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PRESENTED BYA.ARAVIND KUMAR
Classification is defined as the act or method of
distribution into groups.
Our understanding of the etiology and pathogenesis of
periodontal diseases is continually changing with increasing
scientific knowledge.
Classification systems should be viewed as dynamic works-
in progress that need to be periodically modified based on
current thinking and new 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.
why Classification system necessary
Direct research aimed at learning more about the diseases
concerned.
Help 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.
The first classification system for periodontal disease was
recorded in 1806 when Joseph Fox attempted to classify
“gum- disease”.
Alphonse Toirac in 1823 called it Pyorrhea Alveolaris.
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
Clinical characteristic paradigm(1870-1920)
C.G Davis Classification
G.V Black Classification
Classical pathology paradigm ( 1920-1970)
Gottlieb Classification (1928)
Orban’s Classification (1942)
WHO Classification (1961)
Page and Schroeder (1982) ADA Classification (1982) AAP (1986) Topic’s classification (1986) Grant Stern and Listgarten (1988) Suzuki (1988) World workshop in clinical periodontology (1989) Ranney’s classification (1993) European workshop on periodontitis(1993) World workshop classification (1999) Van der velden classification (2000)
> Based on extent of the disease
> Based on severity of disease per tooth
> Based on age
> Based on clinical characteristics
CLINICAL CHARACTERISTICS PARADIGM
(1870-1920)
Very little was known about the etiology and pathogenesis of
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.
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 LL-1894; Mills GA-1877)
John M.Riggs 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.
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
4.Calcic inflammation of the peridental membrane
5.Phagedenic pericementitis
(phagedenic –spreading ulcer or necrosis)
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
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.
In 1923 he described the disease & called it “the diffuse atrophy of
the alveolar bone”.
Gottlieb classified periodontal disease into four types:
1. Schmutz – pyorrhoe
2. Alveolar atrophy or diffuse atrophy
3. Paradental-pyorrhea
4. 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.
1.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.Environmental factors however dictates the inclusion of a third
and different category of pathologic reaction in periodontology
i.e.,‘pathologic reactions’ produced by occlusal trauma.
This was the first classification scheme to be accepted by AAP.
He grouped them according to the “Pathologic” categories of
inflammation.
Inflammation
I. Gingivitis : Local
Systemic
II. Periodontitis: Simplex
Complex
Degeneration
I. Periodontosis : Systemic disturbances
Hereditary
Idiopathic
Atrophy
I. 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 classical‘experimental gingivitis’ studies published by Harald
Löe 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 1976–1977 of microbial specificity at sites
with periodontosis. ( Newman et al -1976,1977)
This finding, coupled with the demonstration in 1977–1979 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-
inflammatory or degenerative forms of periodontal disease
(Ranney-1977)
It was concluded that ‘Periodontosis’ was an infection &
‘Juvenile Periodontitis’ should become the preferred term.
THE 1977 WORLD WORKSHOP CLASSIFICATION
1.Juvenile periodontitis
2.Chronic Marginal Periodontitis
1977 1986 1989
Page & Schroeder (1982) suggested four different forms of
periodontitis.
1. Prepubertal periodontitis:
Localized
Generalized
2. Juvenile Periodontitis
3. Rapidly progressive periodontitis
4. Adult periodontitis
The need to revise classification system for periodontal diseases
was emphasized during the 1996 World Workshop in Periodontics. In 1997
the American academy of periodontology responded to this and formed a
committee to plan and organize an international workshop to revise the
classification system for periodontal diseases.
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.
CHANGES IN THE CLASSIFICATION IN PERIODONTAL DISEASES
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
“Necrotizing periodontal diseases”
Elimination of a separate disease category for “refractory
periodontitis”
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”
Classification of periodontal disease and condition
(1999 international workshop)
The new classification (1999) is as follows:
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 diseases modified by medications
a) drug influenced gingival diseases
1. drug influenced gingival enlargements
2. drug influenced gingivitis a) oral contraceptive assoicated gingivitis b) other
4.Gingival diseases modified by malnutrition
a) ascorbic acid deficiency gingivitis
b) other
B. Nonplaque induced Gingival lesions
1.Gingival disease of specific bacterial origin
a. Nesseria gonorrhea assoicated lesions
b. Treponema pallidum associated lesions
c. Streptococcal species assoicated lesions
d. Others
2.Gingival disease of viral origin
a) herpes virus infection
: primary herpetic gingivostomatitis
: recurrent oral herpes
: varicella zoster infections
b)Others
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 7 .Other
b. Allergic reactions
1) Dental restorative materials
a. Mercury
b. Nickel,
c. Acrylic
d. Other
2) Reactions attributable to
a. Toothpaste’s /dentifrice’s
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
7) Foreign body reactions
8) Not otherwise specified (NOS)
II. Chronic Periodontitis
III. Aggressive Periodontitis
IV. Periodontitis as a manifestation of systemic diseases.
A) Associated with hematological. disorders.
1) Acquired neutropenia 2) Leukemias
3) Other
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 enlargement1 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
D) Occlusal trauma
1. Primary occlusal trauma
2. Secondary occlusal trauma
1.The classification is very long and extensive.
2.The word “Other” is used too freely.
3.Under “drug influenced gingival diseases” it does not mention the
effects of alcohol, cocaine, heroine, crack and heart medications that
are well documented in the literature as causing increased plaque
formation and stimulating gingival over growth.
3.Removal of the term “Localized Juvenile periodontitis” is most
unfortunate because it is the most clearly defined of all periodontal
diseases.
4.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.
5. The developmental & acquired conditions/deformities are not strictly
periodontal conditions.
5. NUG & NUP together called as necrotising periodontal diseases, they
should remain as separate terms.
6. The term ‘necrotizing stomatitis’ does not appear in the
necrotizing periodontal diseases list.
7. There is no discussion of TMJ problems.
8.There is no discussion on stress as aggravating factors in periodontal
disease.
9.There is no mention of biochemical mediators of GCF and their
effects on periodontal tissues.
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).
Plaque-associated gingivitis is designated as Case Type I.
Case Type II (early periodontitis) is characterized by progression of
inflammation into the deeper periodontal structures with slight bone and
attachment loss.
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 IV (advanced periodontitis) is characterized by further
progression of periodontitis with major loss of alveolar bone support that
is usually accompanied by an increase in tooth mobility. Furcation
involvement is a common finding.
Case Type V (refractory periodontitis) includes those patients that
continue to demonstrate attachment loss after good conventional therapy.
Classification based on the extent of the disease
Van der Velden in 2000
Based on the severity of disease per tooth
Based on the age
Based on the clinical characteristics
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
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 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.
Annals of periodontology vol.4 1999
Perio-2000 volume.39 2005
Perio-2000 volume.26 2001
A Chonological classification of periodontal disease: A
review
journal of internal academy of periodontology 2011 7/2 31-39