INSTITUTE OF DENTAL SCIENCES

DEPARTMENT OF PERIODONTICS

CLASSIFICATION OF PERIODONTAL DISEASES

Guided byProf. (Dr.) Malhotra Parvati Prof. (Dr.) Hemalata M. Dr. H.S. Bhattacharya Dr. Mini S. Semi Dr. Sangita Agarwal

Presented byDr. Gunjan Agarwal

CONTENTS
Introduction Definition The need for a periodontal classification system Historical development of classification systems Clinical characteristics paradigm (1870-1920) Classical pathology paradigm (1920-1970) Infection/Host response paradigm (1970-present) Future challenges in the classification system Conclusion References

INTRODUCTION
Our understanding of the etiology and pathogenesis of periodontal diseases is continually changing with increasing scientific knowledge. Any attempt to group the entire constellation of periodontal diseases into an orderly & widely accepted classification system is fraught with difficulty & considerable controversy.

DEFINITION
Classification is defined as the act or method of distribution into groups.

THE NEED FOR A PERIODONTAL CLASSIFICATION SYSTEM

To cluster similar phenotype in more homogenous syndrome. Direct research aimed at learning more about the diseases concerned. To help to determine the evidence base for better-targeted therapy. Guide practitioners towards the best method for treating a disease. Enable the international community to communicate in a common language. Guide public health planning and targeting of therapy. Help practitioners plan treatment protocols to maximize benefit to all their patients. The ideal way to classify any disease is to use the name of the etiological agent. Periodontal diseases are polymicrobial & polyimmuno-inflammatory in nature.

A HISTORICAL PERSPECTIVE OF PERIODONTAL DISEASE CLASSIFICATION

First specific name for periodontal disease was introduced by Fauchard in 1723 using term Scurvy of the gums. The development and evolution of the periodontal classification system was largely influenced by paradigms that reflect the understanding of periodontal diseases at the given historical period. This guided classification of periodontal disease can be placed into 3 dominant paradigms1) The Clinical characteristics paradigm (1870-1920).

2) Classical pathology paradigm (1920-1970). 3) Infection / Host response paradigm (1970-the present). Classification systems should be viewed as dynamic work in progress that needs to be periodically modified based on current thinking and new knowledge.

CLINICAL CHARACTERISTICS PARADIGM (1870-1920)

During this period very little was known about the etiology and pathogenesis of periodontal diseases and most of the diseases were classified almost entirely based on their clinical characteristics and also on unsubstantiated theories about their cause. Many authors considered these diseases to be caused by local factors (G.V.Black-1893) Some believed that systemic disturbances played a dominant etiological role. (Dunbar LL1894; Mills GA-1877) John M.Riggs (1811-1875) called periodontitis as Riggs disease . First: margins of the gums showed inflammatory action & bleeding at slightest touch of the brush. Second: inflammation extends over the thinner alveolar border causing absorption of bone & gum tissue, forming small pockets filled with pus. Third: thicker portions of the process are involved absorbing it most rapidly. Fourth: the disease has swept away all of the alveoli & much of the gum.

C.G.Davis(1879) believed that there were 3 distinct forms of destructive periodontal disease 1. Gingival recession with minimal or no inflammation- due to feeble vascular action and trauma from tooth brushing or other sources. 2. Periodontal destruction secondary to Lime deposits he believed that calculus exerted mechanical pressure on the gingiva causing the alveolar bone to resorb because of lack of nutrition. 3. Riggs disease the hallmark of which was loss of alveolus without the loss of gumperceived problem was a necrosed alveolus or death of the periodontal membrane, so disease is indicated and continued without any visible mechanical irritant in many cases.

G.V.Black-1886 classified periodontal disease into 5 categories 1. Constitutional gingivitis- Include mercurial gingivitis, potassium iodide gingivitis and scurvy. 2. A painful form of gingivitis- Black described a clinical condition that resembled what is now termed necrotizing ulcerative gingivitis but he never used the term. 3. Simple gingivitis- This was associated with accumulation of debris that eventually led to calcic inflammation of the periodontal membrane. 4. Calcic inflammation of the peridental membrane- This was associated with salivary calculus. Usually there was an even or generalized pattern of destruction of alveolar bone. The destruction usually occurred slowly. Blacks description best fits the periodontal disease that is now known as chronic periodontitis. 5. Phagedenic pericementitis (phagedenic spreading ulcer or necrosis)- This condition shared many features with calcic inflammation of the peridental membrane but there was an irregular pattern of destruction and not much dental calculus. Destruction of the alveolar bone can occur slowly or rapidly later Black replaced this term with Chronic suppurative pericementitis (1915).

CLASSICAL PATHOLOGY PARADIGM (1920-1970)

According to this concept there were at least two forms of destructive periodontal disease inflammatory and non-inflammatory (degenerative or dystrophic). Gottlieb in particular postulated that certain forms of destructive periodontal disease were due to degenerative changes in the periodontium. Gottlieb (1928) discovered histological evidence of an impairment in the continuous deposition of cementum, i.e. cementopathia, this defect was presumably initiated by the degeneration of the principal fibers of the periodontal ligament that eventually resulted in detachment of connective tissue from tooth followed by resorption of adjacent bone. Gottlieb (1928) classified periodontal disease into four types: 1. Schmutz pyorrhoe- result of accumulation of deposits on teeth and was characterized by inflammation, shallow pockets and resorption of alveolar crest. 2. Alveolar atrophy or diffuse atrophy- a non-inflammatory disease exhibiting loosening of teeth, elongation and wandering of teeth in individuals who were generally free of carious lesions and dental deposits. Pockets are formed only in later stages. 3. Paradental-pyorrhea- characterized by irregularly distributed pockets varying from shallow to extremely deep. It may have started as Schmutz- pyorrhoe or as diffuse atrophy.
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4. Occlusal trauma- a form of physical overload which was belived to result in resorption of alveolar bone and loosening of teeth. McCall & Box (1925) introduced the term Periodontitis to those inflammatory diseases in which all components of periodontium i.e. gingiva, bone and periodontal ligament, are involved. Orban & Weinmann (1942) coined the term Periodontosis to designate non-inflammatory disease. Classification systems of this period were based on the Orbans principles of general pathology1. Periodontal disease follow the same pattern as do diseases of other organs. 2. The basic pathologic tissue changes, however are the same as those of other organs. 3. There are 3 main tissue reactions- inflammatory, dystrophic and neoplastic. 4. Environmental factors, however dictate the inclusion of a third and different category of pathologic reaction in periodontology i.e.,pathologic reactions produced by occlusal trauma.

Orban`s classification (1942) Orban`s classification is based on a combination of his perceptions of the etiologic,
clinical & pathologic features of disease. He grouped them according to the Pathologic categories of inflammation. This was the first classification scheme to be accepted by AAP. Inflammation 1) Gingivitis : little or no pocket formation, can include ulcerative form, is of two types- Local: seen in case of calculus, food impaction, irritating restorations, drug action. - Systemic: seen in case of pregnancy, diabetes, T.B., syphilis, nutritional disturbances, drug action, allergy, hereditary, idiopathic. 2) Periodontitis: - Simplex (secondary to gingivitis)- have bone loss, pockets, abscesses can form, cases have calculus. - Complex (secondary to periodontitis)- etiologic factors similar to periodontitis, case have little or no calculus.
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Degeneration 1) Periodontosis : as a rule attacks young girls and older men, often carries immunity. a) Systemic disturbances b) Hereditary c) Idiopathic Diabetes Endocrine disorders Blood dyscrasias Nutritional disturbances Nervous disorders Infectious disease (acute and chronic)

Atrophy

1) Periodontal atrophy: recession , no inflammation, no pockets, osteoporosis. Local trauma- from toothbrush Presenile Senile Disuse Following inflammation Idiopathic

Hypertrophy : Gingival hypertrophy - Chronic irritation - Drug action (dilantin sodium) - Idiopathic (gingivoma, elephantiasis, fibromatosis) Traumatism periodontal traumatism- occlusal trauma

In 1966 world workshop questions were raised about the existence of Periodontosis as a distinct disease entity. Butler (1969) introduced term Juvenile Periodontitis instead of periodontitis when describing periodontal condition of young individuals with severe periodontal bone loss.

INFECTION/HOST RESPONSE PARADIGM (1970 TO PRESENT)

W.D. Miller (1890) was an early proponent of the infectious nature of periodontal diseases. His work had very little impact on convincing his contemporaries that periodontal diseases were infections. He was, however, an early advocate of the Infection/Host Response Paradigm. It was not until, the classical experimental gingivitis studies published by Harald Le and his colleagues from 1965 to 1968 that the Infection/Host Response Paradigm began to move in the direction of becoming the dominant paradigm. The next major discovery in periodontal microbiology was the preliminary demonstration in 19761977 of microbial specificity at sites with periodontosis. ( Newman etal -1976,1977). This finding, coupled with the demonstration in 19771979 that neutrophils from patients with juvenile periodontitis (periodontosis) had defective chemotactic and phagocytic activities, (Genco et al 1977 ; Lavine et al 1979), marked the beginning of the dominance of the Infection/Host Response paradigm. Juvenile Periodontitis new name for periodontitis, was an infection.

Page & Schroeder (1982) suggested four different forms of periodontitis. 1. Prepubertal periodontitis: Localized Generalized 2. Juvenile Periodontitis 3. Rapidly progressive periodontitis 4. Adult type periodontitis

Prepubertal Periodontitis Patients under 11 yrs of age, sex ratio approximately equal, localized or generalized lesions, minimal tooth-associated material, caries rate low, depressed neutrophil chemotaxis, genetic implications, possible medical implications

Juvenile periodontitis Patients between 12-26 yrs of age, females affected more than males, first molar & incisor involvement, lack of clinical inflammation with presence of deep pockets, minimal tooth-associated material, depressed neutrophil chemotaxis, genetic implications, possible medical implications.

Features of RPP Age of onset is between puberty and 35yrs, lesions are generalized, affecting most of the teeth, without any consistent pattern of distribution, some, but not all, patients may have had juvenile periodontitis, severe and rapid bone destruction, after which the destruction process may cease spontaneously or greatly slow, during active phaseacutely inflamed gingiva & arrested phase-the tissues appear free of inflammation, microbial deposits highly variable, functional defects in neutrophils or monocytes, systemic manifestations-weight loss,mental depression & general malaise.

Adult Periodontitis Patients over 35 yrs of age. Approximately equal sex distribution, variable lesions, plaque & calculus present, host-response apparently normal, genetic implications unknown.

AAP in 1986adopted the following classification I. Juvenile periodontitis A Prepubertal periodontitis B Localized juvenile periodontitis C Generalized juvenile periodontitis II. Adult periodontitis III. Necrotizing ulcerative gingivo-periodontitis IV. Refractory periodontitis.

Grant , Stern And Listgarten -1988 Bacterially induced diseases Gingivitis

Periodontitis Adult type Post-juvenile Early onset periodontitis- juvenile- localized or generalized. ANUG Acute abscess Pericoronitis Functionally induced diseases : Traumatic occlusion Disuse atrophy Trauma : habits, accidents.

Suzuki Classification-1988 Suzuki stated that Additional clinical observations in our laboratories during investigation on the mode of inheritance of juvenile and rapidly progressing periodontitis have suggested that further qualifications can be made. I. II. Adult periodontitis Rapidly progressive periodontitis- based on factors such as age, microbial deposits, autologus mixed lymphocyte reaction divided intoType A Type B III. Juvenile periodontitis IV. Post juvenile periodontitis V. Prepubertal periodontitis

RPP-Type A Patients usually between 14 & 26 yrs of age Females affected more than males(2:1 to 3:1) Generalized lesions Minimal tooth-associated materials
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Caries rate variable Depressed neutrophil chemotaxis Genetic implications Possible medical considerations

RPP-Type B Patients generally over 26 yrs of age Sex distribution not established Generalized lesions Plaque and calculus present Caries rate variable Neutrophil chemotaxis normal or depressed Genetic implications not known Possible medical considerations

Post-Juvenile Periodontitis Patients generally between 26 &35 yrs of age Females affected more than males(3:1) First molar and incisor lesions Plaque and calculus present Caries rate variable Neutophil function not determined Genetic implications not known Possible medical considerations

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Classification of periodontitis recommended by the 1989 workshop in clinical periodontics I. Adult periodontitis II. Early-onset periodontitis A. Prepubertal periodontitis 1. Generalized 2. Localized B. Juvenile periodontitis 1. Generalized 2. Localized C. Rapidly progressive periodontitis III. Periodontitis associated with systemic disease IV. Necrotizing ulcerative periodontitis V. Refractory periodontitis This classification, although soundly based in the Infection/Host response Paradigm, depended heavily on the age of the patients and the rates of progression.

Problems with the 1989 classification The uncertainty about the proposed Rapidly progressive Periodontitis as a single entity. And secondly the questionable criteria used to determine its presence they were -

1. That the clinician had to actually document that rapid progression had occurred prior to giving the patient the diagnosis. 2. The term rapid was not defined in terms of progression and time period. 3. The disease had to be assumed from a single examination in an adolescent or young adult with massive attachment loss. 4. The concept that the rate of progression might be a useful criterion may itself be flawed

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Shortcomings of the 1989 classification 1. Lack of a category for gingival diseases. 2. Overlap between the disease categories 3. Difficulty in fitting the patients into any one of the existing categories 4. Similarity of microbiological and host response features in different categories 5. An emphasis on age of onset that became a problem as patients aged into a new category. 6. Unclear classification criteria. As a consequence the 1989 classification was criticized and a new system of classification was proposed by Ranney in 1993.

Ranneys Classification (1993) He recommended elimination of the Refractory periodontitis category since it was a heterogeneous group and it was impossible to standardize treatment. He also recommended the elimination of the Periodontitis associated with systemic disease category since the expression of all forms of periodontitis is affected by systemic diseases.

I. Gingivitis A. Gingivitis, Plaque bacterial not systemically aggravated systemically aggravated by sex hormones, drugs, systemic disease.

B. Necrotizing ulcerative 1. Systemic determinants unknown 2. HIV-related C. Gingivitis, Non plaque 1. Associated with skin disease 2. Allergic 3. Infectious II. Periodontitis A. Adult Periodontitis
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- not systemically aggravated - systemically aggravated 1. Diabetes mellitus 2. Neutropenias 3.Leukemias 4. Acquired immunodeficiency syndrome 5. Crohn's Disease 6. Addison's Disease 7. Lazy leukocyte syndrome B. Early Onset Periodontitis 1. Localized early onset periodontitis a. Neutrophil abnormality 2. Generalized early onset periodontitis a. Neutrophil abnormality b. Immunodeficient 3. Early onset periodontitis related to systemic disease- leukocyte adhesion deficiency, hypophosphatasia, Papillon Lefevre syndrome, neutropenias, leukemias, Chediak Higashi syndrome, AIDS, diabetes mellitus type 1, trisomy 21, histocytosis X, Ehlers- Danlos syndrome (type VIII) 4. Early onset periodontitis, systemic determinants unknown. C. Necrotizing Ulcerative Periodontitis 1. Systemic determinants unknown 2. HIV-related 3. Nutritionally related D. Periodontal Abscess

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The consensus reached by the first European Workshop on Periodontology in 1993 was that existing disease classifications were unsatisfactory due to: Extensive overlap between different diagnostic category. The need for assumption concerning previous disease progression. The nessicity for detailed information on the quality of treatment previously provided and the patients compliance and tissue response to this therapy. The lack of a consistent basis for classification.

The European Workshop In Periodontics-1993 The recommendation was that classification should be based on causative factors and host-response factors, and a simple classification was proposed that omits the forms periodontitis associated with systemic disease and refractory periodontitis.

1.Early-onset periodontitis 2.Adult periodontitis 3.Necrotizing ulcerative periodontitis

Drawbacks of 1993 European workshop classification1. Considerable overlap in disease categories. 2. Absence of a gingival disease component. 3. Inappropriate emphasis on age of onset of disease and rate of progression. 4. Inadequate or inappropriate classification criteria.

The AAP international workshop for classification of periodontal diseases, 1999

Problems, inconsistencies and deficiencies associated with the 1989 classification led to many clinicians and investigators to call for a revision in the classification system. What emerged was a classification that was more firmly based on the Infection /host response paradigm In reality, the changes were a course-correction or fine-tuning of the 1989 classification.
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Changes in the Periodontal Classification system 1. Addition of a gingival disease component 2. Replacement of Adult Periodontitis with Chronic Periodontitis 3. Elimination of Refractory Periodontitis as a separate entity. 4. Replacement of Early-onset periodontitis with Aggressive periodontitis 5. Sub classification of Periodontitis as a manifestation of systemic diseases. 6. Replacement of ANUG and ANUP with Necrotizing periodontal diseases. 7. Addition of a category for Periodontal abscesses and Periodontic and Endodontic Lesion 8. Addition of a new category for Acquired deformities and conditions

Addition of a gingival diseases category Gingivitis represents a spectrum of diseases whose onset is commonly attributed to the presence of bacteria

Gingival diseases were classified as 1. Dental plaque induced gingival diseases 2. Non-plaque associated gingival disease

AAP CLASSIFICATION, 1999 Gingival diseases Dental plaque-induced gingival disease

I. Gingivitis associated with dental plaque only A.Without local contributing factors B.With local contributing factors II. Gingival disease modified by systemic factors A.Associated with the endocrine system B.Associated with blood dyscrasias
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III. Gingival diseases modified by medications A. Drug-influenced gingival diseases 1.drug-influenced gingival enlargements 2.drug-influenced gingivitis IV. Gingival diseases modified by malnutrition

Non-plaque induced gingival lesions

I. Gingival diseases of specific bacterial origin II. Gingival diseases of viral origin III. Gingival diseases of fungal origin IV. Gingival lesions of genetic origin V. Gingival manifestations of systemic conditions A. Mucocutaneous lesions B. Allergic reactions VI. Traumatic lesions A. Chemical injury B. Physical injury C. Thermal injury VII. Foreign body reactions VIII. Not otherwise specified

Replacement of Adult Periodontitis with Chronic Periodontitis Adult periodontitis was defined as a disease having its onset after the age of 35 years; approximately 18% of this population has periodontal bone loss. However, the agedependent nature of the adult periodontitis designation was felt to be somewhat arbitrary as similar bone loss patterns can also be seen in adolescents and even in the primary dentition of children. Another difficulty lay in the fact that the age at which a patient presents for treatment does not necessarily reflect the age at which the disease began.
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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. Chronic periodontitis refers to progression of the disease over time without treatment and does not suggest that the disease is untreatable. Chronic periodontitis was defined as an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss. It is characterized by pocket formation & or gingival recession. (Flemming 1999)

Clinical features and Characteristics of Chronic Periodontitis (G. Armitage; Annals1999) 1. Most prevalent in adults but can also occurs in children and adolescents. 2. Amount of destruction is consistent with the local factors 3. Sub gingival calculus is a frequent finding 4. Slow to moderate rate of progression but my have periods of rapid progression. 5. Can be associated with local predisposing factors (eg-Tooth related, iatrogenic factors) 6. Associated with variable microbial pattern. 7.May be modified by and or associated with systemic diseases 8.Can be modified by factors other that systemic diseases such as cigarette smoking and emotional stress. 9. Can further be classified on the basis of extent & severity. Extent localized or generalized Severity slight: 1-2mm CAL moderate: 3-4mm CAL severe: >5mm CAL

Elimination of Refractory Periodontitis category Refractory periodontitis refers to continued attachment loss in spite of adequate treatment. The term recurrent periodontitis is now used to refer to the return of periodontitis and not as a separate disease
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Potentially any patients with a past history of periodontitis can develop recurrent periodontitis if adequate oral hygiene is not maintained.

Chronic Periodontitis

A. Localized B. Generalized Aggressive Periodontitis

A. Localized B. Generalized Periodontitis as a manifestation of systemic diseases A. Hematological disorders B. genetic disorders Necrotizing Periodontal diseases Abscesses of the periodontium Periodontitis associated with endodontic lesions

Replacement of Early onset Periodontitis with Aggressive Periodontitis In the 1989 classification patients were placed into this category based on the age in so the term was replaced . In 1999 Aggressive Periodontitis was defined as a disease in patients who were systemically healthy but had rapid loss of attachment & alveolar bone loss & a high incidence of familial link.

Features common to both Localized and Generalized Aggressive periodontitis (Lang et al 1999)

Primary features 1. Except for periodontitis patients are usually healthy 2. Rapid attachment loss and bone destruction 3. Familial aggregation
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Secondary features 1. Amounts of microbial deposits are inconsistent with the disease severity. 2. Elevated proportions of A.a.comitans and in some populations P.gingivalis may be elevated. 3. Phagocyte abnormalities. 4. Hyper responsive macrophage phenotype including elevated levels of PGE2 and IL . 5. Progression of attachment loss and bone loss may be self arresting.

Localized Aggressive periodontitis 1. Circumpubertal onset 2. Robust serum antibody to infecting agents 3. Localized first molar/incisor disease with proximal attachment loss on at least 2 permanent teeth, 1 of which ia a 1st molar.

Generalized Aggressive Periodontitis 1. Usually affecting persons under 30yrs of age 2. Poor serum antibody response to infecting agents. 3. Pronounced episodic nature of destruction. 4. Generalized proximal attachment loss affecting at least three permanent teeth other than first molars an incisors.

Periodontitis as a manifestation of systemic diseases The term periodontitis as a manifestation of systemic diseases is a misnomer as the conditions listed are strictly systemic diseases that affect the periodontal tissues and are present within them rather than periodontal diseases arising de novo. Diabetes mellitus has not been included in this category as it can modify all forms of periodontal diseases.

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Introduction of the term Necrotizing Periodontal diseases The workshop participants acknowledged that NUG and NUP are clinically identifiable conditions although they were unsure if both were two different diseases or part of the same disease. Diagnostic criteria for ANUG (Corbet 2004) 1. Lesions are painful. 2. Lesions are gingival ulcers, punched out crater like, of interdental papilla and may involve marginal gingiva. 3. The ulcers bleed spontaneously or readily.

Diagnostic criteria for NUP (Corbet 2004) 1. Deep interdental craters with denudation of interdental alveolar bone. 2. Sequestration of interdental and possibly buccal and /or lingual alveolar bone.

Addition of a category for Periodontal abscesses and Periodontic Endodontic lesion Periodontal abscess present diagnosis & treatment challenges they deserve to be classified apart from periodontal diseases. 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. No changes were made to the definition of these diseases; they were simply added to the classification system.

Addition of a category for Developmental or acquired deformities and conditions Although the deformities and conditions listed in this section of the classification are not separate diseases, they are important modifiers of the susceptibility to periodontal diseases or can dramatically influence outcomes of treatment. In addition, since periodontists are routinely called upon to treat many of these conditions they have been given a place in the new classification

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Developmental or acquired deformities and conditions A. Localized tooth-related factors that predispose to plaque-induced gingival diseases or periodontitis B. Mucogingival deformities & conditions around teeth C. Mucogingival deformities & conditions on edentulous ridges D. Occlusal trauma

Shortcomings of the 1999 classification 1. The classification is very long and extensive. 2. Removal of the term Localized Juvenile periodontitis is most unfortunate because it is the most clearly defined of all periodontal diseases. 3. There is no provision for the category of Historical or previous disease for a patient who has suffered periodontal disease in the past and is no longer currently active. 4. The developmental & acquired conditions/deformities are not strictly periodontal conditions. 5. NUG & NUP together called as necrotising periodontal diseases, they shoud remain as separate terms. 6. The term necrotising stomatitis does not appear in the necrotising periodontal diseases list.

Van der Velden in 2000 Van der Velden classification was based on four dimensions, i.e. extent, severity, age, and clinical characteristics. Defining when periodontitis is considered to be present. It is suggested to define periodontitis as the presence of inflamed pathological pockets 4 mm deep in conjunction with attachment loss. If present, then the next steps can be taken. -Classification based on extent of the disease, i.e. number of affected teeth. -Classification based on severity of disease per tooth. The fact that either attachment loss or bone loss can be used for the classification of severity implies that although it may be important to know the actual root length in a given patient, radiographs are not a prerequisite for the classification of severity. -Classification based on age.
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-Classification based on clinical characteristics.

Classification based on the extent of the disease

If teeth are missing, the class description should still reflect the clinical image of the patient. Therefore it was decided for cases with 14 teeth to omit the class semigeneralized and to change the number of teeth for the generalized class to 814

Based on the severity of disease per tooth

Based on the age

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Based on the clinical characteristics

The classification is 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. Ex:- localized severe juvenile periodontitis - semi-generalized minor juvenile periodontitis -generalized severe refractory post adolescent periodontitis

FUTURE CHALLENGES PERIODONTAL DISEASES

IN

THE

CLASSIFICATION

OF

As we enter the postgenomic era with our increased understanding of the bacteria associated with periodontal infections and the genetic factors controlling host responses to these infections, it would seem that a more mechanistic or etiological classification could be devised. Why could modern classifications of periodontal diseases not be based on the
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microbiological features of these infections, or on the genetic factors that seem to control the clinical expression of these diseases? The answer is simple. We do not know enough about periodontal infections to take this next step. It is very likely that Chronic Periodontitis is a constellation of diseases (i.e. it is not a single entity). One of the main problems associated with any attempt at subclassifying this or other forms of periodontitis, is that these infections are polymicrobial and polygenic. In addition, the clinical expression of these diseases is altered by important environmental and hostmodifying conditions (e.g. oral hygiene, smoking, emotional stress, diabetes). It is conceivable that with much more information and the application of sophisticated multivariate analyses, it may eventually be possible to subclassify the multiple forms of Chronic Periodontitis into discrete microorganism/host genetic polymorphism groups such as: group A Set .1 of microorganisms +Set .1 of genetic polymorphisms. group B Set .2 of microorganisms + Set .2 of genetic polymorphisms. group C Set .3 of microorganisms + Set .3 of genetic polymorphisms. group D Set .4 of microorganisms + Set .4 of genetic polymorphisms.

In addition, it will be necessary to superimpose on these microorganism/host genetic polymorphism groupings the effect of environmental or host-modifying factors. It will be necessary to address head on the nagging question, When are host-modifying factors (e.g. smoking, diabetes) so important that they should be a principal part of the disease classification? That is, in an evidence-based classification should there be a smokinginduced periodontitis or a diabetic periodontitis? When do modifying factors become an essential classification characteristic of the disease? The same problems also occur when one addresses the so-called Localized Aggressive Periodontitis and Generalized Aggressive categories. It is likely that these diseases also have multiple forms and are at least as complex as the Chronic Periodontitis group. There is a tendency for clinicians and investigators to jump the gun and to use etiology- or pathogenesis- based classifications or terms prematurely. For example, it is exceedingly difficult to prove in a given subset of patients that the presence of a known periodontal pathogen in the subgingival flora is actually the cause of the periodontal disease in that group of individuals. Indeed, it has been amply shown that known periodontal pathogens, such as Actinobacillus actinomycetemcomitans, can be found in the supra- and subgingival flora of patients without periodontitis. Nevertheless, some authors have referred to the existence of an A. actinomycetemcomitans- associated periodontitis. Although tempting, terms based on assumed etiological or pathogenic associations should be discouraged until there is a body of data to support their use.

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CONCLUSION In the past 130 years classification system for periodontal diseases have evolved based on understanding of nature of these diseases at time the classification were proposed. One consistent feature of the development of classification systems is the guaranteed controversy surrounding any suggested revisions to the previously accepted system of nomenclature. Future systems are likely to be controversial, stimulate much debate & require further modification.

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REFERENCES
Carranzas clinical periodontology 8th & 10th edition Development of a Classification System for Periodontal Diseases and Conditions by Gary C. Armitage. Ann Periodontol 1999;4:1-6. Purpose and problems of periodontal disease classification by Ubele van der velden. Periodontology 2000, Vol. 39, 2005, 1321. The Periodontal Disease Classification System of the American Academy of Periodontology An Update by Colin B. Wiebe, Edward E. Putnins. J Can Dent Assoc 2000; 66:594-7 Classifying periodontal diseases -a long standing dilemma. Gary.C.Armitage. Perio 2000 2002: vol 30; 9-23. Diagnosis of acute periodontal lesions. Corbet EF. Perio 2000 2004: vol 34;204-216. Periodontal diagnoses and classification of periodontal diseases. Armitage GC. Perio 2000 2004: vol 34; 9-12.

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