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A.ARAVIND KUMAR
knowledge.
Classification systems are necessary in order to provide a frame work in which to scientifically study the etiology, pathogenesis and treatment of disease in an orderly fashion.
Help determine the evidence base for better-targeted therapy. Guide practitioners towards the best method for treating a disease.
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.
The first classification system for periodontal disease was recorded in 1806 when Joseph Fox attempted to classify gumdisease.
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
1870-1920
1920-1970
1970-present
Page and Schroeder (1982) ADA Classification (1982) AAP (1986) Topics classification (1986) Grant Stern and Listgarten (1988) Suzuki (1988) World workshop in clinical periodontology (1989) Ranneys classification (1993)
periodontal diseases during this period and most of the diseases were
classified almost entirely based on their clinical characteristics and also on unsubstantiated theories about their cause.
Second: inflammation extends over the thinner alveolar border causing absorption of bone & gum tissue, forming small pockets filled with pus.
Fourth: the disease has swept away all of the alveoli & much of the
gum.
A classical example was the paper published by C.G.Davis(1879) who believed that there were 3 distinct forms of destructive periodontal disease
1.Gingival recession with minimal or no inflammation 2.Periodontal destruction secondary to Lime deposits 3. Riggs disease the hallmark of which was loss of alveolus without the loss of gum
Similarly G.V.Black-1886 classified periodontal disease into 5 categories 1.Constitutional gingivitis 2.A painful form of gingivitis 3.Simple gingivitis
By 1929 Becks.H estimated that there were over 350 theories of pyorrhea and much more confusing terminologies such as
Pyorrhea alveolaris Calcic inflammation of the peridental membrane Phagedenic pericementitis Chronic suppurative periodontitis
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.
In 1923 he described the disease & called it the diffuse atrophy of the alveolar bone.
1. 2. 3. 4.
Gottlieb classified periodontal disease into four types: Schmutz pyorrhoe Alveolar atrophy or diffuse atrophy Paradental-pyorrhea Occlusal trauma
McCall & Box (1925) introduced the term Periodontitis to those inflammatory diseases in which all components of periodontium are involved.
Wannenmacher (1938) Paradontosis marginalis progressiva Thoma & Goldman(1940) called the disease as Paradontosis. Orban & Weinmann (1942) coined the term Periodontosis
Classification systems were dominated by the Orbans principles during this time.
This was the first classification scheme to be accepted by AAP. He grouped them according to the Pathologic categories of inflammation.
I.
Inflammation Gingivitis : Local Systemic Periodontitis: Simplex Complex Degeneration I. Periodontosis : Systemic disturbances Hereditary Idiopathic
II.
I.
Atrophy Periodontal atrophy: Local trauma Senile Disuse Idiopathic Hypertrophy : Gingival hypertrophy - Chronic irritation - Drug action - Idiopathic Traumatism
In 1966 world workshop questions were raised about the existence of Periodontosis as a distinct disease entity.
The term Juvenile Periodontitis was introduced by Chaput & colleagues in 1967 & by Butler (1969) .
In 1971 Baer defined it as a disease of the periodontium occurring in an otherwise healthy adolescent which is characterized by a rapid loss of alveolar bone about more than one tooth of the permanent dentition. the amount of destruction manifested is not commensurate with the amounts of local irritants.
W.D. Miller (1890), in particular, 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 . however, an early advocate of the Infection/Host Response Paradigm.
The classicalexperimental 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 et al -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.
1977 convincing arguments were provided that there was no scientific basis for retaining the concept that there were non-
1989
I. Early-Onset Periodontitis
A. Prepubertal periodontitis B. Juvenile periodontitis C. Rapidly progressive periodontitis II. Adult Periodontitis III. Necrotizing Ulcerative Periodontitis IV. Refractory Periodontitis V. Periodontitis Associated
1.
2. 3. 4.
On October 30 November 2, 1999, the International Workshop for a classification of Periodontal Diseases and conditions was held and a new classification was agreed upon.
Addition of a section on Gingival Diseases Replacement of adult periodontitis with chronic periodontitis Replacement of early onset periodontitis with aggressive periodontitis
Replacement
of
necrotizing
ulcerative
periodontitis
with
Elimination of
periodontitis
a separate
disease
Addition of a category on Periodontal abscess Addition of a category on Periodontic endodontic lesions Addition of a category on Development or acquired deformities and conditions
I : GINGIVAL DISEASES
A) Dental plaque induced gingival disease. (Can occur without attachment loss or on a periodontium with attachment loss that is not progressing) 1.Gingivitis associated with dental plaque only: a) Without other local contributing factors b) With local contributing
2.Gingival diseases modified by systemic factors a) Associated with the endocrine system 1. Puberty associated gingivitis 2. Menstrual cycle associated gigivitis 3. Pregnancy associated a) gingivitis b) pyogenic granuloma 4. Diabetes mellitus associated gingivitis b) associated with blood dyscrasias 1. leukemia associated gingivitis 2. Other
3) Gingival disease of fungal origin a. candida species infections 1.generalized gingival candididosis b. linear gingival erythema c. histoplasmosis d. other 4) Gingival lesions of genetic origin a.hereditary gingival fibromatosis b.other 5. Gingival manifestations of systemic conditions a. mucocutaneous disorders
1. lichen planus 2. pemphigoid 3. pemphigus vulgaris 4. erythema multiforme 5. Lupus erythematosus 6. Drug-induced
b. Allergic reactions
1) Dental restorative materials a. Mercury b. Nickel, c. Acrylic d. Other 2) Reactions attributable to
a. Toothpastes /dentifrices
b. Mouth rinses / mouth washes c. Chewing gum additives d. Foods and additives
3)
Other
6) Traumatic lesions (factitious, iatrogenic, accidental) a. Chemical injury b. Physical injury c. Thermal injury
II. Chronic Periodontitis III. Aggressive Periodontitis IV. Periodontitis as a manifestation of systemic diseases. A) Associated with hematological. disorders.
B) Associated with genetic disorders 1. Familial and cyclic Neutropenia 2. Down syndrome 3. Leukocyte adhesion deficiency syndromes 4. Papillon - Lefevre syndrome 5. Chediak Higashi syndrome 6. Histiocytosis syndrome 7. Glycogen storage disease 8. Infantile genetic agranulocytosis 9. Cohen syndrome 10. Ehlers Danlos syndrome (Types IV and VIII) 11. Hypophosphatasia 12. Other C) Not otherwise specified (NOS)
V. Necrotising Periodontal Diseases A) Necrotising ulcerative gingivitis (NUG) B) Necrotising ulcerative periodontitis (NUP) VI. Abscesses of the periodontium
A) Gingival abscess B) Periodontal abscess C) Periocoronal abscess VII. Periodontitis assoicated with endodontic lesions
VIII. Developmental or Acquired Deformities & conditions A) Localized tooth related factors that modify or predispose to plaque induced gingival disease / periodontitis 1. Tooth anatomic factors 2. Dental restorations / appliances 3. Root fractures 4. Cervical root resorption & cemental tears
B) Mucogingival deformities and conditions around teeth 1. gingival / soft tissue recession a. facial or lingual surfaces b. interproximal (papillary) 2. lack of keratinized gingiva 3. decreased vestibular depth 4. aberrant frenum / muscle position 5. gingival excess a. pseudopocket b. inconsistent gingival margin c. excessive gingival display d. gingival enlargement 1 1 6.abnormal color
C) Mucogingival deformities and conditions on edentulous ridges 1. vertictal and / or horizontal ridge deficiency 2. lack of gingiva / keratinized tissue 3. gingiva / soft tissue enlargement 4. aberrant frenum / muscle position 5. decreased vestibular depth 6. abnormal color
1.The classification is very long and extensive. 2.The word Other is used too freely.
diseases.
10. The section on occlusal trauma does not in our opinion adequately cover the magnitude of the pathology associated occlusion, malocclusion and conutribute to TMJ malfuction. 11. There is still considerable overlap in disease categories
For administrative and third-party insurance reporting purposes, the American Academy of Periodontology classifies gingivitis and periodontitis into five broad case types (1997).
Case Type III (moderate periodontitis) is classified as a more advanced state with increased destruction of the periodontal structures and noticeable loss of bone support, possibly accompanied by increased tooth mobility and furcation involvement on multirooted teeth.
Case Type V (refractory periodontitis) includes those patients that continue to demonstrate attachment loss after good conventional therapy.
First ,the extent of disease Severity Diagnosis made based on the clinical characteristics Based on age.
Ex:- localized severe juvenile periodontitis - semi-generalized minor juvenile periodontitis -generalized severe refractory post adolescent periodontitis
diseases i.e. it is not a single entity, One of the main problems with
any attempt to classify this or any 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 host-modifying conditions.
The facility to study gene expression & the genetic factors underlying the differences in host response to periodontal pathogens between patients may help inform the classification systems of 2010-2020.
Future systems are likely to be controversial, stimulate much debate & require further modification.