICROORGANISMS
OF THE ORAL CAVITY
τvDe P]edominant Genus or Femiιv
Aerobic or Facultative
Gram'positive cocci Streptocφcus sp
S. mutaλs
3:."iδ*i'"
S. salivarius
Gram_positive rods Lactobaci!ιus sρ
Corynebacteium sp
Gram-negative cocci Moraxella sρ
Gram-negative rωs Εnterobacteiaceae sρ
Anaerobic
Gram-positive cocci Peptostreptococcussp
Gram-positive rods Actinomyces sρ
Eubacterium Sρ
Lactobaciιιus sp
Leptotrbhia sρ
Gram-negative cocci veiιlonelιa Sρ
Gram-negative rods Actinobaciιιus sρ
FusobacterΙum sρ
Prevoteιιa sρ
Porphyromonas sp
Bacteroides sp
cempyιobacter sρ
spirochetes τreρonemasρ
Fungi candidasρ
124

127. APPEΝDlx
REFERENCE VALUES FOR ADULTS
Automated chemistry (cHEMlsτRY A)
Values Remarks
SERUM PLASMA
Aοetone
Albumin
Alcohol, ethyl
Aldolase
Ammonia
Amylase
Bilirubin, direct
Bilirubin, total
Calcium
Calcium, ionized
chloridΘ
Cholesterol, total
HDL cholesterol
LDL cholesterol
co,
οreatine kinase (cK) isoenzymes
CK.BB
CK-MB (cardiac)
CK-MM (musle)
cκ-MB levels must be both >47o and
Creatine phosphokinase (CPK)
οreatinine
Ferritin
Folate
GGτ (gamma-glutamyltEnsρeρtidase)
male
female
GLDH
Glucose (2-h postprandial)
Glucosθ, fasting
Glucose, nonfasting (2-h postprandial)
Hemoglobin 41"
Hemoglobin, plasma free
Hemoglobin, total glyΦsylated (Hb A1)
lron
lron binding capacity, total (τlBc)
Lactic acid
Lactate dehydrogenase (LDH)
Lactate dehydrogΘnase (LDH) isoenzymes
LDt
LD,
LD"
LDn
LDu
10 lU/L to meet diagnostic critΘria for CK-MB positive result Φnsistent with myocardial injury
8-150 rU/L
ο.5-1.4 mαdL
13-300 nσmL
3.6-20 ng/dl
1 1-63 rU/L
8-35 rU/L
To be determined
Up to 140 mσdl
60-110 mσdl
60-140 mσdl
I
<2.5 mΦ10ο mL
4γ"-8"/.
65-150 mcg/dL
250-420 mcgldL
0.7-2.1 mΕq/L
56-194 rU/L
20%-340/"
29oλ-41o/"
150/"-250/"
10/"-120/"
10/"-150/"
Specimen to be placed on ice as soon as
ωllected
Fasted blood required _
normal γalue atfected
by dietary habiιs
τhis reference range is tor a general adult
ρopUlation
Fasted blood rθquired _
normal νaιue atfected
by dietary habits
LDLo calculated by Friewald formula... whiοh
has certain inaccuracies and is invalid at trig
levels >3o0 mσdl
specimen to be kept on iΦ and sent to lab as
soon as ρossible
Negative
3.2_5 ΦdL
Negative
1.2-7.6lυlL
20-70 mcg/dl
30-1 10 units,/L
0-0.3 mΦdL
0.1-1.2 mg/dL
8.6-10.3 mΦdl
2.24-2.46 mΕqlL
95-108 mEq/L
Ξ22o mΦdL
40-60 mσdl
65-170 mσdl
23-30 mEq/L
oγ"
oγ"-3'9o/"
960/-10οo/o
Flipρed LD]/LD, ratios (>1 may be consistent with myocardial iniury) particular|y when considered in combination with a reΦnt cK-MB positive result
Lipase
Magnesium
Osmolality
Phosphatase, alkaline
adults 25-60 y
adults 61 y or older
infancy-adolescence
Phosρhate, inorganic
Potassium
Prealbumin
Protein, total
SGoτ (Asτ)
SGPT (ΑLτ) (10-35)
Sodium
τransfeπn
τri9lycerides
Urea nitrogen (BUN)
Uric acid
male
female
lncreased by slight hemoιysis
lncreased by slight hemolysis
23-208 units/L
1.6-2.5 mσdl
289-308 mosm/kg
33-131 lU/L
5'1-153 tU/L
Values range up to 3-5 times higher than
adults
2.8-4'2 mΦdL
3.5-5.2 mEq/L
>15 mΦdl
6.5-7.9 ΦdL
<35 tU/L (20-48)
<35 tU/L
134-149 mΕΦL
>200 mΦdl
45-155 mg/dl
7-2O mg/dL
2.0-8.0 mσdl
2.O-7.5 mgldL
125
Fasted blood required
-

128. APPENDIX
REFERENOE vALUEs FoR ADULτS (Continued)
Automated chemistry (cHEMlsτRY A) (continued)
τest Values Remarks
CEREBROSPINAL FLUID
Glucose
Prolein
adults and children
newborn infants
on csF obtained by cisternai puncture: Aboυt 25 mg/dL
on οsF obtained by ventricular puncture: Αbout 10 mg/dl
Note: Bloody specimen gives erroneously high value due to contamination with blood proteins
URINE
50-70 mg/dl
15-45 mσdl
60-90 mg/dl
(24-hour spΦimen is rΘquired for all thes tests υnless spΦified)
Amylase
Αmylase, fluid (random 9mples)
οalciUm
Creatine
male
lemale
Creatinine
Creatinine clearance (endogenous)
male
female
Glucose
5-hydroxyindoleacetic aοid
lpn
Magnesiυm
Osmolality
Oxalate
Phosρhate
Potassium
Sodium
Poφhobilinφen, qualitative
Porphyrins, qualitative
Proteins
Salicylate
υrea clearance
Urea N
Uric acid
Urobilinogen
Xylos absorption test
children
adults
FECES
Fat, 3-day coι|ection
GAsTRlc AclDlτY
Acidity, total, 12 h
32-64'l unittL
Depends upon dietary intake
150 mσ24 h
25O mgl24 h
10ο0-2000 mg/24 h
85-125 ml/min
75-115 mumin
1 gl24 h
2-a mgl24h
O-15 mgl24 h
146-209 mgl24 h
500-800 mosπ/kg
1O-4O mgl24 h
400-1300 mg/24 h
25-120 mΕql24h
4o-22o mΕq24h
Negative
Negative
0.05-0-1 g/24 h
Negative
6ο-95 mumin
1o-4O gl24 h
25o-75O mgl24 h
0.5-3.5 mg/24 h
16%-33o/" of ingested xylose
>4gin5h
<5 αd
10-60 mEΦL
CSF obtained by lumbar puncture
The value is in units/l and not Φlculated for
toιal volume
lnterρretalion of value |ett for physician,
deρends on the nature of fluid
Higher value on children and during pregnancy
A blood Sample must aΦmpany urine
specimen
Acid-washed container required
νvith normal fluid intake
Varies with diet; the interpretation of urine
electrolytes and osmolality should be left for
the physician
Α blood sample must accompany specimen
Dependent on protein intake
Dependent on diet and therapy
For qualitative deteminalion on random urine,
send samρle to urinalysis section in
Hematology Lab
value depends on fat intake of 100 Φd lor 3
days preceding and during Φllectιon
Titrated at pH 7
BLOOD GASES
Arterial CaDillaru Venous
oΗ 7.35-7.45 7.35-7,45 7.32-7.42
oCO" (mm Ho) 35-45 35-,ι5 38-52
oO" (mm HoΙ 70100 5ο-8o 24-48
HCO" (mEo/L) 19-25 19-25 19-25
τco" 1mEo/L) 19-29 19-29
O" saturation
(o/") 90-95 90-95 40-70
Base exοess (mΕo/L) -5 to i5 -5 to +5 -5 to +5
126

129. APPENDIX
Segs = segmented neutrophils
Bands = band neutroρhilS
HEMATOLOGY
Complete Blood Count
Lymphs = lymphocytes
Monos = monocytes
Erythrocyte Sedimentation Rates and Reticulocμe counts
Sedimentation rate, \Λrestergren
Sedimentation rate, \Λrintrobe
Reticulocyte count
Children 0-20 mm/hour
Adult male 0-15 mm/hour
Adult female 0-20 mm/hour
οhiΙdren 0-13 mm/hour
Adult ma|e ο-10 mm/hour
Adult female 0-15 mm/hour
Newborns 27.-67"
1-6 mo o"/"-2'8γ"
Αdults 0.5%-1.5%
Age
Hgb
(q/dL)
Hcl
ιo/^1
RBC
amill/mm3)
RD\iV
0-3 d 15.0-20.0 45-61 4.0-5.9 <18
1-2 wk 12.5-18.5 39-57
1-6 mo 10.0-13.0 29-42 3.1-4.3 <16.5
7 moΙo2ν 10.5-13.0 33-38 3.7-4.9 <16
l1 5-13 ο 34-39 3.9-5.0 <15
5-8 v 11 5-145 35-42 4.ο-4.9
'13-18 v 12.O-15.2 36-47 4.5-5.1 <14.5
Adult male 13.5-16.5 41 -50 < ι4.5
Adult female 12 o-'15 ο 36-44 4.0-4.9 <14.5
Age
MCV
(fLt
MCH MCHC
ιo/^\
Plts
x 103/mms)
0-3 d ο5-1 29-37 250-450
1-2 wk A6-1 1ο 2Β-36 28-38 25ο-450
1-6 mo 74-96 25-35 30-36 300-700
7 mo'ιo 2 ν 70-84 23-30 31-37 250-600
2-5 75-47 24-30 31-37 250-550
5-8 v 77-95 25-33 31-37 250-550
13-18 r 7A-96 25-35 31-37 150-450
Adult male aο-'1οο 26-34 31-37 150-450
Adult female aο-1οο 26-34 31-37 15ο-450
WBC and Diff
Age
γιrBc
(x 103/mm3)
Segs Bands Lymphs Monos
0-3 d 9_0-35.0 32-62 10-18 19-29 5-7
1-2 wk 5.0-2ο.0 14-34 6- 36-45 6-10
1-6 mo 6.0-17.5
1 3-33 4^12 41-71 4-7
7 moΙo2ν 6_0-17.0
1 5-35 5. 45-76
2-5 ν 5.5-15.5 23-45 5-1 1 35-65
5-8 v 5.0-14.5 32-54 2A-44 3-6
13-18 v 4.5-13.0 34-64 5-1 1 25-45 3-6
Adults 4.5-1 1.0 35-66 5- 24-44 J-O
AgΘ Eosinophils Basophils
Atypical
l νmnhξ
No. of
NRBCs
0-3 d o-2 o-1 0-8 n-t
1-2 wk o-2 ο_1 ο-8 0
'1-6 mo 0-3 ο_1 ο-8 ο
7moιo2 ο-3 o-1 0-θ ο
2_5 ν 0-3 0-1 ο-8 0
5_8 ν ο-3 ο-1 ο-8 0
13-18 v ο-3 ο-1 ο-8 ο
Adults ο-3 0-1 0-8 ο
127

130. APPENDIX
DENTIFRICE PRODUCTS
Brand Name
Abrasive τherapeutic
lnqredient lnqredient
Foaming
Agent
Aim@ Baking soda Gel Ηydrated silica, Sodium bicarbonate sodium monofluorophosphate 0.7ol. sodium lauryl sulfate
(fIuoride ο.14%)
Other lngredients: Sorbitol and related polyols, water, glycerin, SD alcohol 388, flavor, cellulose gum, sodium saccharin, blue #1,
#
Aim@ Extra Strength Gel Ηydrated silica Sodium monofluorophosphate '1.2ol.
Sodium lauryl sulfate
Other tngredients: Sorbitol, water, PEG-32, SD alcohol 388, flavor, cellulose gum, sodium saccharin, sodium benzoate, blue #1,
#10
AimΘ Regular Strength Hydrated silica sodium monofluoroρhosphate 0.8% sodium lauryl sulfate
(ΙtUoride ο.'14%)
αher lngredients: Sorbitol and other related ρolyols, Water, glycerin, sD alcohol 38B, flavor, cellulose gum, sodium saccharin, blue
#1 vellow#10
Aim@ τartar control Gel Hydrated silica sodium monotluorophosphate 0.8% sodium lauryl sulfate
(lluoride 0.14%)
αher lngredients: sorbitol and reIated polyols, water, glycerin, zinc citrate trihydrate, sD alcohol 38B, flavor, cellulose gum, sodium
blυe #1. vellow #'lο
AquafreshΘ Baking soda Toothpaste calcium carbonate, hydrated silica, sodium sodium monotluoroρhosρhate sodium lauryl suIfate
bicarbonate
other lngredients: calcium carrageenan' cellυlose gum, coloE, flavor, glycerin' PEG-8, sodium benzoate, sodiUm saΦharin, sorbitol,
titanium dioxde. water
AquafreshΘ Extra Fresh Toothpaste* Ηydrated silica, οalcium carbonate sodium monofluorophosphate sodium lauryl sulfate
Other lngredients: Sorbitol, water, glycerin, PEG-8, titanium dioxide, cellulose gum, flavor, sodium saccharin, sodium benzoate,
calciυm carraoeenan. colors
AquafreshΘ for Kids τoothpaste* Hydrated silica, caicium carbonate sodium monofΙuorophosphate Sodium lauryl sulfate
other lngredients: Sorbitol, Water, glycerin, PEG_8, titanium dioxide, cellulose 9Um,
flavor, sodium Saοcharin, calcium carrageenan,
sodium benzoate. colors
Aquafresh@ Gum Care Toothpaste Hydrated silica, calcium carbonate Sodium monofluorophosphate Sodium lauryl sulfate
other lngredients: calcium carrageenan, cellUlose gum, colors, flavor, PEG-8, sodium benzoate, sodium Saωharin, sorbitol, titanium
water
AqualreshΘsensitiveτoothpaste Hydratedsilica Potassium nitrate, sodium fluoride Sodium lauryl sulfate
Other lnqredients: Colors, flavor. qlvcerin, sodium
AquafreshΘ Tartar control τoothpaste* Hydrated silica Sodium fluoride sodium |auryl su|Ιate
other ιngredients: τetrapotassium pyrophosphate, tetrasodium pyrophosphate, sorbitol, glycerin, PEG-8, flavor, xanthan gum, sodium
saccharin. sodium benzoate. colors.
AquafreshΘ Triple Protection τoothpaste* Hydrated silica, Φlcium carbonate sodium monofιuorophosphate Sodium lauryl sulfate
Other lngredients: PEG-8, sorbitol, cellulose gum, sodium benzoate, titanium dioxide, calcium carrageenan, flavor, sodium saccharin,
coloE. water
Aquafresh@ νhjtening Gel or Toothpaste HydΙated silica sodium lluoride sodium lauryl sulfate
Other lngredients: Colors, flavor, glycerin, PEG-8, sodium benzoate, sodium hydroxide, sodium saccharin, sodium tripolyphosphate,
BioteneΘ Antibacterial Dry Mouth Hydrated silica, calcium pyrophosphate Lactoperoxidase, glucose oxidase,
τoothpaste lysozyme, sodiυm monofluorophosphate
(o.76γ")
other lngredients: sorbitol, glyοerin, xylitol, isoceteth-2o, cellulose gum, flavor, sodium benzoaie, beta-d-glucose, potassium
close-UpΘ Baking soda Toothpaste (mint) Hydrated siliοa, sodium bicarbonate Sodium monofluorophosphate 0.79% Sodium lauryl suIfate
(fluoride 0.15%)
other lngredients: sorbitol and related ρolyols, water, glycerin, SD alcohol 38B, flavor, cellulose gum, sodium saccharin, sodium
benzoate, red #33' red #4ο, titanium dioxide
close-Up@ οlassic Red Gel Hydrated silica sodium monofluorophosphate 0.8% sodium lauryl sulfate
(lluoride 0.14%)
other lngredients: sorbitol and related polyols, water, g|yοerin, SD alcohol 38B, flavor, cellulose gum, sodium saccharin, sodium
close_Up@ cool Mint Gel Ηydrated silica sodium monofluorophosρhate 0.79% sodium lauryl sulfate
(fluoride 0.15%)
other |ngredients: Sorbitol, water, glycerin, sD alcohol 38B, flavor, cellulose gum, sodium saωharin, po|ysorbate 20, blue #1, mica,
red #33 titanium dioxide
close-UpΘ original Red ιΛ/hitening Hydrated siιiοa Sodium monofluorophosphate 0.8% sodium lauryl sulfate
τoothpaste (Ιluoride 0.14%)
αher lngredients: sorbitoi and related poIyols, water, glycerin, sD alcohol 38B, flavor, celluiose gum, sodium saccharin, sodium
chloride. red iP30 lake. titanium dioxide. blue #1
close-Up@ τartar control Gel (mint) Hydrated silica sodium monof|uorophosphate 0.79% sodium lauryl sulfate
(fluoride 0.15%)
αher lngredients: Sorbitol and related ρolyols, water, glycerin, zinο citrate trihydrate, sD alcohol 38B, flavor, cellulose gum, sodium
saΦharin. red #33. red #4o. caffeine frΦ
close_Uρ@ Tartar contml \Λrhitening Ηydrated silica Sodium monofluorophosphate ο.8% sodium lauryl sulfate
Toothpaste (Ιluoride 0.14ol")
αher lngredients: SoIbitol and related ρolypols, water, glycerin, sD alcohol 38B, Ιlavor, zinc citrate trihydrate, cellulose gum, sodium
titanium dioxide. blue #1. vellow #10
οolgateΘ Baking soda & Peroxide τartar Hydrated silica, sodium bicarbonate Sodium monofluorophosphate 0.76% sodium lauryl sulfate
controΙ Toothpaste'
othe. lngredients: Glycerin, propylene glycol, water, pentasodium triphosρhate, tetrasodium pyroρhosρhate, titanium dioxide, Ιlavor,
sodium hvdroxide. calcium Deroxide, sodium saccharin, carraqeenan, cellulose qum, FD&C blue #1, D&C yellow #10
colgate@ Baking soda & Peroxide Ηydrated Silica, sodium bicarbonate, Sodium monofluorophosphate 0.76% Sodium lauryl sulfate
\Λrhitening τωthpaste* aluminum oxide
other lngredients: GlyΦrin, polypylene glycol, water, penιasodium triphosphate, tetrasodium pyrophosphate, titanium dioxide, tlavor,
sodium hvdroxide. calcium oeroxide. sodium saccharin. carraoeenan, cellulose qum, dietetically sucrose free
colgateΘ Baking Soda Tarlar control Gel Hydrated silica, sodium bicarbonate Sodium tluoride 0.243% Sodium lauryl sulfate
or τoothρaste
other lngredients: Glycerin, tetrasodium ρyrophosphate, PVM/MA coρolymer, cellulose gum, flavor, sodium saccharin, sodium
hvdroxide. titanium dioxide (paste). FD&c blue #'1, D&ο ve|low #10 (οeI), dieteticaιly sucros free
Hydrated siliοa Sodium fluoride 0-243ol" SodΙUm lauryl sulfate
other lngredients: sorbitol, water, PEG-12, flavor, tetrasodium ρyrophosphate, cellulose gum, sodium Saοcharin, mica, titanium
οolgateΘ Junior Gel-
dioxide, colorants,
128

131. APPΕNDlx
Toothpaste
Brand Name
Abrasive τherapeuιic
lnοredient lnq]edient
Foaming
Aqent
colgateΘ PlatinumτM \Λrhitening Toothpaste- Silica, aluminum oxide sωium monof|uorophosρhate SωiUm lauryl sulfate
αher lngrcdients: \Λrater, hydrated silica, Sorbiιol, glycerin, PEG-12, tetrapotassium pyrophosρhate, PVM/MA copolymer, flavor,
sodium hγdrcxide, sodium saΦharin, titanium dioxide
colgate@ PlatinumτM \Λrhitening with Baking Sodium bicarbonate, aluminum oΧide sωium monofluorophosρhate 0.76% sωium lauryl sullate
Soda Toothρaste*
other lngrcdients: \Λrater, glycerin, PEG-12, tetrapotassium pyroρhosphate, PVM/MA copolymer, flavor, sodium hydroxide, sodium
sacοharin, titanium dioxide, celluΙose gum
colgateΘ sensitive Maximum Strength Ηydrated silica, sodium bicarbonate Potassium nitrate 57o, stannous fΙuoride Sodium lauryl sulfate
o.45γ"
Other lngaedients: Glycerin and/or sorbitol, water, PEG-40 castor oil, PEG-12, poloxamer 407, sodium citrate, flavor, titanium dioxide,
sοdium hydroxide, cellu|ose gum, xanthan gum, sodium saccharin, stannous chloride, citric aοid, tetEsodium pyrophosρhate, FD&c
Blue No. 1
colgate@ τartar οontrol Micro cleansing Hydrated si|ica sodium fIuoride 0.243% Sodium lauryl suIlate
Gel or Toothpaste*
other lngredienιs: νater, sorbitol, glycerin, PEG-12, tetrasodium pyroρhosphate, PVλ/VMA copolymer, cellulose gum, flavor, Sodium
hvdroxide. titaniυm dioxide. Sodium saccharin. οarraoeenan, dieteticallv sucros
'@
colgateΘ Tartar control Plus ννhitening HydEted silica, aluminum oxide sodium monofluoroρhosphate 0.76% sodium lauryl sulfate
other lngredients: r/ater, sorbitol, glycerin, pentasodium triphosphate, tetrasodiUm pyrophosphate, PVλ4/MA copolymer, cellυlose
oum. flavor. sodium hvdroxide. titanium dioxide. sodium saccharin. οaΙraoeenan
colgateΘ Toothpaste- Dicalcium phosphate dihydrate sodium monofluorophosphate 0.76% sodium lauryl sullate
other lnoredients: Glvcerin. cellulose oum. tetrasodiUm oγroohosohate' sodium saccharin, flavor, dieteticallv sucroΦ frΦ
Colgate Total@ Toothpaste Hydrated silica Sodium fluoride 0.243ol., triclosan 0.3% Sodium lauryl sulfate
oιher lngredients: \Ι/ater, glycerin, sorbitol, PVM/MΑ copolymer, cel|ulose gum, flavor, sodium hydΦxide, propylene glycol,
sodium saccharin. titanium dioxide
colgate τotalΘ Fresh stripe τoothρaste Hydrated Silica Sodium fluoride 0.243ol", triclosan 0.3% Sodium lauryl sulfate
Other lngredients: Water, glycerin, sorbitol, PVM/MA copolymer, cellulose gum, flavor, sodium hydrcxide, propylene glycol,
carraoeenan. sodium saΦharin. mica' titanium dioxide, FD&c bΙue #1, D&c vellow #10
colgateΘ ιryinterfresh Gel- Hydrated Silica sodium fluoride 0.243% sodium lauryl sulfate
other |ngredients: sorbitol, Water, PEG-12, llaνor, tetrasodium pyrophosphate, cellulose gum, sodium Saccharin, FD&c blue #1,
sucrose free
crest@ Baking Soda τartar Protection Gel Hydrated silica, sodium bicarbonate Sodium fluoride 0.243%
or τoothpaste (mint)-
Sodium lauryl sulfate
other lngredients: \Λ/ater, glycerin, sorbitol, tetrasodium pyrophosphate, PEG-6, fΙavor, celιulose gum, sodium saΦharin, titanium
dioxide (paste), FD&ο blue #'1 (gel), disodium ρyrophosphate,
tetrapotassium pyrophosρhate, carbomer 956, xanthan gum, FD&c
#5
crestΦ cavity Proteοtion with Baking soda Hydrated siΙiΦ, sodium bicarbonate Sodium fluoride 0.243ol"
Gel or Toothpaste (mint)*
Other lngredients: Sorbitol, water, glycerin, sodium carbonate, flavor, cellulose gum, sodium saccharin, titanium dioxide (paste),
Sodium lauryl sulfate
FD&C blue #1
creslo οavity Protection Gel (cool mint)* Hydrated silica Sodium fluoride 0.243%
other ιngredients: Sorbitol, water, trisodium phosphate, flavor, Sodium phosphate, xanthan gum, sodium Saccharin, carbomer 956,
Sodium lauryl sultate
FD&C blue #1,
crest@ οavity Protection ToothpastΘ" (icy Hydrated silica
mint or regular)
Sodium f luoride 0.24Ι}y"
αhe. lngrcdients: Sorbitol, Water, glycerin (mint), trisodium phosρhate, llavor, sodiυm phosphate, cellulose gum (mint), Xanthan gum
(reqular), sodium saccharin, carbomer 956, titanium dioxide, FD&C blue #1. carbomer 9404
Sodium lauryl sulfate
crest@ Extra \Λrhiιening Gel or τoothpaste Hydrated siiica Sodium fluoride 0.15ol. Sodium lauryl sulfate, poloxamer 407
αher lngrcdients: Sorbitol, water, glycerin, tetrasodium pyrophosphate, sodium οarbonate, carboxymethylcellulose sodium, titanium
diοxi.|e carnaltba wax sodium saωharin. flavor. FD&c blue #1. FD&c vellow #5. PEG-6. sodium bicarbonatet
crest@ ror Kids cavity Protection GeΙ Hydrated silica Sodium fluoride 0.243% Sωium lauryl sulfate
other lngredients: sorbitol, Water, trisodium phosρhate, sodium ρhosρhate, xanthan gum, llavor, sodium saΦharin, carbomer 956,
miΦ, titanium dioxide, FD&c blue #1
οrestΘ Gum care Gel or τoothpaste Hydrated silica Stannous fluoride 0.4547o sodium laUryI sullate
Other lngredients: Sorbitol, water, stannous chloride, titanium dioxide (paste), flavor, sodium hydroxide, sodium saccharin, sodium
carraqeenan, FD&C blue #1 (qel), sodium qluconate, hydroxyethylcellulose
οrestΘ Multicare Gel or τoothρaste (cool Hydrated silica, Sodium bicarbonate Sodiυm fiuoride 0.243ol" sodium lauryl sulfate
mint, fresh mint)
oιher lngredients: τetrasodium pyrophosphate, xyιitol, water, glyοerin, PEG-6, poloxamer 407, sodium carbonate, f|avor, cellulose
oum. xanthan οUm- sodium saΦharin. titanium dioxide. FD&ο blue #1. FD&c ve|low #5 (cool mint)
crestΘsensitivityProtectionToothpaste* HydratedSilica
(mild mint)
Potassium nitrate 5olo, sodium rluoride Sodium lauryl sultate
o.150/"
other lngredients: Water, 9lycerin, sorbitol, trisodium phosphate, celIulose gum, flavor, xanthan gum, sodium saΦharin, titanium
dioxide. dve free
crest@ τartar Protection Gel* (fresh mint,
smooth mint)
sodium fluoride ο.243% Sodium lauryl sulfate
other lngredients: ν1,/ater, sorbitol, glyοerin, tetrapotassium pyrophosphate, PEG-6' disodium pyrophosphate, tetrasodium
ovroohosohate. flavor. xanthan oum. Sodium saωharin. carbomer 956. FD&c blue #1
'
FD&c γellow #5 (Smooth mint)
crestΘ τartar Protection Toothpasιe- silica sodium fluoride 0.243% sodium Ιauryl sulfate
(original flavo0
other ιngredients: ι/vater, sorbitol, glycerin, tetrapotassium pyrophosphate, PEG-6, disodium ρyrophosphate, tetrasodium
ovroohosohate. flavor. xanthan αum. sodium saωharin' carbomΘr 956, titanium dioxide, FD&c blue #1
Dr. τichenor's Toothpaste Hydrated siliοa Sodium fluoride Sodium lauryl sulfate
other lngredients: \Λrater, glycerin, sorbitol, insoluble Sodium metaphosphate, peppermint oil, cellulose gum, sodium saccharin,
sodium ohosDhate. titanium dioxide.
EnamelonΘAll-Familyτoothpaste HydratedsiIica Sodium fluoride (fluoride 0.14%) Sodium lauryl sufate
otheΙ lngredients: \Λrater, glycerin, sorbitoI, monoammonium phosphate, calcium sulfate, xanlhan gum, llavor, PEG-60 hydrogenaιed
castor oil, sodium Saοcharin, ammonium οhloride, celIUlose gum, titaniUm dioxide, magnesium chloride, methylparaben, propylparaben,
FD&c bιue #1
First Teeth.u Baby Gel Lactoperoxidase 0.7 units/g, lactoferrin, Sodium lauryl Sulfaιe
glucose oxidase
αher lnαredients: \Λrater.
F|uoride FoamτM"+ lngredients: Fluoride 1.2396 (from sodium fluoride and hydrogen fluoride), Water, phosρhoric acid, poloxamer, sodium saccharin, flavor
gluten free
129
-

132. APPENDIX
DENτIFRICE PRoDUcTs (Continued)
Brand Name
Abrasive
lngredient
Τherapeutic
lngredient
Foaming
Agent
GleemΘ τoothρaste Hydrated silica sodium f luoridΘ 0.243"/" sodium lauryl sυlfate
other lngredienιs: Sorbitol, water, trisodium phosphate, rlavors, sodium phosphate, xanthan gum, sodium saοcharin, caΦomer 956,
titaniυm dioxide. dve free
Listerine@ Gel or Toothρaste Hydrated siliοa
(cool mint)
Sodium monofluorophosphate Sodium lauryl sulfate
Other lngredients: \ivater, sorbitol, glycerin, flavors, cellulose gum, sodium saccharin, phosphoric acid, FD&C blue #1, D&C yellow
#10. sodium DhosDhate. benzoic acid. titanium dioxide (oaste). xanthan
ListerineΦ τartar control Gei or Toothpaste Hydrated silica
(cool mint)
Sodium fluoride Sodium lauryl sulfate
other lngredients: ι/vater, sorbitol, glycerin, PEG-32, flavor, cellUlose gum, sodium saccharin, tetrapotassium pyrophosphate, FD&c
#1. D&C vellow #10. titanium dioxide
Mentadent@ Advanced \Λ,/hitening Gel or Ηydrated silica, sodium bicarbonate Sodium fluoride 0.15%
Toothρaste
sodium lauryl sulfate, hydrogen ρeroxide
other lngredients: Zinο citrate trihydrate, Water, SorbitoI, glyοerin, poloxamer 4o7' PΕG-32' SD alcohol 38B, flaνor, cellulose gum,
MentadentΘ Gum care Gel or Toothpaste Hydrated silica, sodium bicarbonate sodium fluoride 0.24% (fluoride 0.15%) sodiυm lauryl Sulfate, hydrogen peroxide
other lngredients: Zinc citrate trihydrate (1.8old, Water, sorbitol, glycerin, poloxamer 4ο7, PEG-32' SD alcohol 38B, f|avor, cel|ulose
Νrentadent@ τartar control Gel or Hydrated Silica, sodium bicaΦonate sodiυm lluoride 0.24% Sodium lauryl sulfate, hydrogen peroxide
τoothpaste
αher lngredients: \Λrater, sorbitol, glycerin, poloxamer 407, PEG-32, zinc citrate, sD alcohol 38B, flavor, cellulose gum, sodium
#1
MentadentΘ with Baking soda & Peroxide Hydrated silica, sodium bicarbonate Sodium fluoride o.24oλ (Ιlυoride 0j5ok' sodium lauryl sulfate, hydrogen peroxide
Gel or τoothpaste-
other lngredients: ννater, sorbitol, glycerin, poloxamer 407, PΕG-32, sD alcohol 38B, flavor, cellUlose gum, sodiUm saccharin,
ohosohοric acid blιre #1 titanil]m diοxide
ιjly First colgate@ Gel* Hydrated silica Sodium fluoride 0.243ol" sodium lauryl sulfate
other lngredients: \Λrater, sorbitoI, PEG-12, flavor, tetrasodium pyrophosphate, cellulose gum, sodium saΦharin, FD&c red #40, D&c
red f33- dieteticallv sucrose free
Natural \ΛrhiteΘ Toothpaste Hydrated silica Sodium fluoride Sodium lauryl sullate
other lnαredients: solbitoi water οlvcerin sodiιlm ben7οate titaniιlm.|iοxide Ιlavοr cellι]lοsρ ο|lm die-te-ticallv sucrosο lrΦ
Νatural νhite@ Baking soda τoothpaste calcium carbonate Sodium monofluorophosphate sodium lauryl sulfate
other lnσredients: sorbitol. Water olvcerin. sodiιrm bicarbonatef carraοeenan natι]ral flavοr dieteticellv sucrose rrΦ
Natural ννhiteΘ Fights Plaque Toothρaste Hydrated silica Sodium fluoride sodium lauryl Sulfate
other Ιnoredients: sorbitοl Water οlvcelin sodium ben7oale titaniι]m dioxide flavοr celhrlοse οιlm diοtEticrlrv sucrose free
Natural WhiteΦ sensitive TΦthρaste Hydrated silica Sodium monofluorophosphate, potassium Sodium lauryl sulfate
nitrate
other lngredients: Sorbitol, Water, glyοerin, flavor, FD&c red #40, sodium benzoate, titanium dioxide, sodium saccharin, dietetically
sucrose free
Natural \Ι/hite@ Tartar contro| τoothpaste HydΙated silica Sodium flυοride Sodium lauryl sulfate
oιher lngredients: sorbitol, Water, g|ycerin, Xanthan gum, tetrapotassium pyrophosphate, titanium dioxide, celluIose gum, flavor,
sodium benzoate. FD&c blue #1. D&c vellow #10. dietΘtica|lv sucrosΘ ffee
Natural ιΛ/hiteΘ with Peroxide Ge| Hydrogen peroxide
Other lngredients: Vvater, glycerin, flavor, dipotassium phosphate, sodium saccharin, phosphoric acid, poloxamer, dietetically
sucrose f@
oEjelΘ Baby Tooth & Gum cleanser Gel
other lngredients: Poloxamer 407 (2%), simethicone (0.12%), Microdent, carboxymethylοe||ulose, sodium, citric acid, flavor, g|ycerin,
sodium saccharin. sorbitο|. fluoride frΦ
orajelΘ Gold sensitive Teeth Ge| for Adults Hydrated silica Potassium nitrate 5%, sodium Sodium lauryl sultate
monof luorophosphate 0.2%
other lnoredients: FD&c blue #1. flavor. olvcerin. sodiυm laurovl sarcΦinate. sodium
Pearl DropsΘ Toothpolish Paste Hydrated silica, calcium pyrophosρhate, sodium monofluoroρhosphate Sodium lauryl sulfate
dicalcium phosphate, aluminum hydroxide
other lngredients: \,νater, Sorbitol, glycerin, PEG-12, flavor, ceIlulose gum, trisodium ρhosphate, SodiUm ρhosρhate, sodium
saωharjn. dieιeticallv sucrose frΦ. dve free
Pearl DropsΘ τoothpo|ish Gel Hydrated silica sodium monofluorophosphate Sodium laury] sulΙate
Other lngredients: Sorbitol, water, glycerin, PEG-12, flavor, cellulose gum, sodium saccharin, FD&C blue #1, FD&C yellow #10,
sucrose free
Pearl Droρs@ \Λ/hitening Extra strength Hydrated silica, calcium pyrophosphate, Sodium monofluorophosphate sodium Ιauryl sulfate
Paste diοalcium ρhosphate
other lngredients: ιΛ,/ater, sorbitol. glycerin, PEG-12, flavor, cellulose gum, trisodium phosphate, sodium phosphate, sodium
saccharin, titanium dioxide. dieteticallv sucrose fe. dve free
Pearl DropsΘ \Λrhitening Gel
(icy cool mint)
Hydrated silica sodium monoflυorophosρhate sodium lauryl sulfate
other lngredients: sorbitol, Water, glycerin, PEG-12, flavor, οellulose gum, Sodium Saccharin, FD&c blue #'1, FD&ο yellow #10,
PepsodentΘ Baking soda Toothpaste Hydrated Silica sodium monoΙluorophosphate 0.8% sodium lauryl sulfate
(fluoride (0.14%)
Other Ingredients: Sorbitol, water, sodium bicarbonatet, PEG-32, SD alcohol 388, flavor, cellulose gum, sodium saccharin, titanium
Pepsodent@ Original Toothpaste Hydrated silica Sodium monofluorophosphate 0.8% Sodium lauryl sulfate
(fluoride 0.14%)
other lngrcdients: Sorbitol and related polyols, water, glycerin, sD alcohol 38B, flavor, cellulose gum, sodium saccharin, titaniυm
Peρsodent@ Tartar control Toothpaste Hydrated silica sωium monotluorophosρhate 0.8% Sodium lauryl sulfate
(fluoride 0.14%)
Other lngredients: Sorbitol and related polyols, water, glycerin, SD alcohol 388, zinc citrate trihydrate, flavor, cellulose gum, sodium
'l
vcllow #1
Pete & Pamπ Gel (premeasured strips) Hydrated Silica Sodiummonofluorophosphateο.76% sodiumlaurylSarcosinate
other |ngredients: sorbitol, Water, glycerin, xanthan gum, polysorbate 2ο, sodium benzoate, pluronic P84, FD&c blue #1, FD&c red
#33 FD&c νellow #5 flavοr xvlilol
130

133. APPENDIX
Brand Name
Abrasive τherapeutic
lnαredient lnqredient
Foaming
AEent
Promise@ τoothρaste Dicalcium phosρhate Potassium nitrate, sodiυm Sodium lauryl sulfate
monofluorophosphate
other lngrcdients: \Λ/ater, hydroxyethylcellulose, flavor, sodiυm saccharin, methy|paraben, propylparaben, D&c yelιow #10, FD&c
bιue #1
'
οlrοerin. sorbitol. silicon dioxide. dieteticallv sucrose frΦ
Reach Act Adult Antιcavity τreatment ιngredients: sodium fluoride 0.05%, cetylpyridinium chloride, D&ο red #33 (cinnamon), EDTΑ calcium disodium, FD&c yellow #5,
Liquid (cinnamon, mint)+ flavor, glycerin, monobasic sodium phosphale, dibasic Sodium phosphate, poloxamer 407, ρolysorbate 80 (cinnamon), polysorbate 20
(mint), propylene glycol, sodium benzoate, sodium saccharin, water, FD&C green rPJ (mint), menthol (mint), methyl salicylate (mint),
Dotassium sorbate (mint). aιcohol frΦ
Reach Act for KidS*+ lngrΘdients: Sodium fluoride 0.05%, οeιy|pyridinium chloride, D&c red #33, EDτA calcium disodium, flavor, glyΦrin, monobasic
sodium phosρhate, dibasic sodium phosphate, poloxamer 407, polysorbate 80, propylene glycol, sodium benzoate, sodium saccharin,
water, alcohol free
Rembrandι@ Age_Detying Adult τoothpaste Dicalcium orthophosρhate, Soft silica sodium monofluorophosphate (fluoride
(original or mint) 0.15%)
αher lngredients: τrihydroxy proρane,
ρerhydrol
urea, aluminum oxide, acetylated ρectins, sodium ciιrate' iridiυm' papain, carboxyΙ
Mouthwasht flavor. cocamidooroprl betaine, citric aοid, sodium benzoate, sodium saccharin, sodium hvdroxide, alcohol fre
RembrandtΘ Daily \Λ/hitening Gel Silica Sodium monof|uoroρhosphate (fluoride carbamide peroxide, sodium lauryl sullate
ο.15%)
Other lnoredients: Glvcerin, sodium citrate, carbopol, triethanolamine, flavor
Rembrandt@ \Λ/hitening Baking Soda Sodium bicarbonate, silica Sodium monofluorophosphate (fluoride sodium lauryl sulfate
τoothpaste 0.15%)
αher lngrcdients: Glycerin, sorbito|, aiumina, waler, sodium citrate, sodium carrageenan, papain, flavor, sodium hydroxide, FD&c
Rembrandt@ Whitening canker sore Dicalοium phosphate, silica Sodium monofluorophosphate (fluoride
Prevention τoothpaste 0.15%)
αher lnqredients: νater, οlycerin, Xylitol, sodium citrate, natural flavors, Sodium carrageenan, papain, citric acid, dye free
Rembrandt@ ιΛrhiιening Natural Toothpaste Dicalcium phosphate, silica Sodium monofluorophosphate
other lnqredients: \Λrater, glycerin, xylitol, Sodium citrate, natural flavors, Sodium carrageenan, papain, citriο acid, dye free
RembrandtΘ \Λ/hitening sensitive Dicalοium phosρhate dihydrate Potassium nitrate 5%, sodium Sodium lauryl Sulfate
τoothpaste monofluoroρhosphate 0.76%
αher lngredients: Glycerin, sorbitol, Water, alumina, paρain, sodium citrate, flavor, carlcoxymethylοel!ulose Sodium, sodium saccharin,
methylparaben, FD&C red #40, citric acid
Rembrandt@ \,vhiιening Toothpaste Dicalcium phosphate dihydrate sodium monofluorophosphate 0.76% sodium lauryl sulfate
(mint or original)
other lngredients: Glycerin, sorbitol, water, alumina, sodium citrate, flavor, sodium οarrageenan, papain, sodium saccharin,
methylparaben, citric acid, FD&c blue #1, FD&ο yellow #5
ReveΙationΘ τoothpowder Calcium carbonate
other lngredientε: Methyl salicylate, menthol, dye free
vegetable soap ρowder
SensodyneΘ Baking soda τoothpaste Sodium biοarbonate, silica Potassium nitrate, sodium fluoride Sodium lauryl sulfate
other lngredients: νγater, glycerin, flavor, hydroxyethylcellulose, titanium dioxide, sodium saccharin, dietetically sιcrose frΦ, dye
free
Sensodyne@ cool Gel Silica Potassium nitrate, sodium fluoride sodium meιhyl cocoyl taurate
Other lngredients: \i/ater, sorbitol, glycerin, sodium carboxymethylcellulose, flavor, sodium saccharin, FD&C blue #1, trisodium
ohosohaιe. dieteticallv sucrose frΦ
SensodyneΘ Extra \Λ/hitening Toothpaste Silica Potassium nitrate, sodium sodium lauryl Sulfate
monofluoroρhosphate
other lngredients: νγater, flaνor,glycerin, PEG-12, PEG-75, sodium carbonate, sodium sacοharin, titanium dioxide, calcium peroxide,
SensodyneΘ Toothpaste'
(fresh mint)
Dicalcium phosphate Potassium nitrate, sodium
monofluorophosphate
Sodium lauryl sulfate
other lngredients: \Λ/ater, glycerin, sorbitol, hydroxmethylcellulose, flavor, Sodium saccharin, methylρa.aben, proρylparaben, D&ο
#10. FD&C blue #'1, silicon dioxide, dieteticallv sucrose tree
sensodyneΘ Toothpaste (origina|) Silica Potassium nitrate, sodium fluoride sodium methvl cocovΙ taurate
other lngredients: \Λ/ater, glycerin, Sorbitol, ceιlulose 9um, titanium dioxide, sodium Saccharin, flavor, D&c red #28, trisodium
slimeι@ Gel" Hydrated silica Sodium fluoride 0.15%
other lngredients: sorbitol, Water, glycerin, PEG-32' flavor, ethyl alcohol, ρropylene
glycol' glyceryl triacetate, οellulose gum, sodium
saccharin, sodium benzoate, FD&C blue #1
τhermodent Toothpaste Diatomaceous earth, silica Strontium chloride hexahydrate Sodium methyl cocoyl taurate
other lnοredients: sorbitol. olvcerin. titanium dioxide, quar qUm, PEG-40 stearate, hγdroxvethγlcellulose. flavor, preseryative' Water
τom'sΘ Νatural Baking Soda With Propo|is calcium carbonate, sodium biοarbonate sodium lauryl sulfate
& Myrrh Toothρaste
other lnσredients: G|vcerin, Water. carraoeenan, peρρermint oil, mvrrh, ρropolis, fluoride frΦ
τom'sΘ Natural Baking Soda, οalcium, and calοium carbonate, sodium bicarbonate Sodium monofluorophosphate Sodium lauryl sulfate
Fluoride Τoothpaste
τom'sΘ Νatura| calcium and Fluoride ca|cium carbonate sodium monofluorophosphate sodium lauryl sullate
τoothpaste*
other lngredienιs: Glycerin; Water; carrageenan; xylitol (sρearmint); cinnamon, fennel oil, or Spearmint; peppermint oil (cinnamon,
τom's@ Natural calcium and Fluoride calcium carbonate, hydrated silica sodium monofluorophosphate Sodium lauryl sulfate
τoothpaste
otheΙ lnqredients: Glycerin, Water' carraqeenan, xylitol, natural winterqreen oil
Tom'sΘ Natural for children with calcium caΙcium carbonate, hydrated silica Sodium monofluorophosphate Sodium lauryl sulfate
and Fluoride τoothpaste
Other lnqredients: Glvcerin, fruit extracts, carraqeenan, water
Tom'sΘ Natural With Propolis and lνΙyrrh calcium carbonate Sodium lauryl sulfate
τoothpaste
t-.
"'".
raki"*"* *"*
τoothpasιe
Other lngredients; Glycerin, water, propylene glycol, cellulose gum, flavor, sodium saccharin, titanium dioxide, sodium hydroxide,
οalcium peroxide, carrageenan, dietetically sucrose free
131

134. APPENDIX
DENτlFRlcE PRoDυcτs (Continued)
Brand Name
Abrasive Therapeutic
lnαredient lnqredient
Foaming
Aqent
Ultra BriteΘ Gel Hydrated silica sodium monofluorophosphate ο.76% sodium lauryl sulfate
αher lnqredients: sorbilol. water, PEG-12, ,lavor, celluiose qum, sodium saccharin, FD&c blue #1, D&c red #33
Ultra BriteΘ τoothpaste Hydrated silica, alumina sodium monolluorophosphate ο.76% sodium lauryl sulfate
othΘr lngredients: Glycerin, ce|lulose gum, sorbitol, carrageenan gum, titanium dioxide, sodium saωharin, flavor, tetrasodium
suc]ose frΦ
viadentΘ Fluoride Gel Hydrated silica Sodium monofluorophosphate ο.8% sodium lauryl sulfate
other lnoredients: sodium saωharin. zinc οh|oride, teaberry flaγor, sodium οarboxvmethylcellulose, sorbitol, sanguinaria extract
viadentΘ FIuoride TΦthpaste Hydrated silica sodium monofluorophosphate 0.8ol. sodium lauryl sulfate
Other lngredients: Sorbitol, titanium dioxide, carboxymethylcellulose, flavor, sodium saccharin, citric acid, zinc chloride, anhydrous
viadentΘ original Toothpaste Dicalcium phosphate Sodium lauryl sulfate
αher lngredients: Glycerin, sorbitol, titanium dioxide, zinc chloride, carrageenan, flavor, sodium saccharin, citric acid, sanguinaria
extract,
VinΦ Tooth Powder οalcium Φrbonate, sodium carbonate,
tricalcium ρhosρhate
other lnqredients: sodium alum, sodium oerborate monohvdrate, maοnesium trisilicate, sodium saccharin, flavor, D&c red
*carries
American Dental Association (ADA) seal indiΦting safety and etficacy.
tsodium bicarbonate can also be Φnsidered an abrasiνe.
+τopical fluoride product
Adapted with ρermission from Λ/onprescriρtion Products: Formutations & Features' companion to the Handbωk of Nonprescriρtion Drugs,1 1th ed,, \Λ/ashington, Dc, American
Pharmaceutical Association, 1998, 344-58.
132

135. APPENDIX
ORAL RINSE PRODUCTS
Brand Name Antiseptic Other lngredients
Astring-o-SolΘ Liquid SD alcohol 388 75.6%, methyl Water, myrrh extract, zinc chloride, citric acid
salicvιate
BetadineΘ Mouthwash/Gargle Alcohol 8.8% Povidone-iodine 0.5%, glycerin, sodium
saccharin, flavor
Bioteneo Mouthwash Lysozyme (6 mg), lactoferrin (6
mg) glucose oxidase (4000
units)
Water, xylitol, hydrogenated Starch, propylθne
glycol, hydroxyethylcellulose, aloe vera, naturaΙ
peppermint,
ρoloxamer 407, calcium lactate, zinc
gluconate, sodium benzoate, benzoic acid
Cepacolo Mouthwash/Gargle Alcohol 14%, cetylpyridinium
chloride 0.05%
EDTA disodium, color, flavor, glycerin,
polysorbate 80, saccharin, sodium biphosphate,
sodium phosphate, νvater, gluten free,
dieteticallv sucrose free
cepacolΘ Mouthwash/Gargle
(mint)
Alcohol 1 4.5%, cΘtylpyridinιum
chloride 0.5%
Color, flavor, glucono delta-lactone, glycerin,
poloxamer 407, sodium saccharin, sodium
gluconate, \Λ/ater, gluten free, dietetically
sucrose free
Dr. Tichenor'so Antiseptic Liquid SDA alcohol 38B 7oΥo Oil of peppermint, extract of arnica, \ivater, dye
free. qluten free
ListerineΘ- Liquid Alcohol 26.9%, eucalyptol
0.092%, thymol 0.064%,
methyl saliοylate 0.06%,
menthol O.O42"/"
Benzoic acid, poloxamer 407, caramel, water,
sodium benzoate
ListerineΘ- Lιquid
(freshburst, cool mint)
Alcohol 21 .6%, eucalyptol
0.092γ", thymol 0.064%'
methyl salicylate 0.06%,
menthol o.o42"λ
Water, sorbitol solution, poloxamer 4O7, benzoic
acid, flavor, sodium saccharin, sodium citrate,
citric acid, FD&C green #3, D&C yellow #10
(freshburst)
MentadentΘ Mouthwash
(οoo| mint, fresh mint)
Alcohol 10% νvater, Sorbitol, sodium bicarbonate, hydrogen
peroxide, poloxamer 407, sodium lauryl sulfate,
flavor, polysorbate 20, methyl salicylate (cool
mint), sodium sacοharin, phosphoric acid, blue
#1 ,
yellow #5 (cool mint)
Plaxo Advanced Formula
(mint sensation)
Alcohol 8.7% Water, sorbitol solution, tetrasodium
pyrophosphate, benzoic acid, tlavor, poloxamer
407, sodium benzoate, sodium lauryl sulfate,
sodium saccharin, xanthan gum, FD&C blue #1
Plax@ Advanced Formula
(original, SoftMlNT)
Alcohol 8.7% Sodium lauryl sulfate, water, sorbitol solution,
sodium benzoate, tetrasodium pyrophosphate,
benzoic acid, poloxamer 407, sodium saccharin,
ftavor (SoftMlNτ), xanthan gum (SoftMlNT),
flavor enhancer (SoftMlNT), FD&C blue #1
(SoftMlNT), FD&C yellow #5 (SoftMlNT)
S.T. 37Θ Solution Hexylresorcinol 0.1% Glycerin, propylene glycol, citric acid, EDTA
disodium. sodium bisulfite. sodium citrate
Scopeo Baking Soda SD alcohol 38F 9.9olo,
cetylpyridinium chloride,
domiphen bromide
Sorbitol, sodium bicarbonate, sodium saccharin,
flavor
Scopeo
(cool peppermint)
SD alcohol 38F 14%,
cetylpyridinium chloride,
domiphen bromide
Purified water, glycerin, poloxamer 407, sodium
saccharin, sodium benzoate, N-
ethylmethylcarboxamide, benzoic acid, FD&C
blue #1, flavor
TargonΘ Smokers' Mouthwash
(clean taste)
SDA alcohol 388 15.6% Water, glycerin, polyoxyl 40 hydrogenated caster
oil, sodium lauryl sulfate, dibasic sodium
phosphate, benzoic aοid, sodium saccharin,
caramel powder, dietetically sucrose free
TargonΘ Smokers' Mouthwash
(original)
SDA alcohol 388 16% Water, sodium saccharin, sodium benzoate,
glycerin, sodium lauryl sulfate, FD&C green #3,
FD&C yellow #5, polyoxyl 40 hydrogenated
castor oil, dietetically sucrose free
Tom's of Maineo Natural Mouthwash
(cinnamon, original)
Menthol ν1/ater, glyοerin, aloe vera juice' witch hazel,
poloxamer 335, spearmint oil, ascorbic acid,
alcoho! free
Viadent@ Oral Rinse Alcohol 10% Sanguinaria extract, gιycerin, polysorbate 80,
flavor, sodium saccharin, poloxamer 237, citric
acid, zinc chloride 0.2%
-carries
American Dental Αssociation (ADA) seal indicating safety and efficacy.
Note: sD alcohol refers to "sρecially denatured" alcohol.
Αdapted with permission from Nonprescription Products: Formulations & Features, companion to the Handbook of Nonprescriρtion Drugs,11th ed, Washington, Dc, American
Pharmaceutical Association,'1 998, 341-2.
133

136. APPENDIX
PREScRIPτIoN \MRITING
Doctor's Name
Address
Phone Number
Patient's Name/Date
Patient's Address/Age
Rx
Drug Name/Dosage Size
Disp: Number of tablets, caρsules, ounces to be dispensed (roman numerals added aS precaution for abused drugs)
Sig: Direction on how drug is to be taken
Doctor's signature
State license number
DEΑ number (if required)
PRESCRIPTTON REQUIREMENTS
1. Date
2. Full name and address of patient
3. Name and address of prescriber
4. Signature of prescriber
lf Class ll drug, Drug Enforcement Agency (DEA) number necessary.
lf Class ll and Class lll narcotic, a triplicate prescription form (in the state of california) is necessary and it must be handνvritten by the prescriber.
ABBREVIATIONS COMMONLY USED tN MEDICAL ORDERS
Abb.eviation From Meanino
each ear
134

137. APPENDlX
Abbreviation Faom Meaninq
h.
hs
t.M
t.v
ung
USAN
USP.
intramusular
intravenous
kcal..... "
kilocalorie
kg ... . .. .. ... . kilogram
L....... ...... liter
liq...... ...... liquor aliquor,solution
mcg..... ...... microgram
mEq..... ...... milliequivalent
mg...... ...... milligram
mixt..... ...... mixtura. ........ amixture
mL " "
milliliter
mm..... ...... millimeter
NF...... ...... NationalFormulary
no....... ..... numerus. ...... number
noc..... ..... nocturnal ...... inthenight
nonrep.. ..... nonrepetatur. .. donotreρeat,norefiιls
NPO
O, Oct
o.d.
o.l. . .
o.s.
oculuslaevus .... lefteye
oculussinister. ... lefιeye
o.u...,.. ....,. oculouteηue.. eacheye
pc,postcib .... postcibos. ...... aftermeals
ρer......
..... throughorby
PM..... ....,. postmeridiem. ... atternoonorevening
P.O...... ...... peros ........ bymouth
P.R...... ...... perrectum ...... rectally
ρrn.....' ...... prorenata... ... asneeded
ρulv,.... ...... pulvis .. aρowder
q .. . .. . . ... ... every
qad..... ...... quoquealternisdie
qd......
qh...... ...-.. quiaquehora
qs...... ..... quantumsutficiat.
qsad....
quam volueris
recipe......
reρetatur . . .
si opus sit.
statim....
suppositorium
syrupus . .
tabella . . .
every other day
θvery day
every hour
four times a day
every other day
a sutticient quantity
a sutticient quantity to make
quantity
as much as you wish
take, a reciρe
let it be repeated
without
aΦrding to art
saturated
subcutaneous
label, or let it be printed
solution
dissolve
one-half
if there is need
at once, immediately
supρository
syrup
tablet
such
three times a day
tincture
triturate
teaspΦnfuI
ointment
United States Adopted Names
United States PharmacopΘia
as directed
stne.....
sΦundumarlem....
tid...... ...... terindie
lr.ιinct... ...... tincture.
u.d..utdict. ..... utdictum
135
-

138. APPENDIX
SAFE WRITING PRACTICES
Health professionals and their support personnel τ. o.D. is not a safe abbreviation for once daily,
frequently produce handwritten copies of information as it is properly interpreted as meaning
,,right
they see in print; therefore, such information is eye" and has οaused liquid medications such
subjected to even greater possibilities for error or misin- as saturated solution of potassium iodide and
terpretation on the part of others. Thus, particular care Lugol's solution to be administered incorrectly.
must be given to how drug names and strengths are There is no safe abbreviation for once daily. lt
expressed when creating written healthcare documents. must be written out in full.
Τhe following are a few examples of safe writing rules
8' Do not USe chemical names such as 6-
suggested oy tne lnstitute for Safe Medication Prac-
mercaptopurine or 6-thioguaninΘ, as sixfold
tices, lnc.* overdoses have been given when these were
not recognized as chemical names. The proper
1. There should be a space between a number and names of these drugs are mercaptopurine or
its units as it is easier to read. Τhere should be thioguanine.
no periods after the abbreviations mg or mL'
g.
Do not abbreviate drug names (sFc, 6Mp, 5-
correct ]ncorrect ASA, MTX, HcτΖ' cPz' PBz' etc) as they are
'10 mg 10mg misinterpreted and cause error.
100 mg 100ms
10. Do not use the apothecary system or symbols.
2. Never place a decimal and a zero after a whole 11. Do not abbreviate microgram as μg; instead
number (2 mg is correct and 2.0 mg is
use mcg as there is less likelihood of
incorrect). lf the decimal point is not seen
misinterpretation'
because it falls on a line or because individuals 12. When writing an outpatient prescription, write a
are working from copies where the decimal complete prescription. A complete prescription
point is not seen, this causes a tenfold can prevent the prescriber, the pharmacist,
overdose.
and/or the patient from making a mistake and
can eliminate the need for further clarification.
3. Just the opposite is true for numbers less than The legible prescriptions should contain:
one. Always place a zero before a naked a. patient's full name
decimal (0'5 mL is correct' '5 mL is incorrect)'
b. for pediatric or geriatric patients: their age (or
4. Never abbreviate the word unit. The weight where applicable)
handwritten U or u, looks like a 0 (zero), and c. drug name, dosage form and strength; if a
may cause a tenfold overdose error to be drug is neγv or rarely prescribed, print this
made. information
5. lU is not a safe abbreviation for international d. number or amount to be dispensed
units. The handwritten lU looks like lV. Write e. complete instructions for the patient,
out international units or use int. units. including the purpose of the medication
6. e.D. is not a safe abbreviation for once daily, f. when there are recognized contraindications
as when the Q is followed by a sloppy dot, it
for a prescribed drug, indicate to the
looks like QlD which means four times daiΙv.
pharmacist that you are aware of this fact (ie,
when prescribing a potassium salt for a
patient receiving an ACE inhibitor, write "K
serum leveling being monitored")
*From
"Safe Writing" by Davis NM, PharmD and cohen MR, MS, Lecturers and consultants for Safe Medication Practices, 1143 \Ιr'right Drive,
Huntington Valley, PA 19006. Phone: [phone]-
136

139. APPENDlX
INSURANCE coDING FoR THE PERIoDoNTAL PAτIENT
Dealing with insurance is one of the most perplexing and sometimes frustrating aspects of clinical practice.
While the patient's insurance plan is, in actuality, an agreement between the patient and his employer, many
patients lose sight of this fact. Often, patients feel that the dentist has some say in the breadth and depth of
the patient's coverage. Limitations in coverage due to eligibility; waiting periods; deductibles; copayments;
yearly benefit maximums; calculation of the usual, customary, and reasonable (UCR) fee base; least expen-
sive alternative treatment (LEAT); least expensive, professionally acceptable alternative treatment (LΕPAAT),
and preexisting conditions may all play a role in the patient's ultimate coverage. lt is important for the
practitioner and office staff to understand the true nature of this relationship and be ready to assist patients in
understanding this as well. At no time should a practitioner knowingly falsify any insurance claim or use an
inappropriate code in order to gain additional benefits for the patient. This may lead to a charge of insurance
fraud against the practitioner, not the patient.
Sometimes patients will only agree to treatment that is covered by insurance. While this is their right, it is the
practitioner's obligation to treat the patient, not the patient's insurance plan. A comprehensive treatment plan
with sound alternatives covering the patient's dental needs must be presented to the patient with the patient
determining the course of action. Obtaining a predetermination of dental benefits from the insurance carrier
may be of some help to the patient in making treatment decisions. lnsurance carriers often request copies of
periodontal charting and radiographs in order to make payment or predetermination decisions. Maintaining a
record of what supporting documentation an insurance plan requires when a claim or predetermination
request is sent in may expedite payment or a response.
INSURANCE CODES OF PERIODONTAL IMPORTANCE
Adapted and used with permission from lhe Code on Dental Procedures and NomencΙature (CDT-3) available
from the Αmerican Dental Association and Current Procedural Terminology for Periodontics and lnsurance
Reporting Manual available from the American Academy of Periodontology. Commentary following each code
is of a general nature. lt is incumbent upon each clinician and/or office personnel to be apprised of details
related to specific insurance plans.
CLINICAL ORAL EVALUATION
D0120
D0140
D0150
Periodic oral examination: Completed on a patient of record at a specified interval. Additional diagnostic procedures
are reported separately.
Limited oral evaluation - problem focused: Used when a patient has been referred for a specific problem or
presents with an emergency, trauma, infection, or other unusual circumstance.
Comprehensive oral evaluation: This includes medical and dental histories, hard and soft tissue examinations,
caries exam, periodontal charting, occlusal analysis, and oral cancer screening.
RADIOGRAPHS/DIAGNOSTIC IMAGING
D0210
D0220
D0230
D0240
D0250
D0260
D0270
D0272
D0274
lntraoral - complete series (including bitewings): Vertical bitewings preferred for a patient \ivith periodontal disease
(author's note)
lntraoral: Periapical first film
lntraoral: Periapical each additional film
Intraoral: Occlusal film
Extraoral: First film
Extraoral: Each additional film
Bitewing: Single film
Bitewings: 2 films
Bitewings: 4 films
τEsτS AND LABoRAToRY ExAMINAτloNs
D0415 Bacteriologic studies for detΘrmination of pathologic agents: May include culture and sensitivity, DNA probe
analysis, and tests for susceptibility to periodonta| disease. Microbial testing may be payable under thΘ patient's
medical coverage.
Pulp vitality tests
Diagnostic casts
D0460
DO470
137
-

140. APPENDIX
INSURANCE coDING FoR TΗE PERIODONTAL PATIENT (Continued)
PREvΕNTlvE
D1 110 Prophylaxis - adult: lncludes scaling and polishing of supragingival areas. This code may also be used if tνvo visits
are necessary for the completion of the prophy|axis due to thθ heaviness of the tooth accumulated materials. A shod
narrative should accompany the second submission detailing the reason for the extra time needed to complete the
procedure.
D1 120 Prophylaxis - child
D12O4 Topical application of fluoride (prophylaxis not included) - adult
D'l205 Topical application of fluoride (including prophylaxis) - adult
D'l310 Nutritional counseling for control of dental disease
D1320 τobacco counseling for the control and prevention of oral diseasΘ
D1330 Oral hygiene instructions
ENDODONTICS
D3450 Root amputation - per root: Τhis procedure leaves the cro\Λ/n of the tooth intact.
D3920 Hemisection (including any root removal), not including root canal therapy: This entails the separation of the
crown of the tooth. May or may not retain all of the tooth sections
SURGICAL SERVICES-
*See
appropriate sections in the manual for procedure indications and descriptions.
SURGIcAL sERvlcEs (INcLUDING USUAL PosτoPERAτlvE cARE)
D4210 Gingivectomy or gingivoplasty - per quadrant
D4211 Gingivectomy or gingivopiasty - per tooth
D4220 Gingival curettage, surgicaΙ - per quadrant, by report: This is a detinitive surgical procedure requiring a short
narrative explanation for the rationale for use. code D4341 should not be reported with D4220. τhis procedure is not
thought to be any more beneficial than scaling and root planing in the treatment of periodontitis so it may not be
benefited.
D424O Gingival flap procedure, including root planing - per quadrant: This code may be used as the flap entry for a
-
regenerative procedure (combined with D4263, D4264, and/or D4266 or D4267).
D4245 Apically positioned flap
D4249 Clinica! crourn lengthening - hard tissue: Used to increase the clinical crown and is performed in a healthy
environment. This may require submission of a radiograph and a short narrative.
D4260 Osseous surgery (including flap entry and closure) - per quadrant: Performed in the presence of periodontal
disease to treat osseous defects. This procedure may require documentation including charting and possibly
radiographs of the area.
D4263 Bone replacement graft - first site in quadrant: Does not include flap access or cΙosure. Can be applied to
autogenous, allograft, and alloplast materials.
D4264 Bone replacement graft - each additional site in quadrant
D4266 Guided tissue regeneration - resorbable barrier, per site: Does not include flap access or closure.
D4267 Guided tissue regeneration - nonresorbable barrier, per site (includes membrane removal)
D4268 Surgical revision procedure, per tooth: Used to refine the results of the previousΙy described procedures.
D4270 Pedicle soft tissue graft procedure
D4271 Free soft tissue graft procedure (including donor site surgery): one code and fee should be used for one or t\Λ/o
adiacent teeth. Documentation should include the amount of recession, amount of remaining gingiva, influence of the
frenum (if applicable), and thΘ presence of inflammation.
D4273 Subepithelial connective tissue graft procedure (includes donor site surgery): This procedure should be coded
for each tooth that receives a graft.
D4274 Distal or proximal wedge procedure (when not performed in conjunction urith surgical procedures in the same
anatomic area)
NONSURGICAL PERIODONTAL SERVICE
D4320 Provisional splinting - intracoronal: lnterim stabilization for mobile teeth. ldentify the teeth involved and the nature
of the spιint.
D4321 Provisional splinting - extracoronal
D4341 Periodontal scaling and root planing, per quadrant: Used as a therapeutic, not prophylactic procedure. Usually,
only one or t\,,vo quadrants may be submitted on the same day of serviοe. Under special circumstances (ie, medical
considerations), this benefit may be extended to cover three or four quadrants treated at one visit. Many plans ask for
current periodontal charting, and possibly radiographs for an estimate of benefits to be completed.
D4355 Full mouth debridement to enable comprehensive periodontal evaluation and diagnosis: τhis procedure may be
used to remove plaque and calculus in order to complete the periodontal examination. This procedure should not be
interpreted as comprehensive therapy.
138

141. APPENDTX
D4381 Localized delivery of chemotherapeutic agents via a controlled release vehicle into diseased crevicular tissue,
per tooth, by report: This procedure does not replace conventional or surgical therapy required for debridement,
resective procedures, or regenerative therapy. Τhis code is used for any of the locally delivered agents'
OTHER PERIODONTAL SERVICES
D491o Periodontal maintenance procedures (fol]ouring active therapy): lncludes a reviΘ\λ/ of the medical history' plaque
control evaluation, scaling, and polishing. Τhis is done after the completion of active therapy and is not synonymous
with prophylaxis. There may be a 3-month waiting period after the completion of active therapy for some plans before
lhis benefit \,vill take effect.
D4920 Unscheduled dressing change (by someone other than treating dentist)
D4999 Unspecified periodontal procedure, by report
IMPLANτ sERvlcEs
D6010 Surgical placement of implant body: Endosteal implant: lncludes second stage surgery and placement of healing
cap.
D6020 Abutment placement or substitution: Endosteal implant
D6080 lmplant maintenance procedures, including removal of prosthesis, cleansing of prosthesis and abutments,
and reinsertion of prosthesis: lncludes prophylaxis of implant system.
D6o9o Repair implant suppoπed prosthesis, by report
D6095 Repair implant abutment, by report
D6100 lmplant removal, by report
D6199 Unspecified implant procedure, by report
OTHER SURGICAL SERVICES
D7280 Surgical exposure of impacted or unerupted tooth for orthodontic reasons (including orthodontic
attachments)
D7281 Surgical exposure of impacted or unerupted tooth to aid eruption
D7285 Biopsy of oral tissue: Hard, (bone, tooth)
D7286 Biopsy of oral tissue: Soft (all others)
D7291 Transseptal fiberotomy, by report
D732O Alveoloplasty, not in coniunction urith extractions, per quadrant
D734O Vestibuloplasty: Ridgeextension (secondaryepithelialization)
SURGICAL INCISION
D7510 lncision and drainage of abscess: lntraoral soft tissue
D7520 lncision and drainage of abscess: Εxtraoral Soft lissue
D7530 Removal of foreign body, skin' or subcutaneous alveoιar tissue
D754O Removal of reaction producing foreign bodies, musculoskeletal system
D7550 Sequestrectomy for osteomyelitis
oτHER REPAIR PRoCEDUREs
D7960 Frenulectomy (freneοtomy or frenotomy): Separate procedure
D7970 Excislon of hyperplastic tissue: Per arch
D7971 Excision of pericoronal gingiva
MISCELLANEOUS SERVICES
D91 10 Palliative (emergency) treatment of dental pain - minor procedure: Reported on a per visit basis for emergency
lreatment of dental pain.
D9230 Analgesia, anxiolysis, inhalation of nitrous oxide
D9248 Nonintravenous conscious sedation
D9310 Consultation (diagnostic service provided by dentist or physician other than practitioner providing treatment)
D9410 House/extended care facility call
D9910 AppΙicationofdesensitizingmedicament
D991 1 Application of desensitizing resin for cervical and/or root surface, per tooth
D9920 Behavior management, by report
139

142. APPENDIX
INSURANCE coDlNG FoR THE PERIODONTAL PATIΕNT (Continued)
D9930 Treatment of complications (postsurgical) - unusual circumstances, by report
D9940 Occlusal guard, by report
D9951 Occlusal adiustment: Limited
D9952 Occlusal adiustment: Complete
D9971 odontoplasty 1-2 teeth; includes rΘmoval of enamel proiection
D9999 Unspecified adiunctive procedure, by report
**NOTE:
Related procedures may be grouped together lvith the benefit being limited to the most inclusive procedure. This
may be true for the various steps involved in osseous surgery (incisions, flap, cleanout, scaling, ostectomy/
osteoplasty, flap apposition, and suturing). Any regenerative procedures done in conjunction with this (guided
tissue regeneration, bone replacement graft) would be considered additional procedures to the flap operation
itseif, even when performed in the same area at the same time.
There are a number of procedures where it would be inappropriate to repoft both services on the same treatment
date. Among those combinations that should not be reported together are:
D4341 and D4220 on the same day
D4355 and D0150 on the same day. The patient should be allowed to heal and the gingival edema to
resolve before completing the periodontal examination. This will allow for more accurate probe measure-
ments.
D4381 and D4341 Ιor the same teeth on the same day of Service. While the tooth to receive the locally
delivered antibiotic may be scaled before placement of the medication, definitive scaling should have been
completed at a previous appointment.
D4249 and D4260 for the same teeth on the same day of service. The clinical crown Ιengthening is
performed in a healthy environment and the osseous Surgery peι'formed where disease has been present.
Τhe American Αcademy of Periodontology has published a checklist for filing dental δlaims:
1. ls the form typed or printed legibly so that third party personnel can read and process the information
provided?
2. Are the "patient" and "dentist" sections completed accurately and completely, including employee identifica-
tion numbers, dates of birth, and information on the spouse for coordination of benefits?
3. Has the diagnosis been noted on the claim form? (Use the AAP disease classification found in Chapler 4 on
page 31.)
4. Have all procedures been identified by ADA codes and properly related to dates of services and fees?
5. Have the treatment areas and/or missing teeth been identified on the tooth chart?
6. Ηave "by report'' procedures and unusual services been noted in Section 61 on the claim form or described in
more detail on a separate sheet?
7. Has notation been made regarding specialty status, if any?
8. Has the patient signed and dated the claim form, or has a valid authorization/assignment form been signed by
the patient and has this been noted in the appropriate places as "signature on file?"
9. Has the insured person signed the form in the appropriate space in order for benefits to be paid directly to the
dentist if so desired (assignment of benefits)?
10. Has notation been made regarding prior (financial) agreement with the patient?
11. Has the form been signed and dated by the dentist?
12. Has a copy been filed in the office records?
Much of the paperwork involved with submitting insurance information has been eliminated by the use of
electronic filing. ln this way, the dental office may submit a paperless claim as soon as it is generated by the office
business software program to a clearinghouse for checking for completeness and then forwarded to the appro-
priate carrier. This decreases the busywork involved and often leads to more rapid return of a predetermination
decision and payout by the 3rd party carrier.
SELEcτED READINGS
Code on Dental Procedures and Nomenclature, CDT-3, Chicago, lL: American Dental Association, 1999.
Current Procedural TerminoΙogy for Periodontics and lnsurance Reporting Manual, CΛΙcago, lL: Ameriοan Academy of Periodontology, 20ο0
140

143. APPENDTX
SELECTED READINGS - GENERAL
Books
Cohen ES, Atlas of Cosmetic and Reconstructive Peiodontal Surgery,
2nd ed, Philadelphia, PA: Lea & Febiger, 1994.
Hall WB, Decision Making in Periodontology, 3rd ed, St Louis, MO:
Mosby-Year Book, 1998.
Lindhe J, Karring T, and Lang NP' Clinical PeriodontoΙogy and Implant
Dentistry, 3rd ed, Copenhage: Munksgaard, 1997.
Ne\Λ/land JR, Meiller TF, Wynn RL, and crossley HL' oral Soft Tissue
Diseases: A Reference ManuaΙ for Diagnosis & Management,2nd
ed, Hudson, OH: Lexi-Comp, lnc,2OO2-
Ne\Λrman MG, τakei HΗ, and CarranzaFA, carranza'S Clinical Periodon-
tology,glh ed, Philadelρhia, PA: WB Saunders' 2002'
Periodontal Literature Reviews: A Summary of Current ΚnowΙedge,
Chicago, lL: American Academy of Periodontology, 1996.
Sato N, Perlodontal Surgery: A Clinical Atlas, Chicago, lL: Quintessence,
2000.
Schluger S, Yuodelis R, Page RC, et al, Periodontal Diseases: Basic
Phenomena, Clinical Management, and Occlusal and Bestorative
ιnterreΙationships, 2nd ed, Phi|adeιphia, PA: Lea & Febiger, Phila-
delphia, 1990.
Stedman's Medical Dictionary, 27th ed, Philadelphia, PA: Lippincolt
Wiliiams & Wilkins, 2000.
The Merck Manual, 17th ed, West Point, PA: Merck, 1999.
τroνvbridge Ho and Emling Rc, lnfιammation: A Beview of the Process,
sth ed, Chicago, lL; Quintessence, 1997.
Wynn RL, Meiller TF, and Crossley HL' Drug ιnformation Handbook for
Dentistry, Tth ed, Hudson, OH: Lexi-Comp, lnc, 2001.
Proceedings
Proceedings of the 1989 World Workshop in Clinical Periodontology,
Chicago, lL: American Academy of Periodontoιogy, 1989.
"Proοeedings of the 1996 World Workshop in Periodontics," Ann Peri-
odontoΙ' 1 996' 1 :1 -932.
"Proceedings of the 1 997 Sunstar-Chapel Hill Symposium on Periodontal
Diseases and Human Health: Neι,v Directions in Periodontaι Medi-
cine," Ann Periodontol, 1998, 3:1-380.
"Proceedings of the 1999 lnternational Workshop for a Classification of
Periodontal Diseases and Conditions," Ann Periodontol 1999, 4:1-
1 08.
141

144. APPENDIX
SELECTED READINGS . SPECIFIC
CHAPTER 1: Problem-Based Periodontal
Diagnosis and Disease Management
Armitage G, "DevelopmΘnt oJ a Classification System 1or Periodontal
Diseases and Conditions," Ann Periodontol, 1 999, 4(1
):1
-6.
Dorlands's ΙtΙustrated Medicat Dictionary,23'd ed, Philadelphia, PA: WB
Saunders Co., 1957.
Goodson JM, τanner Αc, Haffajee ΑD, "Pafterns of Progression and
Regression of Αdvanced Destructive Periodontal Disease,'' J c/,n
P e ridonto Ι, 1 9a2' 9 :47 2-81'
Haffajee AD, socransky Ss, and Goοdson JM, "comparison of Different
Data Analysis Ιor Detecting Changes in Attachment Leνel,'' J clin
PeiodontoΙ, 1 983, 1 0:298_31 0.
Kornman K, Ne\,vman MG, Alvarado R, et al, "Clinical and Microbiologic
Patterns of Adults With Periodontitis," J Periodontol 1991, 62:634-
42.
Neν\,man MG, "lmproved clinical Deοision Making Using the Εvidence-
Based Approach," Ann Peiodontol 1996, 1(1):i-ix.
Socransky Ss, Haffajee ΑD, Goodson JM, et al, "New Concepts of
Destructive Periodontal Disease," J Clin Peridontol, 1984, 11:21-32.
The American Academy of Periodontology, Preceedings of the World
Workshop in Clinical Periodontics, Chicago, lL: American Academy
of Periodontology, 1989.
The American Academy of Periodontology' τhe Parameters of care,
Chicago, lL: American Academy of Periodontology, 2OO1.
CHAPτER 2: Anatomy, HistoIogy, and PhysioIogy
of the Periodontium
Bartold PM, Walsh LJ, and Narayanan AS, "Molecular and Cell Biology of
the Gingiva," PeridontoΙ 2000, 2ooo' 24i2a-55'
Beertsen W, Mcoulloch CA, and Sodek J, '"fhe Periodontal Ligament: A
Unique, Multifunctional connectiνe τissue," Periodontol 2000' 1997'
13:2O-4O.
Berkovitz BK, Moxham BJ, and Neγvman HN, Ihe Periodontal Ligament
in HeaΙth and Disease,2nd ed, St Louis' Mo: Mosby-\Λ/olfe' 1995.
Bosshardt DD and Selvig KA, "Dental cementum: Τhe Dynamic Tissue
covering of the Root," Periodontol 2000,1997, 13:41-75.
Cho Ml and Garant PR, "Development and General Structure of the
Periodontium," Peiodontol 2000, 20OO, 24(1):9-27 -
Gargiulo AW, Wentz FM, and Orban B, "Dimensions and Relations of the
Dentogingival Junction in Humans," J Periodontol, 1961, 32:261-7.
Hassell τM' '"Γissues and cells of the Periodontium,'' PeriodontoΙ 2000'
1993,3:9-38.
Mariotti A, '"fhe Extracellular Matrix of the Periodontium: Dynamic and
lnteraοtive τissues," Periodontol 2000, 1993' 3:39-63.
Nuki K and Hock J, '"Τhe organization of the Gingival vasculature," J
Periodontal Res, 1 974, 9(5):305-1 3.
Saffar JL, Lasfargues JJ, and Cherruau M, "Alveolar Bone and the Alve-
olar Prοcess: The Socket That ls Never Stable,'' Periodontol 2000'
1997, 13:76-90.
schroeder ΗE and Listgarten MA, '"The Gingival Tissues: The Architec-
ture o{ Periodontal Protection," Periodontol 2000,1997, 13:91-120.
sodek J and McKee MD, "Molecular and Cell Bio|ogy of Αlveolar Bone,''
Periodontoι 2oo0' 24(1
):99-1 26.
stern lB, "current concepts of the Dentogingival Junction: τhe Epithelial
and connective τissue Attachements tb the Tooth," J Peiodontol,
1981, s2(9):465-76.
τen cate AR' oraι HistoΙow: Deνelopment, Structure, and Fυnction /
A.R. τen Cate,41h ed, St Louis, Mo: Mosby, 1994.
OHAPτER 3: EtioIogy and cIassification of the
Periodontat Diseases
Aldred MJ and Bartold PM, "Genetic Disorders of the Gingivae and
Periodontium," Periodontoι 20oo' 1998' 18:7-20.
Armitage Gc, "Development oΙ a Classification System for Periodontal
Diseases and Conditions," Ann Periodontol, 1 999, 4(1
):1
-6.
Blieden τM, '"[ooth-Related lssues," Αnn Peiodontol, 1999, 4(1):91-7.
Brunsvold MA and Lane JJ, '"The Prevalence of Overhanging Dental
Restorations and Their Relationship to Periodontal Disease," J C/rn
P e riodontoΙ' 1 99o' 17 (2):67 -7 2'
Carnevale G, Sterrantino s, and DiFebo G' "Soft and Hard τissue
Healing Follo\Λ/ing Tooth Preparation to the Alveolar crest," /nt J
Periodontics Restorative Denf,'l 983, 3(6):36-53.
Caton J, "Periodontal Diagnosis and Diagnostic Aids," Proceedings of the
1989 World workshop in ClinicaΙ Peiodontics, chicago, lL: Amer-
ican Academy of Periodontology, 1989, l-1-32.
chandler JA and Brudvik Js' "clinical Evaιuation of Patients Eight to
Nine Years After Placement of Removable Partial Dentures," J Pros-
thet Dent, 1984, 51 (6):736-43.
Darueau RR, Tanner A, and Page RC, "The Microbial Challenge in Perio-
dontitis," Periodontol 2000, 1997, 1 4:12-32.
Flemmig τF, "Periodontitis,'' Ann Periodontol, 1999' 4(1):32-8.
Friedman RB, Gunsolley J, Gentry A, et al, "Periodontal status of ΗlV-
Seropositive and AIDS Patients," J Periodontol, 1991, 62(10):623-7.
Ηaber J and Kent RL, "cigarette Smoking in a Periodontal Practice," J
Periodontaι, 1 992, 63(2):1 00-6.
Ηaffajee A, Socransky s, Smith C, et al' "Microbial Risk lndicators for
Periodontal Attachment Loss," J Periodontal Res, 1991 , 26:292-6.
Hallmon WW, "occlusal Trauma: Effect and lmpaοt on the Periodon-
tiυm,'' Ann Periodontol, 1999, 4(1):102-8.
Holmstrup P, "Nonplaque-lnduced Gingival Lesions," Ann Periodontol,
1 999, 4(1 ):2ο-31
.
Holmstrup P and Westergaard J, "HlV lnfeοtion and Periodontal
Disease," Periodontoι 2o0o' 1998, 18:37-46.
"1999 lnternational Workshop {or a Classification of Periodontal Diseases
and conditions. Papers. oak Brook, lllinois, oοtober 3o-November
2,1999,' Ann PeriodontoΙ, 1999' 4(1):i' 1-112.
Kay Η, "criteria for Restorative contours in the Altered Periodontal Envi-
ronment,'' ιnt J Peiodontics Rest Dent,1984, 5(3):42-63.
Kinane DF, "Periodontitis Modified by Systemic Factors," Ann Peri-
od ontoι, 1 999, 4(1
):54
-64.
Kornman K, Crane A, Wang HY, et al, '"Γhe lnterleukin-1 Genotype As a
Severity Factor in Adult Periodontal Disease," J cΙin Periodontoι,
1997 , 24(1)i72-7.
Lalla E, Lamster lB, Drury S, et al, "Hyperglycemia, Glycoxidation and
Receptor for Αdvanced Glycalion Endproducts: Potential Mecha-
nisms Underlying Diabetic Complications, lncluding Diabetes-Asso-
ciated Periodontitls,'' Periodontoι 2oo0' 2oo0' 23:5o-62.
Listgarlen MA, "Structure of the Microbial Flora Associated With Perio-
dontal Health and Disease in Man. Α Light and Electron Microscopic
Study," J Periodontol, 1976, 47(1):1-18.
Loe H, Theilade E, and Jensen S, "Experimenlal Gingivitis in Man," J
P e riodontol, 1 965, 36:1 77 -87.
Mariotti A, "Dental Plaque-lnduced Gingival Diseases," Ann Periodontol,
1999,4(1):7-19.
Mealey B, PeiodontaΙ Medicine, Rose L, Genco R, cohen DW, et al,
eds, Hamilton, Ontario, Canada: BC Decker lnc, 2000, Chapter I,
121-5ο.
Meng ΗX, "Periodontal Αbscess,'' Ann Periodontoι, 1 999, 4(1 ):79-83.
Meng HX, "Periodontiο-Endodontic Lesions,'' Ann Periodonιo1 1999'
4(1 ):84-90.
Νovak MJ, "Necrotizing Ulcerative Periodontitis"' Ann Periodontol, 1999,
4(1):74-8.
αomo-corgel J and Steinberg B, "Periodontal Management and the
Female Patient," Periodontal Medicine, Rose L, Genco R, Cohen
DW, et al, eds, Hamilton, Ontario, Canada: BC Decker lnc, 2000,
chaρter 9, 151-66.
142

145. APPENDIX
Pack AR, Coxhead LJ, and McDona|d BW, "Periodontal Management oΙ
Overhanging Margins in Posterior Amalgam Restorations and Perio-
dontal consequences," J clin Periodontoι, 1990, 17(13):145-52'
Papapanou PN, "Periodontal Diseases: Epidemiology," Ann Periodontol,
1996,1(1):1-36.
Pini Prato GP, "Mucogingival Deformities," Ann Periodontol 1999,
4(1
):98-1
01 .
Preber H and Bergstrom J, "EΙfect of cigarette Smoking on Periodontal
Healing Following Surgical τherapy,'' J cιin Periodonfol 1990'
17(5)t324-8.
Preber H and Bergstrom J,'"τhe Effect of Nonsurgical τherapy on Perio-
dontal Pockets in Smokers and Nonsmokers," J CIin Periodontol,
1 986, 1 3(4):31 9-23.
RamS T, ''Γhreshold Values," oMTS Newsletter' 1993' 2(2). oral Microbi-
ology Testing Service, Medical College of Pennsylvania.
Rees TD, "Drugs and Oral Disorders," Periodontol 2000, 1998, 18:21-36.
Rees T, "Periodontal Management ol the Patient With Diabetes Mellitus,"
Periotontol 2000, 2O0O, 23(1):63-72.
Rowland RW, "Necrotizing Ulcerative Gingivitis," Ann Periodontoι, 1999,
4(1 ):65-73.
Scully C and Laskaris G, "Mucocutaneous Disorders," Periodontol 2000,
1998,18:81-94.
Ten cate AR, oraΙ Histology: Deveιopment, Structure, and Function /
A.R. Ten Cate,4h ed, St Louis, MO: Mosby, 1994.
Theilade Ε, \,γright WH, Jensen SB, et al, "Experimental Gingivitis in
Man. ll. A Longitudinal Clinical and Bacteriological lnvestigation," J
Periodontal Fes, 1966, 1:1-13.
Tonetti MS and Mombelli A, "Early-onset Periodontitis," Ann PeriodontoΙ'
1 999, 4(1 ):39-53.
zambon JJ, Grossi SG, Maοhtei EΕ, et al, "Cigarette Smoking lncreases
the Risk of Subgingival lnfection Vyith Periodontal Pathogens," J
Periodontol, 1 996, 67(10 Suppl):1050-4.
Zambon JJ, "Periodontal Diseases: Microbial Factors," Ann Periodontol,
1 996, 1 (1
):879-925.
CHAPTER 4: Clinical Assessment, Diagnosis, and
Treatment Planning
Aeppli DM, Boen JR, and Bandt CL, "Measuring and lnterpreting
lncreases in Probing Depth and Attachment LoSs," J Periodontoι,
1 985, s6(5):262-4.
American Academy of Periodontology. The Parameters of Care,
Chicago, lL: Αmerican Aοademy of Periodontology, 2001.
American Academy of Periodontology. chemicaι Agents for Control of
Plaque and Gingivfflb, Chicago, lL: Αmerican Αcademy of Periodon-
tology,1994.
Armitage Gc, "Development of a Classification System for PeriodontaΙ
Diseases and Conditions," Ann Periodontol, 1999, 4(1):1-5.
Armitage Gc, "οlinical EvaΙuation of Periodontal Diseases," Periodontol
2000, 1995, 7:39-53.
Atassi F, Nel,vman ΗN, and Bulman JS, "Probe Tine Diameter and
Probing Depth,'' J cιin PerΙodontoΙ' 1992, 19(5):301-4.
Beck JD, Koch GG, Zambon JJ, et al, "Evaluation of Oral Bacteria as
RiSk lndicators for Periodontitis in older Adults"' J Periodontoι,
1 992, 63(2):93-9.
Greenstein G, Polson A, lker H, et al, "AssociaΙions Betνveen crestal
Lamina Dura and Periodontal status," J Periodontoι' 1981
'
52(7):362-6.
Jeffcoat MK, Wang lC, and Reddy MS, "Radiographic Diagnosis in Perio-
dontiοS,'' Periodontol 2000, 1995, 7:54-68.
Kennedy JE, Bird WC, Palcanis KG, et al, "A Longitudinal Evaιuation of
varying Widths of Attached Gingiva,'' J CΙin Periodonιol 1985,
12(8)i667-75.
Kornman K and Wilson T, '"τhe Presumptive Diagnosis and Diagnosti-
cally Driven Therapy," Fundamentals in PerΙodontics, Chicago, lL:
Quintessence Publishing Company lnc, 1996, Chapter 16, 293-317.
Lamster lB and Grbic JΤ, "Diagnosis of Periodontal Disease Based on
Analysis of the Host Response," Periodontol 2000,1995, 7:83-99.
Lindhe J, Socransky SS, Nyman S, et al, "Critical Probing Depths in
Periodontal τherapy," J CΙin PeriodontoΙ' 1982, 9(4):323-6.
Listgarten MA, "Periodontal Probing: What Does lt Mean?" J Clin Peri-
odontoι, 1980, 7(3):1 65-76.
Listgarten MA, Mao R, and Robinson PJ, "Periodontal Probing and the
Relationship oΙ the Probe Tip to Periodontal τissues,'' J Periodontol,
1 976, 47(9):51 1 -3.
McGuire MK, "Prognosis versus Actuaι outcome: A Long-Term Survey
of 100 τreated Periodontal Patients Under Maintenance Care,'' J
Periodontoι, 1991, 62(1 ):51-8.
McGuire MK and Nunn ME, "Prognosis Versus Actual outcome. ll' Τhe
Effectiveness of clinical Parameters in Developing an Aοcurate
Diagnosis," J PeriodontoΙ, 1996, 67(7):658-65'
McGuire MK and Nunn ME, "Prognosis Versus Αctual outcome. lll. τhe
Effectiveness o{ Clinical Parameters in Accurately Predicting Tooth
Survival," J Periodontol, 1 996, 67(7):666-74.
Papapanou PΝ and Tonetti MS, "Diagnosis and Epidemiology of Perio-
dontal Osseous Lesions," Periodontol 2000, 20OO, 22(1):8-21.
Perlitsh M, "Periodontal Risk Assessment, Diagnosis and Treatment
Planning," Dent CΙin North Am, 1980' 24(2):177-93.
Pihlstrom BL, "Periodontal Risk Αssessment, Diagnosis and τreatment
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CHAPTER 5: Prevention of Disease and
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ffi;"'ΞLx'ι:a:Ψ:l
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143

146. APPENDIX
SELECTED READINGS - SPECIFIC (Continued)
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PeriodontaΙ 2000' 2oo1
'
25:.110-3.
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OHAPτER 6: NonsurgicaI Treatment: ScaIing and
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CHAPTER 7: Surgical Treatment: Principles
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Hawley CE and serio FG, "PeriodontaΙ Wound Healing'', clark'S cΙinicaΙ
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Malamed s, "Physical and Psyοhological Evaluation," Sedation: A Guide
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144

147. APPENDIX
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CHAPTER 8: Surgical Treatment: Repair,
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McOΙain PK and schallhorn RG, "Focus on Furcation Defeοts - Guided
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):681
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Polson AM, ed, Peiodontaι Regeneration: current Status and Directions,
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Ramfjord SP, Εngler Wo, and Hiniker JJ, "A Radioautographic Study o,
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Rosen PS, Reynolds MA, and Bowers GM, "Τhe Τreatment of lntrabony
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Samchukov ML, cope JB, cherkashin AM, eds, CraniofaciaΙ Distraction
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Sanz M and Giovannoli JL, "Focus on Furcation Defects: Guided Tissue
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Schallhorn RG, "Postoρeralive Problems Associated \Λ/ith lliaο Trans-
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Schallhorn RG and McClain PK, "Combined Osseous Composite
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Schluger S, "osseous Resection - A Basiο Principle in Periodontal
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Wagenberg BD, Εskoνv RN, and Langer B, "Exposing Adequate Tooth
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'or
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OΗAPτER 9: SurgicaI Treatment: Periodontal
Plastic Surgery
Αllen EP and Miller PD Jr, "coronal Positioning of Existing Gingiva:
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'
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'
7o(3)i24-8'
Garber DA and Salama MA, '"τhe Aesthetic Smile: Diagnosis and Treat-
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145

148. APPENDIX
SELEOTED RΕADINGS
_ sPEclFlc (Continued)
Jorgensen MG and Noνvzari H,'Aesthetic cro\,νn Lengthening,'' Peri- ννennstrom JL, "Mucogingival τherapy," Ann Periodontoι 1996,
odontol 2000, 2OO1, 27:45-58. 1 (1
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Kois Jc, "τhe Restorative-Periodontal Interface: Biological Parameters," \Λ/ennstrom J and Pini Prato GP, "Mucogingival Τherapy," cιinicaΙ Perio-
Peiodontol 2000' t996' 11:29-38
'".,AE:?{tr:"EξHι";ιEift.'"];'J'[1}:',ffi:1sT"g.1s::
Langer B and calagna L,
*Γhe
subepithelial connective Tissue Graft,"
Prosthet Dent, 1 98ο, 44(4):363-7.
Langer B and Langer L, "subepithelial Conneclive Tissue Graft Tech- CHAPTER 10: Periodontal EmergenCieS
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Dumsha Tc and Gutmann JL, CΙinician's Εndodontic Handbook,
Miller PD, "Periodontal Plastic Surgical Techniques for Regeneration," Hudson, OH: Lexi-Comp, lnc, 2OOO.
Peiodontal Regeneration: Current Status and Directions, Polson
AM, ed' Chicago, lL: Quinlessence Books, 1994,53-70.
Holmslrup P,
,,Νonplaque_lnduced
Gingival Lesions,,, Ann Periodontoι,
Miller PD Jr, "Root coverage Using the Free soft τissue Autograft
1999,4(1):20-9.
FollowingCitricAcidApplication.|ll'Asuccessful andPredictable
MengHX,,,Periodontal Αbscess,,,AnnPeriodontoΙ,1999,4(1):79-83.
Procedure in Areas of Deep-Wide Recession," ιnt J Periodontics
Restorative Denl 1985' 5(2):14'37'
Meng HX, "Perιodontic-Endodonic Lesions,'' Ann Periodonfol 1999,
Miller PD Jr and Αι|en EP,'"rhe Development of Periodontal Plastic
4(1):84-9-
Surgery"', Periodontal 2oo0' 1996' 1 1 :7-17'
Ne\Λ,land JR, Meiller TF, Wynn RL, et al, orat Soft Tissue Diseases: A
Pini Prato GP, clauser c, τonetti MS, et al, "Guided Τissue Regenera- 1?!9',:!::
Manual for Diagnosis and Management' 2"d ed' Hudson'
tion in Gingivat Recessions,"
periodontot 2000,1996, 11;;9:#.
oH: Lexi-comp' lnc' 2001'
sato N, Periodonta! Surgery: A cιinΙcat Attas, chicago lL: Quintessence
Rowland^RW, "Necrotizing Ulcerative Gingivitis," Ann Periodontoι'
Publishing company, iooo.
4(1):65-73'
Seibert JS, 'Reconstruction of Deformed, Partially Edentulous Ridges,
H]}YJy'::Η:}?"Z?i};ΙΕ!'1!";#itr::xiij,%?and
Wound
cHAPTER 11: Considerations in tmplant Dentistry
seibert JS and Lindhe J, "Esthetics in Periodontal Theraρy,'' Ctinicat Donley τG and Gillette WB, "Titanium Endosseous lmplant-soft τissue
PeriodontoΙogy and Ιmplant Dentistry,3,d ed, Lindehe
j,'karring
τ, lnterface: A Literature Review,'' J PeriodontoΙ, 1991' 62(2):153-60.
and Lang NP, eds, Copenhagen, Denmark: Munksgaard lnterna-
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Seibert JS and Salama H, 'Αlveolar Ridge Preservation and Reconstruc- 1994, 5(4):191-201 .
tion,'' Periodontoι 2000' 1996' 11:69_84.
Meffert RM, "Maintenance of Dental lmplants"' contemporary Ιmplant
Serio FG and strassler HΕ, "Perio_esthetic Troubleshooting: Solutions for Dentistry,2nd ed' Misch CE ed, St Louis, Mo: Mosby-Yearbook, lnc,
the Unexpected,'' J Εsthet Dent,1997, 9(6):317_26.
1 999, 647-61 .
Sullivan HC and Αtkins JH, "Free Autogenous Gingival Grafts: l. Princi- Wilson TG Jr, "A Typical Maintenance visit for Patients With Dental
ples of Successful Grafting," Periodontics, 1 968, 6(3):1 21 -9. |mplants," Periodontoι 2000, 1996' 12:29.
146

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A Patient Guide to Dental lmplants and
A Patient Guide to Root Ganal Therapy
An idealtoolto educate your patients
81/2" x 1 1 " colorJul tabbed flip chart explaining each of the steps involved
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151. l
D]ug Informa$οn
Handhoolι fοr
Defiistry
The most complete and
concise drug reference for
all dental professionals
COMPREHENSIVE:
Covers over 6,980 dental &
medical drugs!
Each monograph gives local
anesth etic/vasoconstrictor
precautions, effects on dental
treatment, and drug interactions.
It includes sections on medically-
compromised patients and management of patients \ivith
specific oral conditions (with sample prescriptions) including:
oral pain, oraUbacterial infections, periodontal disease, etc.
EASY-TO-USE:
This book is alphabetically organized like a dictionary and
fully cross-referenced by page number. There are 7 unique
tabbed sections, and Therapeutic Category and Αlphabetical
lndices.
Oral soΙlι
Tisue
Iliseases
A Reference Manual
for Ιliagnosis &
Management
Designed for all
dental professionals
This pictorial reference is
visually-cued with over
160 high quality color
photos. lt is designed to
assist in the diagnosis and
management of oral soft
tissue diseases. The easy to use sections include the
diagnosis proοess: obtaining a history examining the patient'
establishing a differential diagnosis, selecting appropriate
diagnostic tests, interpreting the resuιts, etc. The sections
cover the following topics: White Lesions; Red Lesions;
Blistering-sloughing Lesions; Ulcerated Lesions; Pigmented
Lesions; Papillary Lesions; Soft Tissue Swelling (each lesion
is illustrated with a color representative photograph); Drug
Section (specific medications for treatment); and a Special
Topics section.
Glinician's
End0dοntic
Handhο0lι
Designed for all dentists with
21 endodontic topics every
dentist can use.
Designed for all general practice
dentists, this is a quick reference
addressing current endodontics. lt
has a easy-to-use format and
alphabetical index. lncludes latest techniques, procedures,
and materials including: root canaΙ therapy: why's and why
nots; a guide to diagnosis and treatment of endodontic
emergencies; facts and rationale behind treating
endodonticaΙly-involved teeth; straight{orward dental trauma
management information; pulpal histology, access openings,
bleaching, resorption, radiology, restoration, and
periodontal/endodontic complications. Also includes a
Frequently Αsked Questions (FAQ) section and "Clinical
Note" sections throughout.
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Medical
EmergenGiθs
Designed specifically
for general dentists
during times of
emergency. A tabbed
paging system allows
for quick access to
specific crisis events.
Created with urgency in
mind, it is spiral bound
and drilled with a hole in
the upper left corner for hanging purposes. The easy to use
sections include: Basiο Action Plan for Stabilization; Αllergic /
Drug Reactions; Loss of Consciousness / Respiratory
Distress / Chest Pain; Altered Sensation / Changes in Affect;
Management of Aοute Bleeding; office Preparedness /
Procedures and Protocols; Automated External Def ibrillator
(AED); and Oxygen Delivery
New soon t0be
fu:finamia:Ι
Lεx.CoιηB lιιc
www.lexi.com
For more information or
to order call:
1 -800-837-5394
released!titles
in the Dental Practice +F
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152. Manual 0Ι Glinical Periοdontics
) Uisually_cued with oυer 220 high quality color photos
) Organized by basic principles
) Presented in a "Question & Answer" format
) Recοmmendations for treatment, inοluding sample
treatment plans
12 Ghapters Tabbed for Easy Access:
o PROBLΕM-BASΕD PER|ODONTAL D|AGNOS|S
Θ ANATοMY HISΤοLοGY AND PHYSIοLοGY
Θ ETIοLoGY AND DISEASΕ cLASSlFlcATloN
Θ ΑSSESSMENI DIAGNoSIS, AND TRΕATMENT PLANNlNG
Θ PREVΕNTιON AND MA|NTΕΝANCE
Θ NοNSURGIcAL TREATMΕNT
Θ SURG]OAL TRΕAΤMENΤ: PRlNClPLES
Θ REPAIR, RΕSECTION, AND REGENERATION
Θ PERIoDοNTAL PLASTIc SURGERY
@ PERIODONΤAL EMERGENcIES lm
Θ IMPLΑNΤ cOΝSIDERAΤIΟNS
v
Lεxl,Coιηη lπc
@ APPENDIX.
u,urw.texi.com
- Medical Considerations
- Oral Health Products
- Prescription Writing
- lnsurance Coding
- Selected Readings
Category: Dentistry, Periodontics, Dental Hyσiene
Providing unique publishing serviοes
to the healthcare industry
TSBN * 1_ΞΞE5Ξθ_θΞ-Ξ
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