PERIODONTAL ABSCESS

PERIODONTAL ABSCESS

1. ABSCESS OF THE
PERIODONTIUM
PRESENTED BY
SHILPA SHIVANAND
II MDS

2. Contents
Introduction
Abscess of the periodontium
Periodontal abscess
ODefinition
OPrevalence
OClassification
OEtiology
OClinical features

3. OPathogenesis and histopathology
OMicrobiology
ODiagnosis
ODifferential Diagnosis
OTreatment
OComplications and postoperative care.
Gingival abscess
Pericoronal abscess
Conclusion
References

4. INTRODUCTION
O Abscess- Localised collection of pus purulent material
collected in a cavity caused by destruction of tissues.
(GPT)
OAbscesses of the periodontium have been classified
primarily, based on their anatomical locations in the
periodontal tissue. There are three types:
OGingival abscess
OPericoronal abscess
OPeriodontal abscess.

5. OAmong all the abscesses of the periodontium, the
periodontal abscess is the most important one, which
often represents the chronic and refractory form of the
disease.
O It is a destructive process occurring in the
periodontium, resulting in localized collections of pus,
communicating with the oral cavity through the
gingival sulcus or other periodontal sites and not arising
from the tooth pulp

6. Periodontal Abscess
OA localized purulent infection within the tissues
adjacent to the periodontal pocket that may lead to the
destruction of periodontal ligament and alveolar bone

7. DEFINITION
OA periodontal abscess is a localized
purulent infection in the periodontal tissue

(GLICKMAN)
OA localized purulent inflammation of the periodontal
tissues. It is also known as Lateral periodontal abscess
or Parietal Abscess.

(AAP GLOSSARY 1992)

8. OAn acute, destructive process in the periodontium
resulting in localized collection of pus communicating
with the oral cavity through the gingival sulcus or other
periodontal sites & not arising from the tooth pulp.
(RANNY 1977)

9. OA lesion with an expressed periodontal break down
occurring during a limited period of time & with easily
detectable clinical symptoms with a localized
accumulation of pus located within the gingival wall of
the periodontal pocket.
(Hafstrom et al-1994, Dewitt et al1985)

10. CLASSIFICATION
I) Depending on the location of the abscess
(Gillette and Van House-1980, AhI et al 1986)
 Gingival Abscess – localized painful swelling
affecting only the marginal and interdental gingiva
Mainly due to impaction of foreign objects
May be present on a previously healthy gingiva
 Periodontal Abscess – with similar symptoms,
usually affect deeper periodontal structures, including
deep pockets, furcations and vertical osseous defects.
usually located beyond Mucogingival junction.

11. II) Depending on the course of the lesion
(Galego-Feul et al-1995, Carranza - 1990)
 Acute periodontal abscess.
• Presents with symptoms like pain, tenderness,
sensitivity to palpation and suppuration upon
gentle pressure.
 Chronic periodontal abscess.
• Normally associated with a sinus tract.
• Usually asymptomatic, can refer mild
symptoms

12. III. Depending on the number
(Topell et al 1990)
Single periodontal abscess – related to local factors,
which contribute to the closure of the drainage of a
periodontal pocket.
Multiple periodontal abscess
OSeen in uncontrolled diabetes mellitus,
Omedically compromised patients,
Oin patients with untreated periodontitis after systemic
antibiotic therapy for non-oral reasons .

13. IV. According to periodontal tissue affected
(Meng -1999)
Gingival abscess - in previously healthy sites and
caused by impaction of foreign bodies.
Periodontal abscess – either acute or chronic
developing into a periodontal pocket.
Pericoronal abscess – in incompletely erupted
teeth.

14. V. Depending on the cause of acute infectious
process
(Lindhe)
 Periodontitis related abscess: - when the acute
infection originates from biofilm present in a
deepened periodontal pocket.
 Non-periodontitis related abscess: - when the
acute infection originates from other local source,
such as foreign body impaction or alteration in
root integrity.

15. VI. Based on location of abscess
(Carranza)
Abscess in the supporting periodontal tissues along
the lateral aspect of the root, sinus tract present.
Abscess in the soft tissue wall of a deep periodontal
pocket.

16. PREVALENCE
O3rd most prevalent emergency infection, after acute
alveolar (14-25%) and periodontitis (10-11%).
OMore likely to occur in a pre-existing periodontal
pocket.
OMore in molar sites (> 50%)

17. OThe prevalence of periodontal abscesses has been
studied in emergency dental clinics (Galego-Feal et al.
1996, Ahl et al. 1986)
OIn general dental clinics (Lewis et al. 1990)
OIn periodontitis patients before and during periodontal
treatment (Gray et al. 1994) and
OIn periodontitis patients during periodontal maintenance

18. OGray et al (1994) monitored periodontal patients in an
army clinic and found that periodontal abscess had
prevalence of 27.5%. In this population, 13.5% of
patients undergoing active periodontal treatment had
abscess formation and while in untreated patients it is
59.7%.

19. OKaldahl et al (1996) in a 7-year prospective
longitudinal treatment study for occurrence of
periodontal abscess. From the 51 patients included, 27
developed abscesses were detected.
O16 out of the 27 abscess sites had an initial probing
pocket depth greater than 6 mm, and in about 8 sites
the periodontal probing depth was 5-6 mm.

20. ETIOLOGY
OPeriodontal abscesses have been either directly
associated to periodontitis or to sites without the
prior existence of a periodontal pocket.
1.Periodontal abscesses in periodontitis
(Periodontitis – Related Abscess)
OIn periodontitis, a periodontal abscess represents a
period of active bone destruction (exacerbation).
OThe existence of tortuous pockets, with cul-de-sac,
which eventually become isolated, may favor the
formation of abscesses .

21. OThe marginal closure of a periodontal pocket, may lead
to an extension of the infection into the surrounding
periodontal tissues due to the pressure of the
suppuration inside the closed pocket.
OThe fibrin secretions leading to the local accumulation
of pus may favor the closure of the gingival margin to
the tooth surface.
OChanges in the composition of the microflora, bacterial
virulence, or in host defenses (Kareha et al. 1981)
could also make the pocket lumen inefficient to drain
the increased suppuration.

22. OThe development of a periodontal abscess in
periodontitis may occur at different stages during the
course of the infection:
OAs an acute exacerbation of an untreated periodontitis
(Dello Russo 1985)
ODuring periodontal therapy (Dello Russo 1985,
Carranza 1990)
OIn refractory periodontitis (Fine 1994) or
ODuring periodontal maintenance (Chace & Low 1993,
McLeod et al. 1997)

23. Different mechanisms behind formation are
A.Exacerbation of chronic lesions:
Occur without any obvious external influences.
B. Post therapy periodontal abscess
Post scaling periodontal abscess –occur
immediately after scaling or routine prophylaxis.
Odue to inadequate scaling which will allow calculus
to remain in the deepest pocket area,

24. Owhile the resolution of the inflammation at the coronal
pocket area will occlude the normal drainage and then
cause the abscess formation.
OWhen the periodontal abscess occurs immediately after
scaling or after a routine prophylaxis, it has been related
to the dislodging of calculus fragments, which can be
pushed into the tissues.

25. Post-surgery periodontal abscess.
OIncomplete removal of sub gingival calculus or the
presence of foreign substance. Ex-sutures, regenerative
devices or periodontal pack.
Oclinical study on guided tissue regeneration reported
that 10 out of 80 controls (non-resorbable barrier) and 4
out of 82 tests (bio-absorbable barrier) showed abscess
formation or suppuration at the treated sites.
(Garrett et al 1997)

26. Post-antibiotic periodontal abscess.
OTreatment with systemic antibiotics without subgingival
debridement in patients with advanced periodontitis
may also cause abscess formation.
OIt is Attributed to a likely change in the composition of
subgingival microbiota, leading to a super infection and
massive inflammation.

27. OTopell et al (1990) reported on the development of
multiple abscess (4-10) in 10 untreated periodontal
patients who received systemic antibiotic therapy.
(Penicillin, tetracycline) for non-oral infections.
OHelovuo et al. (1993) studied 72 patients with untreated
periodontitis, who were followed for 12 weeks, after
intake of systemic antibiotics for non-oral reasons.
Patients were divided into 3 groups according to the
antibiotic used,

28. O10 out of 24 patients (42%) in the penicillin group
developed abscesses within the next 4 weeks.
OThe number of abscesses ranged between 1-10. No
abscesses were detected in the erythromycin or the
control groups.
OKoller-Benz et al. (1992) showed that after initiation of
nifedipine therapy, 8 abscesses appeared in 5 days.
OThe nifedipine therapy was discontinued, and the
abscesses resolved. 3 weeks later the treatment was
resumed, and after 2 weeks another abscess was
detected.

29. 2. Periodontal abscesses in the absence of Periodontitis
OImpaction of foreign bodies. Periodontal abscesses
caused by foreign bodies, related with oral hygiene
aids, have been named "oral hygiene abscesses“.
OPerforation of the tooth wall by an endodontic
instrument (Carranza 1990)
OInfection of lateral cysts (Kareha et al. 1981)
OLocal factors affecting the morphology of the root
may predispose to periodontal abscess formation

30. PATHOGENESIS AND
HISTOPATHOLOGY
OThe entry of bacteria into the soft tissue pocket wall
could be the first event to initiate the periodontal
abscess.
OInflammatory cells are then attracted by chemotactic
factors released by the bacteria, and
OThe concomitant inflammatory reaction leads to
destruction of the connective tissues, the encapsulation
of the bacterial infection and the production of pus.

31. OHistologically, the intact Neutrophils are found
surrounding a central area of soft tissue debris and
destroyed leukocytes.
OAt a later stage a pyogenic membrane, composed of
macrophages and neutrophils is organized.
OThe rate of destruction in the abscess will depend on the
growth of bacteria and its virulence as well as the local
pH, since an acidic environment will favour the activity
of lysosomal enzymes

33. De Witt et al. (1985) studied biopsy punches taken from
12 abscesses. They observed, from the outside to the
inside:
(a) A normal oral epithelium and lamina propria;
(b) An acute inflammatory infiltrate;
(c) An intense foci of inflammation (neutrophil-
lymphocyte) with the surrounding connective tissue
destroyed and necrotic;
(d) A destroyed and ulcerated pocket epithelium;
(e) A central region, as a mass of granular, acidophilic,
and amorphous debris.

35. MICROBIOLOGY
OThe most frequent type of bacteria were gram-negative
anaerobic rods and gram-positive facultative cocci. In
general, gram-negatives predominated over gram-
positives and rods over cocci.
OThe periodontal abscess microbiota is usually
indistinguishable from the microflora found in the
subgingival plaque in adult periodontitis.
OThe microflora from abscesses and deep pockets was
similar and harbored higher proportions of pathogens
when compared to the microflora of shallow pockets.

36. OBacterial species with capacity of producing proteinases,
such as P. intermedia, are important, since they may in-
crease the availability of nutrients, and thereby, increasing
the number of bacteria inside the abscess (Jansen & Van
der Hoeven 1997)

37. Culture studies of periodontal abscesses have revealed
high prevalences of
Porphyromonas gingivalis (55-100%),
Prevotella intermedia (25-100%), and
Fusobacterium nucleatum (44-65%) other pathogens
Which have been reported are
Actinobacillus actinomycetemcomitans (25%)
Campylobacter Rectus (80%)
Prevotella Melaninogenica (22%)

38. OClinical Features
 Smooth, shiny swelling of the gingiva
 Painful, tender to palpation
Purulent exudate
Increased probing depth
Mobile and/or percussion sensitive
Tooth usually vital

41. DIAGNOSIS
Diagnosis should be based on
OPatients chief complaint
OClinical signs and symptoms
OAdditional information can be obtained through a
careful medical and dental history, and radiographic
examination.
OSymptoms range from light discomfort to severe pain,
tenderness of the gingiva, swelling, tooth mobility,
tooth elevation, sensitivity of the tooth to palpation

42. OAnother common finding is suppuration, either
spontaneous or after pressure on the abscess combined
with rapid tissue destruction and deep pocket formation.
OThe radiographic examination may reveal a normal
appearance, or some degree of bone loss, ranging from
a widening of the periodontal space to a dramatic
radiographic bone loss.
OSystemic involvement has been reported in some severe
cases, including fever, malaise, leukocytosis and
regional lymphadenopathy.

43. Van Winkelhoff et al (1985) established 4 diagnostic
criteria
O Association of pocket of >/= 6 mm,
O Presence of bleeding on probing,
O Evidence of radiographic bone loss &
O Absence of periapical lesion.

44. OOther recommended additional diagnostic tools: include
the use of Dark-Field Microscopical examination of
the abscess microflora in order to exclude an
endodontic origin, due to the higher percentage of
spirochetes in periodontal abscesses.
OPositron Emission Tomography and a Fluorine-18-
Fluoromisonidazole marker for detection of
periodontal abscesses and other anaerobic infections in
the mouth. Results from the clinical study showed that
100% of periodontal abscesses were found with this
procedure.

45. DIFFERENTIAL
DIAGNOSIS
OGingival abscess
OPeriapical abscess,
OLateral periodontal cyst,
OPericoronitis
OVertical root fracture,
OOsteomyelitis
OEosinophilic granuloma

46. Periodontal abscess Gingival abscess
Involves supporting periodontal
structure
Confined to marginal and / or
interdental gingiva.
Often occurs in the course of
chronic destructive periodontitis
Occurs in previously disease free
areas.
X-ray- bone loss present Acute inflammatory response to
forcing of foreign material into the
gingiva. No bone loss
Pocket present No pockets

47. Periodontal abscess Gingival abscess
Pain – diffuse. Pain – dull
May affect the entire side of the
face.
localized.
Affected by thermal changes Not affected by thermal changes.

48. Periodontal abscess Periapical abscess
Associated with preexisting
periodontal pockets, caries or
both.
Associated with deep restoration,
caries or Tooth wear
Pulp test- vital. Non-vital
Swelling generalized and located
around the involved tooth and
gingival margin, seldom with a
fistulous tract.
Swelling localized often with
fistulous tract opening in the
apical area.

49. Periodontal abscess Periapical abscess
Pain – dull, constant, less severe,
localized and patient usually can
locate the offending tooth
Pain - severe, throbbing, last for
long, deep, unable to locate the
offending tooth
Pain associated with the
movement or percussion is not as
severe as with a pulpal disease
Severe than periodontal abscess.
Lateral radiolucency Apical radiolucency

50. Periodontal abscess Periapical abscess
Angular bone defects,
Furcation involvement
Endodontic filling or
Endodontic or post perforations
Responds dramatically well to
sub gingival debridement.
Responds poorly or not at all to
periodontal therapeutic
interventions

51. Periodontal cyst (non-infected)
ONo inflammatory signs
OMore common in mandibular canine – premolar
region
OOn radiograph well defined oval radiolucency on the
lateral surface of the root, with chronic border, < 1
cm in diameter.
OMicroscopically thin, non-keratinized stratified
squamous epithelia with focal epithelial thickening.
Inflammatory cells seen if secondarily infected.
OTreatment – Enucleation.

52. Pericoronitis
O Usually seen in incompletely erupted tooth
O Commonly associated with mandibular 3rd molar.

Osteomyelitis
ORapid diffuse bone destruction may occur with in a few
days
ODeeper pain being only symptom.
OX-ray – indistinct trabecular and disappearance of
lamina dura
OAs infections increases, lymphadenopathy, fever and
malaise are more common.

53. Eosinophilic granuloma
ODiagnosed by the rapid bone destruction after periodontal
therapy
OBiopsy.
Vertical root fracture
OLoupes or operating microscopes assist in visualization of
cracks/fractures
OThe bite test, Transillumination with fiber optic light and
use of dyes helps in detecting the suspected fracture

54. ODifferential diagnosis should also be made with self-
inflicted gingival injuries.
OSome lesions caused by patient's habits can mimic
periodontal abscesses, such as trauma of the gingiva
with a pencil (Rodd 1995) or with a safety pin (Beckett
et al. 1995)
OA careful evaluation is the main factor to solve these
cases, since conventional treatments usually fail unless
the habit is discontinued.

55. TREATMENT
Treatment of acute periodontal abscess usually
involves two stages
OManagement of the acute lesion.
OThe appropriate treatment of the original and / or
residual lesion, once the acute situations has been
controlled.
The purpose of treatment of acute periodontal abscess
is
OAlleviate pain,
OControl the spread of infection, and
OTo establish drainage.

56. Protocol recommended.
OIncision and drainage (closed or open approach)
OScaling and Root planning
OCompression and debridement of soft tissue wall.
OUse of different systemically administered
antibiotics
OTooth extraction.

57. Incision and drainage
OThrough the pocket (Closed approach)
O Incision from the outer surface (Open approach)
Closed approach
OAnesthesia
OFlat instrument /probe – carefully introduced into the
pocket.
O Distend the pocket wall for drainage.
OFurther drain and gently curettage the mass of tissue
internally.

58. Open approach
OVertical incision through the most fluctuant part of the
swelling, extending to an area just apical to the abscess.
OCurette the granulomatous tissue internally.
OExternal aspect of the abscess is gently pushed to drain
the remaining pus.
OSaline irrigation
OApproximate to wound margin
ONo sutures required.

59. Antibiotic administration
OMetronidazole – 200 mg, tid, 5 days –Smith and
Davies(1986)
OTetracycline – 1 gm / day – 2weeks -Hafstrom(1994)
OAzithromycin, 500mg, OD, 3 days.
OAmoxicillin + Clavulanate, 500 + 125 mg, tid, 8days.

61. Chronic periodontal Abscess
Surgical therapy
OGingivectomy
OFlap procedures
OMainly in abscess associated with deep vertical defects,
where the resolution of the abscess may only be
achieved by a surgical operation.
OObjective : To eliminate the remaining calculus and to
obtain drainage at the same time.

62. For the treatment of Gingival Abscess, the protocol
should include the following:
OElimination of the foreign object, through careful
debridement (Abrams 1983)
ODrainage through the sulcus with a probe or light
scaling,
ORinsing with warm saline and follow-up after 24-48
hours

63. COMPLICATIONS
 Tooth Loss
OSuggested as the main cause for extraction in the
maintenance phase.
OHistory of repeated abscess formation is considered as a
“hopeless” prognosis for the tooth.
OIn a retrospective study, 45% of teeth with periodontal
abscesses in a maintenance population were extracted
(McLeod et al. 1997)

64. Dissemination of the infection
Two possibilities have been described:
I. The dissemination of the bacteria during therapy
(bacteraemia); or
II. Bacteraemia related with an untreated abscess.
The Dissemination of the bacteria during therapy
OSuzuki & Delisle (1984) related a case of pulmonary
actinomycosis due to a periodontal abscesses, which was
ultra-sonically scaled. it was suggested that during
treatment, Actinomyces sp. from the subgingival
microflora had passed to the lungs.

65. OGallaguer et al. (1981) described a healthy patient with
a periodontal abscess who was treated with drainage
and curettage, but without systemic antibiotic.
O2 weeks later a brain abscess was diagnosed,
Microbiology of the lesions demonstrated, among other
bacteria, Bacteroides melaninogenicus and other
bacteroides, species.

66. II.Bacteraemia related with an untreated abscess.
OCellulitis in breast cancer patients has been claimed to
follow gingivitis or an abscess (Manian 1997)
Odue to transient bacteraemia and reduced host defenses
(radiation therapy and axillary dissection). The breast
and the upper extremities are particularly susceptible to
infections of oral origin (Manian 1997)
Operiodontal abscess is also associated with the
development of a cervical necrotizing fascitis. it is
frequently associated with oropharyngeal infections.

67. Necrotising cavernositis:-
OInflammation and necrosis of the Corpora
Cavernosa or Corpus Spongiosum of male
external genital organ leading to impotency.
OCulture from corposa carvernosa showed
Peptostreptococcus species and Fusobacterium
species. ( Pearle and Wendel 1993)

68.  Sickle cell crisis in patient with sickle cell anemia:
OA periodontal abscess may also cause a sickle cell
crisis, in patients with sickle cell anaemia (Rada et al.
1987)
ODuring the crisis, the abscess must be treated with
antibiotics, aiming to avoid pain and to prevent
dissemination of the infection.
ODefinitive treatment should be delayed until resolution
of the crisis.

69. Gingival Abscess
OA localized purulent infection that involves the
marginal gingiva or interdental papilla

70. Gingival Abscess

71. OEtiology
OAcute inflammatory response to foreign substances
forced into the gingiva
OClinical Features
OLocalized swelling of marginal gingiva or papilla
OA red, smooth, shiny surface
OMay be painful and appear pointed
OPurulent exudate may be present
ONo previous periodontal disease

72. OTreatment
OElimination of foreign object
ODrainage through sulcus with probe or light scaling
OFollow-up after 24-48 hours

73. Pericoronal Abscess
OA localized purulent infection within the tissue
surrounding the crown of a partially erupted tooth.
OMost common adjacent to mandibular third molars in
young adults; usually caused by impaction of debris
under the soft tissue flap

74. Pericoronal Abscess

75. OClinical Features
•Operculum (soft tissue flap)
•Localized red, swollen tissue
•Area painful to touch
•Tissue trauma from opposing tooth common
•Purulent exudate, trismus, lymphadenopathy, fever,
and malaise may be present

76. OTreatment Options
•Debride/irrigate under pericoronal flap
•Tissue recontouring (removing tissue flap)
•Extraction of involved and/or opposing tooth
•Antimicrobials (local and/or systemic as needed)
•Culture and sensitivity
•Follow-up

77. OThe treatment of pericoronal abscess is aimed at
Managemant of acute abcess,followed by
Resolution of the chronic condition.

78. OThe acute pericoronal abscess is properly anaesthetized
ODrinage is established –lifting the soft tissue operculum
with periodontal probe or currette
OIf the underlying debris is accessible, It must be
removed-followed gentle irrigation

79. OSystemic antibiotics are given- swelling,regional
lymphadenopathy.
OThe patient is then instructed to rinse with warm water
for every 2 hours and reassesed for 24 hours.
OAnalgesics also prescribed-discomfort.

80. OAcute phase has been controlled, the partially erupted
teeth may be definitely treated with ;
OSurgical excision of the overlying gingiva
ORemoval of the offending tooth.

81. CONCLUSION

82. REFERENCES
OClinical Periodontology : Carranza,
Newman 9
th
Edition
OClinical Periodontology and implant
dentistry – Lindhe 4th edition
O Periodontal abscess: a review. JCDR-2011
OPeriodontal Abscess review, JCP-2000,
27:377-386.
OPerio 2000 volume 34, 2004.