Classification of Periodontal Diseases.pptx

Periodontal disease is a disease, or more likely a number of diseases of the periodontal tissues that results in attachment loss and destruction of alveolar bone. The natural history of periodontal disease, in some but not all patients, results in tooth loss. Periodontal disease, however, encompasses a wider spectrum of diseases than just periodontitis and the recognition of these diseases requires a diagnosis be made.
Classification is the process of identifying and grouping objects or ideas into predetermined categories.

1. CLASSIFICATION OF PERIODONTAL DISEASES Dr Akriti II MDS 1

2. CONTENT INTRODUCTION NEED FOR CLASSIFICATION HISTORY EVOLUTION OF CLASSIFICATION 1999 CLASSIFICATION RESPONSE TO 1999 CLASSIFICATION NEED FOR 2017 CLASSIFICATION REFERENCES PART 1 2

3. PART 1 3

4. INTRODUCTION 4

5. Periodontal disease is a disease, or more likely a number of diseases of the periodontal tissues that results in attachment loss and destruction of alveolar bone. The natural history of periodontal disease, in some but not all patients, results in tooth loss. Periodontal disease, however, encompasses a wider spectrum of diseases than just periodontitis and the recognition of these diseases requires a diagnosis be made. Classification is the process of identifying and grouping objects or ideas into predetermined categories. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 5

6. NEED FOR CLASSIFICATION 6

7. Allows clinicians to develop a structure which can be used to identify diseases in relation to aetiology, pathogenesis and treatment Allows to organize effective treatment of the patient’s disease, predict the outcome of treatment as well as to explain to the patient about the disease Allows the clinicians and researchers everywhere to communicate with a common language Assembles similar disease phenotypes in more homogeneous syndromes Helps to differentiate between various types of disease and their process Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. Tonetti MS. Etiology and pathogenesis. In: NP Lang, T Karring, editors. Proceedings of the 1st European Workshop on Periodontology . Berlin: Quintessence Publishing Co., 1994: 120– 126. Baelum V, Lopez R. Defining and classifying periodontitis: need for a paradigm shift? Eur J Oral Sci 2003: 111: 2– 6 7

8. HISTORICAL PERSPECTIVE 8

9. Descriptions of treatment are found in ancient Egyptian and Chinese writings and would suggest that periodontal diseases were recognized possibly 5000 years ago. Pierre Fauchard published the first dental textbook, “The Surgeon Dentist” in 1728 John Hunter published “The Natural History of the Human Teeth” in 1771 and “A Practical Treatise on the Diseases of the Teeth” in 1778. Joseph Fox in 1806 tried to classify gum disease and gave the first periodontal classification. Adolph Witzel (1847–1906) was the first individual to identify bacteria as the cause of periodontal disease. The first true oral microbiologist was WD Miller (1853–1907). John W Riggs (1811–1885) clearly recognized the importance of local irritants in the aetiology of periodontal disease. The term “pyorrhea alveolaris” was introduced early in the 19th century to describe periodontitis and literally meant “pus oozing out of the alveolus”. Gold SI. Periodontics. The past. Part (1). Early sources. J Clin Periodontol 1985; 12: 79– 97. Fauchard P. Le chirurgien dentiste, au traité des dens . Paris: Pierre-Jean Maruiette, 1728. Reprinted in facsimile, Paris: Prèlat, 1961. English translation by Lillian Lindsay, London: Butterworth, 1946. Hunter J. The natural history of the human teeth . 3rd edn. London: Johnson, 1803. Milward MR, Chapple IL. Classification of Periodontal Diseases: Where were we? Where are we now? Where are we going?. Dental update. 2003; 30(1):37-44. Witzel A. The treatment of of pyorrhea alveolaris or infectious alveolitis. Br J Dent Sci 1882; 153: 209– 263. Miller WD. The micro-organisms of the human mouth . Philadelphia: The S. S. White Dental Mfg. Co., 1890: 321– 336. Riggs JW. Suppurative inflammation of the gums and absorption of the gums and alveolar process. Pa J Dent Sci 1876; 3: 99– 104. Reprinted in Arch Clin Oral Pathol 1938;2:423. 9

10. Armitage described three major paradigms of understanding which have had a major influence on our attempts at classifying periodontal diseases: the clinical characteristics paradigm was in vogue from 1870 to 1920 from 1920 to 1970 the major influence was the classic pathology paradigm from 1970 to the present day the infection/host response paradigm is of main influence In the late 1800s and early 1900s clinicians used case descriptions and their personal interpretation of what they saw clinically as the primary basis for classifying periodontal diseases. C.G. Davis in 1879 gave three distinct forms of destructive periodontal disease, that was in accordance with the clinical characteristics paradigm: Gingival recession with minimal or no inflammation. Periodontal destruction secondary to ‘lime deposits’ ‘Riggs’ Disease' Armitage G. Classifying periodontal diseases–a longstanding dilemma. Periodontol 2000 2002; 30: 9– 23. Davis CG. Gum and alveolar diseases. Dental Cosmos 1879: 21: 192 – 201. 10

11. In 1886 G.V. Black gave his classification of periodontal diseases based on their clinical characteristics and his understanding of their cause into five separate groups: Constitutional gingivitis A painful form of gingivitis Simple gingivitis Calcic inflammation of the peridental membrane Phagedenic pericementitis, replaced with “chronic suppurative pericementitis” In 1942 , Orban proposed a classification scheme based on the principles of basic pathology (in accordance with the classic pathology paradigm), which was accepted by the American Academy of Periodontology (AAP) and gained wide acceptance. Periodontal disease was classified into 5 broad groups: Inflammation Degeneration Atrophy Hypertrophy Traumatism. 11 Black GV. Diseases of the peridental membrane having their beginning at the margin of the gum. In: WF Litch editor. American System of Dentistry , Vol. I. Philadelphia: Lea Brothers, 1886: 953 – 979. Orban B. Classification and nomenclature of periodontal diseases. J Periodontol 1942; 13: 88– 91.

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13. EVOLUTION OF CLASSIFICATION 13

14. The AAP further addressed the issue of classification in the 1966 World Workshop in Periodontics . The term chronic marginal periodontitis was accepted but the workshop failed to produce a definite system of classification for periodontitis. The outcome of the workshop resulted in only one form of periodontitis, chronic marginal, being recognized. In 1977 , however, the term juvenile periodontitis, which had largely replaced the term periodontosis, was accepted by the AAP. The Academy then recognized two distinct forms of periodontitis. age and rate of disease progression was considered important for classification of diseases In 1982 , Page and Schroeder stated they could identify at least five distinctly different forms of periodontitis in humans. subclassified marginal periodontitis as adult periodontitis and rapidly progressive periodontitis They designated the forms of periodontitis as prepubertal, juvenile, rapidly progressive, adult and acute necrotizing ulcerative gingivo-periodontitis. The 1989 periodontal disease classification was a significant improvement over previous classifications. the effect of systemic disease on periodontal health was recognized and added as a category The American Academy of Periodontology. Proceedings of the World Workshop in Periodontics . Ann Arbor, MI: University of Michigan, 1966: 69– 126. Page RC, Schroeder HE. Periodontitis in man and other animals. A comparative review. Karger , 1982: 222– 239. 14

15. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology -an update. Journal- canadian dental association. 2000 Dec 1;66(11):594-9. 15

16. 1999 CLASSIFICATION 16

17. Drawbacks of 1989 Classification lack of a category for strictly gingival diseases overlap between disease categories difficulty in fitting certain patients into any of the existing categories similarity of microbiological and host response features in purportedly different disorders an emphasis on age of onset that became a problem as patients aged into a new category some unclear classification criteria A new periodontal disease classification system was recommended by the 1999 International Workshop for a Classification of Periodontal Disease and Conditions and has been accepted by the AAP. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology -an update. Journal- canadian dental association. 2000 Dec 1;66(11):594-9. 17

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19. Changes to the 1999 periodontal classification system Addition of a Gingival Disease component Replacement of “Adult Periodontitis” with “Chronic Periodontitis” Elimination of “Refractory Periodontitis” as a separate entity Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis” Further subclassification of “Periodontitis as a Manifestation of Systemic Diseases” Replacement of “Necrotizing Ulcerative Periodontitis” with “Necrotizing Periodontal Diseases” Addition of categories for “Periodontal Abscess” and “Periodontic-Endodontic Lesion” Addition of a category for “Developmental or Acquired Deformities and Conditions” 19

20. Addition of a Gingival Disease component Gingival lesions are classified into two broad categories: Plaque induced Non-plaque induced Dental plaque induced lesions (gingivitis) may be purely plaque related with or without local contributing factors or may be modified by systemic factors, medications or by malnutrition. Non-plaque induced gingival lesions encompass those caused by specific bacterial, fungal or viral infections, genetic origin, systemic conditions (dermatological conditions, allergic reactions), foreign body reactions, trauma lesions and a catch all, not otherwise specified, for forms of gingivitis that do not fit neatly into any of the other areas Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 20

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24. Replacement of “Adult Periodontitis” with “Chronic Periodontitis” Workshop participants concluded that the term adult periodontitis was misleading and should be replaced with the term chronic periodontitis because there is no histopathological uniqueness nor natural determination point as to when disease onset is most likely to occur. The term “chronic” was chosen as it was felt to be non-specific and not age dependent and thus less restrictive. Localized periodontitis is described as 30 percent or less of sites affected and generalized periodontitis being more than 30 percent of sites affected. The workshop also produced the following working definition and features of chronic periodontitis: “An infectious disease resulting in inflammation within the supporting structures of teeth, progressive attachment and bone loss. It is characterized by pocket formation and/or gingival recession. It is recognized as the most frequently occurring form of periodontitis. Its onset may be at any age but is most commonly detected in adults. The prevalence and severity of the disease increases with age. It may affect a variable number of teeth and has variable rates of progression.” Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 24

25. Features of chronic periodontitis listed in the 1999 International Workshop are: most prevalent in adults, but can occur in children and adolescents; amount of destruction is consistent with the presence of local factors; subgingival calculus is a frequent finding; associated with a variable microbial pattern; slow to moderate rate of progression, but may have periods of rapid progression; can be further classified on the basis of extent and severity; can be associated with local predisposing factors (e.g., tooth-related or iatrogenic factors); may be modified by and/or associated with systemic diseases (e.g., diabetes mellitus, HIV infection); can be modified by factors other than systemic disease such as cigarette smoking and emotional stress. The workshop categorized a general guide for severity on the basis of clinical loss of attachment (CAL) as follows: slight = 1–2mm CAL; moderate = 3 to 4mm CAL; and severe = 5mm CAL. Lindhe J, Ranney R, Lamster I, et al. Consensus report: Chronic periodontitis. Ann Periodontol 1999; 4: 38. 25

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27. Elimination of “Refractory Periodontitis” as a separate entity Refractory periodontitis refers to continued attachment loss in spite of adequate treatment and proper oral hygiene. Factors: lack of response to periodontal therapy extent of disease prior to therapy type of therapy provided (nonsurgical vs. surgical, with or without antibiotics, etc.) tooth type and furcation involvement species and strains of microflora degree of host response (particularly immune response) whether the patient smokes Given that these factors can affect treatment response, it was felt that refractory periodontitis was likely not a separate entity and the category was discontinued. The term recurrent periodontitis is used to indicate a return of periodontitis and not a separate disease. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. 27

28. Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis” In the 1989 classification, patients were placed into the early-onset category if they exhibited significant attachment loss in the presence of little local factors (plaque and calculus) and were less than 35 years of age. Aggressive periodontitis replaces the category “early onset periodontitis” which in the 1989 AAP and 1993 European classifications embraced a number of diseases affecting young patients. Issues addressed: addressed the clinical characteristics of the disease while avoiding the controversial age barrier avoids the dilemma frequently confronted using the 1989 classification as to where to place certain patients The workshop decided to discard all classifications that were age dependant or where knowledge of rates of progression was required. Patients previously classified as having rapidly progressive periodontitis were classified as having either generalized aggressive periodontitis or chronic periodontitis, depending upon their clinical characteristics. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 28

29. Common features of localized and generalized forms of aggressive periodontitis listed in the 1999 workshop: except for the presence of periodontitis, patients are otherwise clinically healthy; rapid attachment loss and bone destruction; familial aggregation Secondary features that are generally, but not universally, present are: amounts of microbial deposits are inconsistent with the severity of periodontal tissue destruction; elevated proportions of Actinobacillus actinomycetemcomitans ( Aggregatibacter actinomycetemcomitans ) and, in some populations, Porphyromonas gingivalis may be elevated; phagocyte abnormalities; hyper-responsive macrophage phenotype, including elevated levels of PGE 2 and IL-1β; progression of attachment loss and bone loss may be self arresting. Lang N, Bartold PM, Cullinan M, et al. Consensus report: aggressive periodontitis. Ann Periodontol 1999; 4: 53. 29

30. Further specific features were identified- Localized aggressive: circumpubertal onset; localized first molar/incisor presentation with interproximal attachment loss on at least two permanent teeth, one of which is a first molar, and involving no more than two teeth other than first molars and incisors; robust serum antibody response to infecting agents. Lang N, Bartold PM, Cullinan M, et al. Consensus report: aggressive periodontitis. Ann Periodontol 1999; 4: 53 Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 30

31. Generalized aggressive: usually affecting persons under 30 years of age, but patients may be older; poor serum antibody response to infecting agents; pronounced episodic nature of the destruction of attachment and alveolar bone; generalized interproximal attachment loss affecting at least three permanent teeth other than first molars and incisors Lang N, Bartold PM, Cullinan M, et al. Consensus report: aggressive periodontitis. Ann Periodontol 1999; 4: 53 Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 31

32. Further subclassification of “Periodontitis as a Manifestation of Systemic Diseases” Systemic diseases that affect immune function, inflammatory response and tissue organization can modify the onset and progression all forms of periodontal disease. This category has been redefined to include only those diseases where the periodontal disease is a manifestation of the disease process and excludes those which act as modifiers of all types of periodontal disease. Diseases such as HIV and diabetes were considered to be modifiers of both chronic and aggressive periodontitis. It was concluded that there was insufficient evidence that there is a specific periodontitis associated with these diseases. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999; 4: 1– 6. 32

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34. Cyclic neutropenia: Note the very inflamed, erythematous and oedematous gingiva, anterior migration, the advanced premature exfoliation that is apparent and the generalized severe bone loss on the radiograph. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 34

35. Down syndrome: Note the gingival inflammation, splayed teeth and macroglossia. The radiograph shows severe bone loss. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 35

36. Periodontitis modified by systemic disease: (a) and (b) Severe necrotizing ulcerative periodontitis in a patient with HIV infection (previously classified as HIV associated periodontitis). Note the severe interproximal gingival destruction, recession and necrotizing lesions. (c) A patient with advanced periodontitis modified by poorly controlled insulin dependant diabetes. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 36

37. Replacement of “Necrotizing Ulcerative Periodontitis” with “Necrotizing Periodontal Diseases” The workshop recognized that necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative peridontitis (NUP) were clinically distinguishable disease entities but were unsure as to whether they were part of the same disease process or were two distinct diseases. They concluded that there was insufficient data to resolve this problem, thus they decided to place both conditions in the one category of “necrotizing periodontal disease” . Necrotizing ulcerative gingivitis tends to be recurrent if predisposing factors remain and progresses to necrotizing ulcerative periodontitis, in some cases causing severe destruction of the periodontal tissues. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26 Lang N, Soskolne WA, Greenstein G, et al. Consensus report: necrotizing periodontal diseases. Ann Periodontol 1999; 4: 78. 37

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39. Addition of categories for “Periodontal Abscess” and “Periodontic-Endodontic Lesion” In most cases periodontal abscess formation reflects the acute exacerbation of a pre-existing periodontal pocket . It may be more correctly called an acute periodontitis. Abscesses may occur because of other causes such as: foreign body impaction trauma, including occlusal trauma causing vertical and horizontal root fractures cemental tears. It presents as a distinct clinical entity that requires specific diagnosis and treatment and thus deserves a separate classification. The term periodontic-endodontic lesion is not based on the initial etiology of the lesion but simply indicates there is both a periodontic and an endodontic component. Wiebe CB, Putnins EE. The periodontal disease classification system of the American Academy of Periodontology-an update. Journal-canadian dental association. 2000 Dec 1;66(11):594-9. Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. 39

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41. Addition of a category for “Developmental or Acquired Deformities and Conditions” This category appears to have been added for completeness. It includes tooth related factors and conditions which may modify or predispose to disease . Many of these conditions do not constitute disease entities in their own rights but they modify and alter susceptibility to disease. 41 Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26.

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43. RESPONSE TO 1999 CLASSIFICATION 43

44. Milward and Chapple , while recognizing the 1999 World Workshop attempted to produce a classification from an evidence-based perspective, criticized the 1999 classification as being unnecessarily complex and not suited for routine general dental practice. Lopez and Baelum argued from an epidemiological point of view that there is little justification for the use of complicated classification systems and favour an approach based upon simple clinical attachment loss measurements such as ≥ 3 mm etc., a minimalist approach that does not try to differentiate between different types of periodontitis. Van der Velden argued that the 1999 reclassification was not helpful and suggested a classification based on age, which appears to be a simplified version of the 1989 AAP classification, and further classified on the basis of extent, severity and clinical characteristics. 44 Milward MR, Chapple ILC. Classification of periodontal diseases: Where were we? Where are we? Where are we going? Dental Update 2003; 30: 37– 44. Lopez R, Baelum V. Classifying periodontitis among adolescents: implications for epidemiological research. Community Dent Oral Epidemiol 2003; 3: 136– 143. Van der Velden U. Diagnosis of periodontitis. J Clin Periodontol 2000; 27: 960– 961.

45. Essentialistic or Nominalistic disease classification 45 As Sherp noted in 1964, one obvious problem is that one of the most important components of periodontitis is expressed in all the patients in the same way, i.e., the amount of loss of attachment. The essentialistic idea implies the real existence of a disease caused by a class of agents. Since periodontitis has to be regarded as a syndrome, present and future classifications of periodontitis have to be based on the nominalistic concept. For clinicians the most important characteristic of a patient is the extent and severity of the periodontal destruction in relation to age. Van der Velden’s classification according to the nominalistic concept was based on four dimensions. The classification was ascertained in the following way: first, the severity category is determined for each tooth; next, the extent category is determined by counting the number of teeth with the most severe condition; diagnosis on the basis of clinical characteristics is added if applicable; diagnosis on the basis of age Sherp HW. Current concepts in periodontal disease research: epidemiological contributions. J Am Dent Assoc 1964: 68: 667– 675. Van Der Velden U. Diagnosis of periodontitis. J Clin Periodontol 2000: 27: 960– 961 Van Der Velden U. Purpose and problems of periodontal disease classification. Periodontology 2000. 2005 Oct;39(1):13-21..

46. 46 CLASSIFICATION ACCORDING TO SEVERITY

47. CLASSIFICATION ACCORDING TO EXTENT 47

48. CLASSIFICATION ACCORDING TO CLINICAL CHARACTERISTICS 48

49. CLASSIFICATION ACCORDING TO AGE 49

50. heterogenicity of the clinical presentation lack of understanding of the true nature of the differences between the different clinical presentations of the disease Armitage stated that “the classification system proposed by the ‘1999 International Workshop for a Classification of Periodontal Diseases and Conditions’ has corrected some of the problems associated with the previous system that had been in use since 1989. Nevertheless, the new system is far from perfect and will need to be modified once there are sufficient new data to justify revisions”. He is of the opinion that current disease designations such as “chronic periodontitis” are constellations of polymicrobial and polygenic infections whose clinical expression is altered by important environmental and host modifying conditions . 50 Why is classification of periodontal disease so difficult and controversial? Highfield J. Diagnosis and classification of periodontal disease. Australian dental journal. 2009 Sep;54:S11-26. Armitage G. Classifying periodontal diseases–a longstanding dilemma. Periodontol 2000 2002; 30: 9– 23.

51. PART 2 51

52. CONTENT PART 2 2017 CLASSIFICATION ADVANTAGES DISADVANTAGES IMPLEMENTATION IN CLINICAL PRACTICE CLINICAL DECISION TREE CONCLUSION REFERENCES 52

53. NEED FOR 2017 CLASSIFICATION 53

54. It did not serve as therapeutic guide It did not elaborate the effect of risk factors Categorizing aggressive & chronic periodontitis – cumbersome & confusing (required assessment of rate of progression spread over multiple visits & chronic periodontitis exacerbation phase may also show rapid progression) Current evidence does not support the distinction between chronic and aggressive periodontitis as separate clinical entities (similar microbiology, pathogenesis, and histopathology). Confusion in diagnosing a case of plaque-induced gingival inflammation on a reduced but healthy periodontium – periodontitis or gingivitis? Categories of gingival disease modified by medication & diabetes mellitus exist but no such periodontitis class exists. The classification did not give clue regards correct treatment plan as it depended on correct diagnosis of the disease No mention of peri-implant diseases 54 Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3). Das N. Critical Analysis of AAP 1999 and 2017 the World Workshop Classification Systems: An Insight. Saudi J Oral Dent Res. 2021;6(7):304-12.

55. 2017 CLASSIFICATION 55

56. Aim 56 The aim of the 2017 World Workshop was to introduce a new classification that was driven by better understanding of periodontal disease since the last classification workshop in 1999. The aims of the 2017 workshop set out by the management committees of the European Federation of Periodontology (EFP) and the American Academy of Periodontology (AAP) were to produce a new evidence based classification that could be implemented in general practice and that breaks down a complex disease process into key components that are important in determining disease severity, extent and susceptibility to further disease progression, something the previous classifications have failed to achieve. Milward, M & Roberts, A 2019, 'Assessing periodontal health and the British Society of Periodontology implementation of the new classification of periodontal diseases 2017', Dental Update,46,10,918- 929

57. Salient Features 57 The major development in this classification is the re-categorization of all three forms of periodontal diseases, in various stages and grades for the periodontal disease and addition of peri-implant diseases and conditions. Periodontitis characterization is now based on a multi dimensional staging and grading system, which maximizes the significance of diagnostic processes in comprehensive case management. considers not only the principal disease (staging) but also the systemic influences both to and from the diseased periodontium (grading) avoids the misconception that disease severity can be reduced by extraction of the compromised teeth The definition & specific criteria of Gingival health & Periodontal health for cases with intact and reduced periodontium have been established. It resolved the discrepancies of previous classification by clarifying the definition of a gingivitis case (differentiates from gingival inflammation at >1 sites). Rearrangement of the non-dental-biofilm induced gingival diseases and conditions is based on the etiology of the lesions. Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

58. The classification laid down the case definition for periodontitis & excluded CAL observed due to non-periodontitis causes. This classification has stated a single term and no chronic/aggressive periodontitis terms remain. Periodontitis as manifestation of systemic diseases has been grouped according to primary systemic disease based on International Classification of Diseases (ICD). All abscesses of periodontal tissues are now termed as periodontal abscess, which are classified based on the etiology and patient's periodontitis history. Mucogingival conditions have been described by the periodontal phenotype i.e. gingival thickness keratinized tissue width bone morphotype The new classification & case definitions related to treatment of gingival recession are based on gingival phenotype interproximal loss of clinical attachment assessment of exposed root cemento-enamel junction 58 Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

59. Changes in Terminologies 59 Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

60. Changes in Terminologies 60 Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

61. Changes in Terminologies 61 Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

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64. 64 According to WHO, “Health is a state of complete physical, mental and social well being and not merely the absence of disease or infirmity”. Thus, PERIODONTAL HEALTH should be defined as a state free from inflammatory periodontal disease that allows an individual to function normally and avoid consequences (mental or physical) due to current or past disease. Periodontal health - should be predicated upon the absence of disease, as assessed clinically, associated with gingivitis, periodontitis, or other periodontal conditions may include patients who have had a history of successfully treated gingivitis or periodontitis, or other periodontal conditions, who have been and are able to maintain their dentition without signs of clinical gingival inflammation. embraces physiological immune surveillance involving levels of biological and inflammatory markers compatible with homeostasis Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

65. 65 CLINICAL GINGIVAL HEALTH is generally associated with an inflammatory infiltrate (predominantly neutrophilic) and a host response consistent with homeostasis. On the site level , clinical gingival health can be classified as: Clinical gingival health on an intact periodontium Clinical gingival health on a reduced periodontium Stable periodontitis patient Non-periodontitis patient (e.g. recession, crown lengthening) Clinical features of Gingival Health - on an intact periodontium on a reduced periodontium following treatment of gingivitis on an intact periodontium following successful treatment of periodontitis Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

66. 66 ABSENCE OF BLEEDING ON PROBING ABSENCE OF ERYTHEMA AND EDEMA ABSENCE OF PATIENT SYMPTOMS ABSENCE OF ATTACHMENT LOSS AND BONE LOSS BONE LEVEL 1-3mm APICAL TO CEJ INTACT PERIODONTIUM Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

67. 67 ABSENCE OF BLEEDING ON PROBING ABSENCE OF ERYTHEMA AND EDEMA ABSENCE OF PATIENT SYMPTOMS PRESENCE OF REDUCED CLINICAL ATTACHMENT PRESENCE OF REDUCED BONE LEVELS REDUCED PERIODONTIUM Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

68. 68 ABSENCE OF BLEEDING ON PROBING ABSENCE OF ERYTHEMA AND EDEMA ABSENCE OF PATIENT SYMPTOMS ABSENCE OF ATTACHMENT LOSS ABSENCE OF BONE LOSS TREATMENT OF GINGIVITIS ON AN INTACT PERIODONTIUM Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

69. 69 ABSENCE OF BLEEDING ON PROBING ABSENCE OF ERYTHEMA AND EDEMA ABSENCE OF PATIENT SYMPTOMS PRESENCE OF REDUCED CLINICAL ATTACHMENT PRESENCE OF REDUCED BONE LEVELS SUCCESSFUL TREATMENT OF PERIODONTITIS Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

70. 70 Gingival inflammation (gingivitis) case can be defined and graded by: using a bleeding on probing score (BOP%) assessing the proportion of bleeding sites when stimulated by a standardized periodontal probe with a controlled (∼0.25 N) force to the apical end of the sulcus at six sites (mesio-buccal, buccal, disto-buccal, mesio-lingual, lingual, disto-lingual) on all teeth present. Case Definitions Epidemiologically, for an intact periodontium and a reduced and stable periodontium, gingival health is defined as <10% bleeding sites with probing depths ≤3 mm. In clinical practice, periodontal health may exhibit one or two sites with some evidence of clinical gingival inflammation, localized mild and delayed bleeding to probe at isolated sites is ubiquitous. Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

71. 71 Following treatment of periodontitis, periodontitis patients may not attain a status of complete gingival health. However, evidence has demonstrated that a patient may achieve periodontal stability. PERIODONTAL STABILITY is characterized by : successful treatment through control of local and systemic risk factors minimal (< 10% of sites) BOP no probing depths of 4 mm or greater that bleed on probing optimal improvement in other clinical parameters lack of progressive periodontal destruction. The treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis and accordingly must be closely monitored. Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

72. The transition from periodontal health to gingivitis is reversible following treatment that resolves gingival inflammation. The transition to periodontitis results in attachment loss which is irreversible (high risk of recurrent periodontitis). Optimal periodontal therapy can restore gingival health on a reduced periodontium, or may result in mild marginal gingival inflammation at shallow probing pocket depths (≤ 3 mm). However, a history of periodontitis places patients at high risk of recurrent periodontitis and such patients require careful site-specific monitoring during periodontal maintenance programs. 72 Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

73. 73 There are broadly two categories of gingival disease : Dental plaque biofilm-induced gingivitis Non–dental plaque-induced gingival diseases Dental plaque biofilm-induced gingivitis is defined at the site level as “an inflammatory lesion resulting from interactions between the dental plaque biofilm and the host's immune-inflammatory response, which remains contained within the gingiva and does not extend to the periodontal attachment (cementum, periodontal ligament and alveolar bone). Such inflammation remains confined to the gingiva and does not extend beyond the mucogingival junction and is reversible by reducing levels of dental plaque at and apical to the gingival margin” . Determinants of the rate of development of gingivitis, its severity and extent: local risk factors, known as predisposing factors systemic risk factors, referred to as modifying factors Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84. Murakami S, Mealey BL, Mariotti A, Chapple ILC. Dental plaque– induced gingival conditions. J Periodontol. 2018;89(Suppl 1):S17– S27.

74. LOCAL RISK FACTORS: Local risk factors for gingivitis are those that encourage plaque accumulation at a specific site by either inhibiting its removal during daily oral hygiene practices, and/or creating a biological niche that encourages increased plaque accumulation . Dental plaque biofilm retention factors Tooth anatomical factors Subgingival restoration margins Oral dryness Sjögrens syndrome Mouth breathing habit 74 SYSTEMIC RISK FACTORS: Systemic risk factors are those which negatively influence the immune-inflammatory response to a given dental plaque biofilm burden, resulting in exaggerated or “hyper” inflammation. Smoking Metabolic factors Hyperglycemia with or without diabetes Nutritional factors Severe Vit C deficiency Pharmacological agents drugs that reduce salivary flow drugs that impact endocrine function drugs that may induce gingival enlargement Elevations in sex steroid hormones at puberty during pregnancy Haematological conditions Blood malignancies Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

75. 75 Clinical, radiological, and biological signs and symptoms of GINGIVITIS: Gingivitis is a clinical diagnosis. Radiographs cannot be used to diagnose gingivitis. The clinical signs of inflammation are erythema, edema, pain (soreness), heat, and loss of function. These may manifest clinically in gingivitis as: Swelling, seen as loss of knife-edge gingival margin and blunting of papillae Bleeding on gentle probing Redness Discomfort on gentle probing The symptoms a patient may report include: Bleeding gums (metallic/altered taste) Pain (soreness) Halitosis Difficulty eating Appearance (swollen red gums) Reduced oral health–related quality of life Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

76. 76 For epidemiological purposes , gingivitis on an intact periodontium and gingivitis on a reduced periodontium in a patient without a history of periodontitis, is defined as ≥10% bleeding sites with probing depths ≤3 mm . Localized gingivitis is defined as 10%-30% bleeding sites. Generalized gingivitis is defined as > 30% bleeding sites. For epidemiological purposes alone, a periodontitis case cannot simultaneously be defined as a gingivitis case. Therefore, a patient with a history of periodontitis, with gingival inflammation is still a periodontitis case. Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84.

77. 77 Non-dental plaque-induced gingival conditions encompass a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity.Although these lesions are not caused by the dental plaque biofilm, the severity of the clinical manifestations often depends on plaque accumulation and subsequent gingival inflammation. Chapple ILC, Mealey BL, et al. Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S74–S84. Holmstrup P, Plemons J, Meyle J. Non–plaque-induced gingival diseases. J Periodontol. 2018;89(Suppl 1):S28–S45.

78. 78

79. 79

80. 80 In the new periodontitis classification scheme, forms of the disease previously recognized as “chronic” or “aggressive” are now grouped under a single category ( “periodontitis” ) and are further characterized based on a multidimensional staging and grading system. PERIODONTITIS is a chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilms and characterized by progressive destruction of the tooth-supporting apparatus. Its primary features include: loss of periodontal tissue support, manifested through clinical attachment loss (CAL) and radiographically assessed alveolar bone loss presence of periodontal pocketing gingival bleeding. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

81. Staging is largely dependent upon the severity of disease at presentation as well as on the complexity of disease management. Grading provides supplemental information about biological features of the disease including - history-based analysis of the rate of periodontitis progression assessment of the risk for further progression analysis of possible poor outcomes of treatment assessment of the risk that the disease or its treatment may negatively affect the general health of the patient 81 Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

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83. 83

84. 84

85. 85 A periodontitis case definition system should include three components: identification of a patient as a periodontitis case, identification of the specific type of periodontitis, and description of the clinical presentation and other elements that affect clinical management, prognosis, and potentially broader influences on both oral and systemic health. In the context of clinical care, a patient is a “periodontitis case” if: Interdental CAL is detectable at ≥2 non-adjacent teeth, or Buccal or oral CAL ≥3 mm with pocketing ≥3 mm is detectable at ≥2 teeth but the observed CAL cannot be ascribed to non-periodontitis-related causes such as: gingival recession of traumatic origin; dental caries extending in the cervical area of the tooth; the presence of CAL on the distal aspect of a second molar and associated with malposition or extraction of a third molar, an endodontic lesion draining through the marginal periodontium; and the occurrence of a vertical root fracture Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

86. 86 Necrotizing periodontal diseases , whose characteristic clinical phenotype includes typical features (papilla necrosis, bleeding, and pain) and are associated with host immune response impairments, remain a distinct periodontitis category. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

87. 87 NECROTIZING GINGIVITIS is an acute inflammatory process of the gingival tissues characterized by presence of necrosis/ulcer of the interdental papillae, gingival bleeding, and pain. Other signs/symptoms associated with this condition may include halitosis, pseudomembranes, regional lymphadenopathy, fever, and sialorrhea (in children). Necrotizing gingivitis lesions have four zones : superficial bacterial zone, neutrophil-rich zone, necrotic zone and a spirochetal/bacterial infiltration zone NECROTIZING PERIODONTITIS is an inflammatory process of the periodontium characterized by presence of necrosis/ulcer of the interdental papillae, gingival bleeding, halitosis, pain, and rapid bone loss. Other signs/symptoms associated include pseudomembrane formation, lymphadenopathy, and fever. NECROTIZING STOMATITIS is a severe inflammatory condition of the periodontium and the oral cavity in which soft tissue necrosis extends beyond the gingiva and bone denudation may occur through the alveolar mucosa, with larger areas of osteitis and formation of bone sequestrum. It typically occurs in severely systemically compromised patients. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

88. 88

89. 89 There are many DISEASES AND CONDITIONS AFFECTING THE PERIODONTAL TISSUES , either by: influencing the course of periodontitis mainly rare diseases that affect the course of periodontitis (e.g., Papillon Lefevre Syndrome, leucocyte adhesion deficiency, and hypophosphatasia) have a major impact resulting in the early presentation of severe periodontitis mainly common diseases and conditions that affect the course of periodontitis (e.g., diabetes mellitus) magnitude of the effect of these diseases and conditions on the course of periodontitis varies but they result in increased occurrence and severity of periodontitis affecting the periodontal supporting tissues independently of dental plaque biofilm-induced inflammation mainly rare conditions affecting the periodontal supporting tissues independently of dental plaque biofilm induced inflammation (e.g., squamous cell carcinoma, Langerhans cell histiocytosis) result in breakdown of periodontal tissues and some of which may mimic the clinical presentation of periodontitis Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

90. 90

91. 91

92. 92 Endodontic-periodontal lesions , defined by a pathological communication between the pulpal and periodontal tissues at a given tooth, occur in either an acute or a chronic form, and are classified according to signs and symptoms that have direct impact on their prognosis and treatment. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

93. 93 Periodontal abscesses are defined as acute lesions characterized by localized accumulation of pus within the gingival wall of the periodontal pocket/sulcus, rapid tissue destruction and are associated with risk for systemic dissemination. Papapanou PN, Sanz M, et al. Periodontitis: Consensus report of Workgroup 2 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S173–S182.

94. 94 RECESSION is defined as an apical shift of the gingival margin caused by different conditions/pathologies. It is associated with clinical attachment loss. This may apply to all surfaces (buccal/lingual/interproximal). Possible consequences of gingival recession and root surface exposure to oral environment: Impaired esthetics Dentin hypersensitivity Caries/non-carious cervical lesions (NCCL) Biotype: (Genetics) group of organs having the same specific genotype. Phenotype: Appearance of an organ based on a multifactorial combination of genetic traits and environmental factors (its expression includes the biotype). Periodontal phenotype is determined by GINGIVAL PHENOTYPE (gingival thickness, keratinized tissue width), and bone morphotype (thickness of the buccal bone plate). Thin phenotype increases risk for gingival recession Periodontal phenotype can be assessed by using a periodontal probe ( CPU 15 UNC, Hu-Friedy, SE Probe SD12 Yellow, American Eagle Instruments) to measure the gingival thickness observing the periodontal probe shining through gingival tissue after being inserted into the sulcus: Probe visible: thin (≤1 mm) Probe not visible: thick (> 1 mm) Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

95. 95 GINGIVAL RECESSION CLASSIFICATION with reference to the interdental clinical attachment loss: Recession Type 1 (RT1): Gingival recession with no loss of interproximal attachment. Interproximal CEJ is clinically not detectable at both mesial and distal aspects of the tooth. Recession Type 2 (RT2): Gingival recession associated with loss of interproximal attachment . The amount of interproximal attachment loss (measured from the interproximal CEJ to the depth of the interproximal sulcus/pocket) is less than or equal to the buccal attachment loss (measured from the buccal CEJ to the apical end of the buccal sulcus/pocket). Recession Type 3 (RT3): Gingival recession associated with loss of interproximal attachment . The amount of interproximal attachment loss is higher than the buccal attachment loss Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

96. 96

97. 97 TRAUMATIC OCCLUSAL FORCE is defined as any occlusal force resulting in injury of the teeth and/or the periodontal attachment apparatus. These were historically defined as excessive forces to denote that the forces exceed the adaptive capacity of the individual person or site. OCCLUSAL TRAUMA is a lesion in the periodontal ligament, cementum and adjacent bone caused by traumatic occlusal forces. It is a histologic term; however, a clinical diagnosis of occlusal trauma may be made in the presence of one or more of the following: progressive tooth mobility adaptive tooth mobility (fremitus) radiographically widened periodontal ligament space tooth migration discomfort/pain on chewing root resorption Evidence from observational studies suggest that traumatic occlusal forces may be associated with the severity of periodontitis. There is no evidence that traumatic occlusal forces can accelerate the progression of periodontitis in humans. Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

98. 98 PRIMARY OCCLUSAL TRAUMA has been defined as injury resulting in tissue changes from traumatic occlusal forces applied to a tooth or teeth with normal periodontal support. This manifests itself clinically with adaptive mobility and is not progressive. SECONDARY OCCLUSAL TRAUMA has been defined as injury resulting in tissue changes from normal or traumatic occlusal forces applied to a tooth or teeth with reduced support. Evidence suggests that certain ORTHODONTIC FORCES can adversely affect the periodontium and result in root resorption, pulpal disorders, gingival recession and alveolar bone loss. Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

99. 99

100. 100 Biologic width is a commonly used clinical term to describe the apico-coronal variable dimensions of the supracrestal attached tissues. The term biologic width is now replaced by SUPRACRESTAL TISSUE ATTACHMENT. Supracrestal attached tissues are composed of the junctional epithelium and the supracrestal connective tissue attachment. Placement of restorative margins within the supracrestal connective tissues is associated with inflammation and loss of periodontal supporting tissues. Optimal restoration margins located within the gingival sulcus do not cause gingival inflammation if patients are compliant with self-performed plaque control and periodic maintenance. Tooth anatomical factors (cervical enamel projections, enamel pearls, developmental grooves), root proximity, abnormalities and fractures, and tooth relationships in the dental arch are related to dental plaque biofilm-induced gingival inflammation and loss of periodontal supporting tissues. Dental materials may be associated with hypersensitivity reactions which can clinically appear as localized inflammation that does not respond to adequate measures of plaque control. Altered passive eruption is a developmental condition with abnormal dento-alveolar relationships. Clinically, this condition is characterized by the gingival margin (and sometimes bone) located at a more coronal level, which leads to pseudopockets and esthetic concerns. Jepsen S, Caton JG, et al. Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1):S237–S248.

101. 101

102. 102 HEALTHY PERI-IMPLANT SITE is characterized by absence of erythema, bleeding on probing, swelling and suppuration. However, the probing depths are usually greater at implant versus tooth sites. The clinical methods to detect the presence of inflammation include visual inspection, probing with a periodontal probe (light probing force) and digital palpation. Probing helps in assessment of presence of bleeding, probing depth changes and mucosal margin migration. The histological characteristics of a healthy peri-implant site are: healthy peri-implant mucosa averages 3 to 4 mm in height and is covered by either a keratinized (masticatory mucosa) or non-keratinized epithelium (lining mucosa) portion of the peri-implant mucosa that is facing the implant/abutment contains a “coronal” portion that is lined by a sulcular epithelium and a thin junctional epithelium and a more “apical” segment in which the connective tissue is in direct contact with the implant surface. Berglundh T, Armitage G, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1): S313–S318.

103. 103 Characteristic of PERI-IMPLANT MUCOSITIS : bleeding on gentle probing erythema swelling and/or suppuration increase in probing depth well-defined inflammatory lesion lateral to the junctional/pocket epithelium with an infiltrate rich in vascular structures, plasma cells, and lymphocytes the inflammatory infiltrate does not extend “apical” of the junctional/pocket epithelium into the supracrestal connective tissue zone Plaque is the etiological factor for peri-implant mucositis. Smoking, diabetes mellitus, and radiation therapy may modify the condition. Non–plaque-induced peri-implant mucositis is not commonly seen. Peri-implant mucositis can resolve in more than 3 weeks following reinstitution of plaque/biofilm control. Berglundh T, Armitage G, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1): S313–S318.

104. 104 PERI-IMPLANTITIS is a plaque-associated pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant mucosa and subsequent progressive loss of supporting bone. Characteristics of Peri-implantitis : clinical signs of inflammation bleeding on probing and/or suppuration increased probing depths and/or recession of the mucosal margin radiographic bone loss lesions extend apical of the junctional/pocket epithelium and contain large numbers and densities of plasma cells, macrophages and neutrophils Peri-implant mucositis is assumed to precede peri-implantitis . Peri-implantitis, in the absence of treatment, seems to progress in a non-linear and accelerating pattern . Patients with a history of severe periodontitis, poor plaque control, and no regular maintenance care after implant therapy have high risk for developing peri-implantitis. Berglundh T, Armitage G, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1): S313–S318.

105. 105 The healing process following tooth loss leads to diminished dimensions of the alveolar process/ridge representing HARD AND SOFT TISSUE DEFICIENCIES. Larger deficiencies may occur at sites exposed to the following factors: loss of periodontal support endodontic infections longitudinal root fractures thin buccal bone plates buccal/lingual tooth position in relation to the arch extraction with additional trauma to the tissues injury pneumatization of the maxillary sinus medications systemic diseases reducing the amount of naturally formed bone agenesis of teeth pressure from soft-tissue supported removable prosthesis The principal factors for recession of the peri-implant mucosa are malpositioning of implants, lack of buccal bone, thin soft tissue, lack of keratinized tissue, status of attachment of the adjacent teeth and surgical trauma. Berglundh T, Armitage G, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1): S313–S318.

106. 106 Diagnosis of peri-implant health requires: Absence of clinical signs of inflammation. Absence of bleeding and/or suppuration on gentle probing. No increase in probing depth compared to previous examinations. Absence of bone loss beyond crestal bone level changes resulting from initial bone remodeling Diagnosis of peri-implant mucositis requires: Presence of bleeding and/or suppuration on gentle probing with or without increased probing depth compared to previous examinations. Absence of bone loss beyond crestal bone level changes resulting from initial bone remodeling. Diagnosis of peri-implantitis requires: Presence of bleeding and/or suppuration on gentle probing. Increased probing depth compared to previous examinations. Presence of bone loss beyond crestal bone level changes resulting from initial bone remodeling Berglundh T, Armitage G, et al. Peri-implant diseases and conditions: Consensus report of workgroup 4 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions. J Periodontol. 2018;89(Suppl 1): S313–S318.

107. ADVANTAGES OF 2017 CLASSIFICATION 107

108. 108 It is evidence-based and clinically relevant classification system. It encourages research, helps in accurate case selection. The difficulty to differentiate aggressive and chronic periodontitis previously is overcome by clarity within stages of periodontitis. Grading of periodontal disease introduces biomarkers (C-reactive protein). 1999 classification classes showed only limited differences with regards to disease risk and complexity factors but has been taken care of by the new classification. New classification was able to reflect on tooth loss while the 1999 classification showed only limited association with tooth loss. Generalised or localised - The 1999 classification used the percentage of sites, while the new one used percentage of teeth (more clinically practical). It assesses the progression of periodontal destruction (bone loss/age) in the patient's past, which is associated with future tooth loss, & may support treatment planning in periodontitis patients. The diagnosis of periodontitis based on CAL was error prone due to CEJ misinterpretation, but in new classification radiographic bone loss & factors including microbiological, host, and environmental determinants increase accuracy. Periodontal & gingival health have been defined. Endo-Perio lesion- classification based on clinical findings in contrast to primary lesion as in the past. Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

109. DISADVANTAGES OF 2017 CLASSIFICATION 109

110. 110 The classification is very extensive and more complicated than 1999 classification and its understanding & implementation by practitioners is bound to take time. Some degree of overlap exists between the following categories: Periodontitis as a Manifestation of Systemic Conditions Systemic Diseases/Conditions Affecting the Periodontal Supporting Tissues Systemic diseases, such as uncontrolled diabetes mellitus, grade modifiers in periodontitis Due to large number of changes from 1999 classification, the effort in the incorporation of this classification in periodontal disease diagnosis is yet to be determined. Necrotizing gingivitis is included in the periodontitis category, despite it being confined to the interproximal soft tissues, and no bone loss. Periodontal abscess is a clinical manifestation and not a disease yet is considered as a diagnosis (reason behind it maybe different treatment regime). Evidence for a distinct pathophysiology between an endo-periodontal and a periodontal lesion have not been established, still it is classified separately. Gingival diseases modified by medications have been included in “dental biofilm induced gingival diseases”, but they cause gingival features independent of biofilm. There is no distinction between periodontal and gingival abscesses. Jain T. The New Periodontal disease classification: Analysis and Review. UNIVERSITY JOURNAL OF DENTAL SCIENCES. 2021 Sep 2;7(3).

111. IMPLEMENTATION IN CLINICAL PRACTICE 111

112. 112 Classification, as described by the World Workshop, is not the same as diagnosis ; classification is historical and tells nothing about current disease status. Diagnosis includes classification but should also include current disease status, based on pocket depths (PPD) bleeding on probing (BoP) risk factor profile of the patient As an example , the classification may be ‘chronic periodontitis’ (using the 1999 system) but an appropriate diagnosis may be ‘generalized moderate chronic periodontitis with widespread pocketing of 4−6 mm and bleeding on probing and with smoking and poorly controlled diabetes as risk factors. Dietrich T, Ower P, Tank M, West NX, Walter C, Needleman I, Hughes FJ, Wadia R, Milward MR, Hodge PJ, Chapple IL. Periodontal diagnosis in the context of the 2017 classification system of periodontal diseases and conditions–implementation in clinical practice. British dental journal. 2019 Jan;226(1):16-22. Ower P. New classification system for periodontal and peri-implant diseases. Dental Update. 2019 Jan 2;46(1):8-11.

113. 113

114. 114 Following the publication of the World Workshop Proceedings, it was also speculated that there would be no place for the Basic Periodontal Examination (BPE) once the new system was adopted. BSP implementation group felt strongly that BPE should be present as an important means of periodontal screening.. Dietrich T, Ower P, Tank M, West NX, Walter C, Needleman I, Hughes FJ, Wadia R, Milward MR, Hodge PJ, Chapple IL. Periodontal diagnosis in the context of the 2017 classification system of periodontal diseases and conditions–implementation in clinical practice. British dental journal. 2019 Jan;226(1):16-22.

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116. 116

117. 117 CLINICAL DECISION TREE

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125. CONCLUSION 125

126. 126 New classification provides new insights for the better understanding and treatment of gingival and periodontal conditions. However, time will decide how the new classification will help periodontists and general dentists to understand the etiology of disease in a better way and choose an optimal treatment plan for periodontal disease. AREAS REQUIRING FURTHER RESEARCH : Develop improved methodologies for accurate assessment of soft and hard tissue changes associated with periodontitis progression longitudinally. Identify genetic, microbial, and host response-associated markers to enable differentiation between periodontitis subtypes, or which can determine the initiation and progression of periodontitis. Expansion of the existing epidemiological databases & integration of clinical, radiographic data to facilitate the study of periodontal and peri-implant diseases and conditions. With regard to the effect of periodontitis on systemic diseases, this classification can help guide future research and lead to prevention of co-morbid effects. Research into the aetiology and natural history of the periodontal diseases is taking giant leaps and will empower us with the knowledge about the mechanisms underlying the etio-pathogenesis of periodontal diseases, generating a need for modifications in the classification schemes.

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