classification of periodontal diseases

1. Classification of periodontal diseases
Contents:
1. Definition
2. Need for classification
3. History
4. Dominant Paradigms in the historical development of classification systems
5. Classification systems
6. Conclusion
7. References
Definition:
Systematic arrangement into classes or groups based on perceived common characteristics.
A means of giving order to a group of disconnected facts.
Need for classification:
 Provides a framework for scientifically studying
Etiology
Pathogenesis
Treatment
 To assess the prognosis, outcome and determine the treatment plan.
The periodontal condition is clinically characterized by three symptoms: loss of connective tissue
attachment, loss of alveolar bone support, and inflamed pathological pockets. On the basis of
these three symptoms one diagnostic name for this condition would be appropriate, e.g.
destructive periodontal disease. However, if age, distribution of lesions, degree of gingival
inflammation, putative rate of breakdown, response to therapy, etc., are also taken into account,
numerous diagnostic names are needed.
History
Giralamo Cardono was the first to differentiate periodontal diseases. He differentiated them into
two main types:
 Disease that occurs with advancing age and leads to progressive loosening and loss of
teeth.
 Very aggressive type that occurs in younger patients.

2. The first specific name for periodontal disease was introduced by Fauchard in 1723 using the
term scurvy of the gums (Gold et al(1985)).
In the early 19th century, periodontitis was known as “Riggs Disease”.
Gottlieb is considered to be the first author who clearly distinguished various forms of
periodontal disease. In the 1920s he classified periodontal disease into four types
 Schmutz-Pyorrhoe: thought to be the result of the accumulation of deposits on the teeth
and was characterized by inflammation, shallow pockets, and resorption of the alveolar
crest.
 Alveolar atrophy or Diffuse atrophy: diffuse atrophy was described as 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. In this disease,
manifesting pockets are formed only in later stages
 Paradental-Pyorrhoe: Paradental-Pyorrhoe was characterized by irregularly distributed
pockets varying from shallow to extremely deep. This form of disease may have started
as Schmutz-Pyorrhoe or as diffuse atrophy.
 Occlusal trauma: a form of physical overload which was believed to result in resorption
of the alveolar bone and loosening of teeth.
More or less at the same time, McCall & Box (1925) introduced the term periodontitis to denote
those inflammatory diseases in which all three components of the periodontium, i.e. the gingiva,
bone, and periodontal ligament, were affected.
Periodontitis was subclassified, on the basis of presumed etiologic factors,
 Simplex periodontitis, considered to be the result from local bacterial factors, and
 Complex periodontitis, a result of systemic etiologic factors.
Becks (1931) made a distinction between paradentitis, a disease which originates from the
gum tissue in the form of gingivitis and genuine paradentosis, which originates in the bony
alveolus, perhaps in the form of an osteopathy. Orban & Weinmann (1942) adopted this
nomenclature using the anglicized term periodontosis to designate non inflammatory disease.
During the 1950s and 1960s the importance of dental plaque as the major etiologic factor for
periodontal diseases became more and more evident. The ultimate proof of the association
between plaque and gingival inflammation was shown by Loe and coworkers in their
experimental gingivitis study. The influence of this way of thinking was clearly evident during
the 1966 Workshop in Periodontics when the entity periodontosis was revisited. Soon after the
Workshop, Butler introduced the name juvenile periodontitis instead of periodontosis when
describing the periodontal condition of young individuals with severe periodontal bone loss.

3. According to Butler there was no proof of any degenerative process, as the suffix “osis” would
imply.
Dominant paradigms in the historical development of classification
systems
The development and evolution of classification systems for periodontal diseases have been
largely influenced by paradigms that reflect the understanding of the nature of periodontal
diseases during a given historical period
The classification of periodontal diseases can be placed into three dominant paradigms primarily
based on
1870–1920: The clinical features of the diseases
1920–1970: The concepts of classical pathology
1970–present: Infectious etiology of the diseases
As classification systems have evolved, newer thoughts about periodontal diseases have been
superimposed on a matrix of older ideas. Ideas that are believed to be clearly incorrect have been
discarded. In the sense, the newest or dominant paradigm rests on a foundation of the still valid
components of the older or previous paradigms.
I) Clinical characteristics paradigm (1870-1920)
During this period, very little was known about the etiology and pathogenesis of periodontal
diseases and one of the main debates was whether they were caused by local or systemic factors.
Most authors like GV Black (1894), WD Miller (1890), Patterson (1885), JM Riggs(1882) and
many more considered these diseases to be primarily caused by local factors whereas some like
Peirce (1892), GA Mills (1881), LL Dunbar (1894)believed that systemic disturbances played a
dominant etiological role. Many of the advocates for the etiological role of local factors like WD
Miller (1890), Patterson (1885), also acknowledged that in some cases both local and systemic
factors were important
C.G. Davis in 1879 believed that there were three distinct forms of destructive periodontal
disease:
 Gingival recession with minimal or no inflammation.
 Periodontal destruction secondary to ‘lime deposits’.

4. Davis apparently believed that calculus exerted mechanical pressure on the gingiva
causing the alveolar bone to resorb because of lack of nutrition.
 ‘Riggs’Disease’
Davis believed the hallmark of which was, ‘... loss of alveolus without loss of gum.’
The perceived problem was a ‘necrosed alveolus’ or death of the periodontal membrane.
‘... we get a disease that is initiated and continued without any visible mechanical irritant
in many cases; and I believe the death of the peridental membrane, depriving the
alveolus of nutrition, accounts for the death and disintegration of the bone.”
In 1886, G.V. Black classified periodontal diseases based on their clinical characteristics into
five separate groups:
 Constitutional gingivitis: including mercurial gingivitis, potassium iodide gingivitis and
scurvy.
 A painful form of gingivitis: Black described a clinical condition that resembled what is
now termed necrotizing ulcerative gingivitis (NUG), but he never used the term.
 Simple gingivitis: This was associated with the accumulation of debris that eventually led
to ‘calcic inflammation of the peridental membrane.’
 Calcic inflammation of the peridental membrane: This was associated with ‘salivary’
and/or ‘serumal’ calculus. Usually there was an even or generalized pattern of destruction
of alveolar bone. The destruction usually occurred slowly. Black’s description best fits
the periodontal disease that is now known as chronic periodontitis.
 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. In a later publication Black replaced the term
‘phagedenic pericementitis’ with ‘chronic suppurative pericementitis’
Drawbacks/ Limitations:
 Little or no scientific evidence was used, it was only based on their personal
interpretation of what they saw clinically as the primary basis for classifying periodontal
diseases
 No generally accepted terminology or classification system for periodontal diseases was
adopted during this era. As a result, in the latter part of the 19th century periodontitis
went under numerous names including: ‘pyorrhea alveolaris’ ‘Riggs’ disease’ ‘calcic
inflammation of the peridental membrane’ ‘phagedenic pericementitis’ and ‘chronic

5. suppurative pericementitis’. During this period, the dominant term used for destructive
periodontal disease was pyorrhea alveolaris.
II) Classical pathology paradigm (1920-1970)
As the field of periodontology began to mature there was a belief that there were at least two
forms of destructive periodontal disease inflammatory and non inflammatory (‘degenerative’ or
‘dystrophic’).
This conclusion was given by a group of investigators led by Gottlieb and Orban. Gottlieb, in
particular, postulated that certain forms of destructive periodontal disease were due to
degenerative changes in the periodontium
He believed that he had discovered histological evidence of an impairment in the continuous
deposition of cementum (i.e. ‘cementopathia’). This cemental defect was presumably initiated by
the degeneration of the principal fibers of the periodontal ligament that eventually resulted in
detachment of connective tissue from the tooth followed by resorption of adjacent bone
Gottlieb’s ideas were probably widely accepted because they appeared to explain clinical
observation that some young patients with relatively clean mouths had massive and localized
bone loss with only minimal or no overt signs of gingival inflammation As a result of Gottlieb’s
theory, almost all classification systems used in this era, included disease categories labeled as
‘dystrophic’, ‘atrophic’, or ‘degenerative’.
Classification of periodontal diseases following the “classical pathology” paradigm
ORBAN, 1942
I. INFLAMMATION
A. Gingivitis (little or no pocket formation; can include ulcerative form – Vincent’s)
1. Local (calculus, food impaction, irritating restorations, drug action etc)
2. Systemic

6. a. Pregnancy
b. Diabetes
c. Other Endocrine Dysfunctions
d. Tuberculosis
e. Syphilis
f. Nutritional Disturbances
g. Drug Action
h. Allergy
i. Hereditary
j. Idiopathic. Etc.
2. Periodontitis
A. Simplex (secondary to gingivitis) – bone loss, pockets, abscesses can form: cases
have calculus
B. Complex (secondary to periodontosis) – etiologic factors similar to periodontitis;
cases have little, if any calculus.
II. Degeneration
A. Periodontosis (as a rule attacks young girls and older men; often caries immunity)
1. Systemic disturbances
a. Diabetes
b. Endocrine dysfunctions
c. Blood dyscrasias
d. Nutritional disturbances
e. Nervous disorders
f. Infectious diseases (acute and chronic)
2. Hereditary
3. Idiopathic
B. Atrophy
1. Periodontal atrophy (recession. No inflammation no pockets; osteoporosis)
a. Local trauma
b. Presenile
c. Senile
d. Disuse
e. Following inflammation
f. Idiopathic
C. Hypertrophy

7. Gingival hypertrophy
a. Chronic irritation
b. Drug action
c. Idiopathic (e.g gingivoma, elephantiasis, fibromatosis)
D. Traumatism
1.Periodontal traumatism
2. Occlusal trauma
In the 1966 World Workshop in Periodontics serious questions were raised about the existence of
‘periodontosis’ as a distinct disease entity. It was not until the next World Workshop, held in
1977, that there was no scientific basis for retaining the concept that there were non
inflammatory or degenerative forms of destructive periodontal disease. Information summarized
at that meeting supported the conclusion that ‘periodontosis’ was actually an infection and
‘juvenile periodontitis’ should become the preferred term for this group of diseases
III) Infection/ host response Paradigm (1970- present)
In 1876, Robert Koch provided experimental proof of the germ theory of disease, following
which some dentists like ES Tablot (1886), W.D. Miller (1890) began to suggest that periodontal
diseases might be caused by bacteria. W.D. Miller, in particular, was an early proponent of the
infectious nature of periodontal diseases:
He believed that there are three factors are to be taken into consideration in every case of
pyorrhea alveolaris:
(1) predisposing circumstances
(2) local irritation
(3) bacteria (also that it is not caused by any specific bacterium, but various bacteria)
Miller also recognized that certain systemic conditions (e.g. diabetes, pregnancy) could
modify the course of the disease. Part of the reluctance of the profession to accept the idea that
most periodontal diseases were infections was an unfortunate belief that some forms of
destructive periodontal diseases were degenerative in nature (i.e. domination of the ‘Classical
Pathology’ paradigm).
In addition, microbiological studies revealed that no clear group of microorganisms could be
causally linked to the diseases. It was not until 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
PAGE AND SHROEDER. 1982

8. GINGIVITIS
Chronic Marginal Gingivitis
Acute Necrotizing Ulcerative Gingivitis (ANUG)
PERIODONTITIS
Juvenile Periodontitis
Rapidly Progressive Periodontitis
Adult Type Periodontitis
In this classification, with the exception of ANUG⁄ P, the age of onset is of decisive importance.
SUZUKI , 1988
 Modification of Page & Schroeder 1982
 For pathogenesis of periodontal lesion, 4 stages have been described: initial, early,
established and advanced
 3 plausible hypothesis for the pathogenesis of the disease:
 Direct tissue destruction by bacteria & metabolic products
 Immune hyper-responsiveness
 Immune deficiencies involving neutrophil function (chemotaxis and
phagocytosis)
Page and Schroeder presented 4 major forms of periodontitis, but based on additional clinical
observations and investigations, Suzuki made further qualifications in these forms. Based on
factors such as age, microbial deposits, and the autologous mixed lymphocyte reaction, rapidly
progressive periodontitis, as introduced by Page & Schroeder, can be subdivided into type A and
type B. In addition, the term postjuvenile periodontitis delineated a slow progression- type of
juvenile periodontitis.
Adult Periodontitis >35 yrs
Rapidly Progressing Periodontitis
Type A 14 - 26 yrs
Type B >26 yrs
Juvenile Periodontitis 12 – 26 yrs
Post juvenile Periodontitis 26 – 35 yrs
Prepubertal Periodontitis < 14 yrs
Advantages:
Short and Easy
Shortcomings :
Does not include all criteria and conditions like gingival conditions
WORLD WORKSHOP IN CLINICAL PERIODONTITIS, 1989

9. The next major landmark in the classification of periodontal diseases emerged from the 1989
World Workshop in Clinical Periodontics where a new classification of periodontitis based on
the Infection/Host Response paradigm was suggested
I. Adult Periodontitis
II. Early Onset Periodontitis
A. Prepubertal Periodontitis
1. Generalised
2. Localised
B. Juvenile Periodontitis
1. Generalised
2. Localised
C. Rapidly Progressive Periodontitis
III. Periodontitis Associated With Systemic Diseases
IV. Necrotising Ulcerative Periodontitis
V. Refractory Periodontitis
‘89 classification critical evaluation :
1. Depended heavily on the age of the affected patients Baab DA(1986), Page RC (1983)
and the rates of progression Page RC (1983).
2. In this classification the dividing line between adult and early onset categories was
arbitrarily set at 35years of age. There is no question that the patient’s age is an important
variable in evaluating the nature of an individual’s periodontal disease. For example, a
15- year-old patient with multiple sites with 3mm of clinical attachment loss (CAL) has a
different kind of periodontal problem compared to a 90-year-old with the same amount of
damage. However, when age is used as the single most important determinant in
classifying various forms of periodontitis, difficult questions arise. As a child or
adolescent with periodontitis gets older, should the periodontal diagnosis change (i.e.
with time does Prepubertal Periodontitis become Juvenile Periodontitis which then
becomes Rapidly Progressive Periodontitis)? Indeed, it is just as likely that the
subcategories of Early Onset Periodontitis are the same disease rather than three separate
forms of periodontitis.

10. 3. The disease category of ‘Prepubertal Periodontitis’ was the first to be seriously
questioned. Indeed, it is likely that most prepubertal children with severe periodontal
destruction affecting the deciduous teeth probably have a systemic disease that increases
their susceptibility to bacterial infections such as: LAD. J Meyle (1994), Waldrop TC et
al (1987), congenital primary immunodeficiency El Batista et al (1999), chronic
neutrophil defects LL Dunbar(1894), JJ Kamma (1998) and cyclic neutropenia JF
Prichard (1984). Such patients should probably have been properly placed under the
general category of ‘Periodontitis Associated with Systemic Disease’.
4. Among the other problems with the 1989 classification were firstly, the uncertainty about
the proposal that ‘Rapidly Progressive Periodontitis’ was a single entity, To be
designated as ‘rapid’, how much progression has to occur and over what time period?
The concept that the rate of progression might be a useful criterion upon which to base a
disease category may in itself be flawed. The rate at which periodontitis progresses is
highly variable and depends on such factors as
 Innate and acquired host susceptibility (Van Dyke (1997), GJ Seymour (1997)
Ishikawa et al(1997)).
 Composition and quantity of the subgingival flora (Page RC(1997)).
 Nature of genetically determined host–bacterial interactions (TC Hart(1997), Page
RC(1997)).
Almost any form of periodontitis can progress rapidly or slowly depending on the set of
circumstances governing the nature of the host–bacterial interactions during a given time
period.
5. The existence of a group of periodontal diseases that would eventually be termed
‘Refractory Periodontitis’ came from a series of studies of private practice patients who
unexpectedly did not respond to treatment (Hirschfeld (1997),Lundstrom et al (1984) The
reasons for the unresponsiveness to conventional therapy are not clear, but it is probably
due to the emergence of resistant or super-infecting microorganisms, tissue invasion by
periodontal pathogens, and innate or acquired alterations or defects in host responses (KS
Kornman (1996) Whatever the reasons, it has been demonstrated that some patients with
periodontitis ‘refractory’ to treatment harbor enteric rods, staphylococci and Candida at
unresponsive sites (H Loe (1993).Whereas other patients who responded poorly to
treatment, or who developed recurrent disease, continued to harbor in the subgingival
flora at nonresponding sites elevated levels of Porphyromonas gingivalis (Choi et
al1990), Prevotella intermedia (Lee et al 1995), Eikenella corrodens (Lee et al 1995),
Streptococcus intermedius (Magnusson 1991), or microbial complexes consisting of
various combinations of P. gingivalis, S. intermedius, Treponema denticola,
Campylobacter rectus, Bacteroides forsythus, Peptostreptococcus micros and
Fusobacterium nucleatum (Haffafjee et al 1997). In addition, perturbations in host
responses, such as altered neutrophil chemotaxis MacFarlane GD et al(1992), over-
production of certain proinflammatory cytokines Lee et al(1995), and elevated serum

11. Magnusson(1991), or gingival crevicular fluid (GCF) antibody Chapple ILC (1993)
against putative periodontal pathogens, have been reported. The striking feature of the
microbiological and host response results in refractory patients is their extensive
variability and heterogeneity.
6. Overlap exists among different diagnostic categories and cases exist that do not clearly fit
into any single category’ (AAP Consensus Report 1989) different forms of periodontitis
proposed in the classification shared many microbiologic and host response features,
which suggested extensive overlap and heterogeneity among the categories Armitage et
al(1996).
7. In addition, it was acknowledged that considerable ‘heterogeneity’ existed within the
Refractory Periodontitis category since, ‘... it includes patients who are unresponsive to
any treatment provided – whatever the thoroughness or frequency – as well as patients
with recurrent disease at few or many sites. Assignment of refractory cases to other
categories may be expected to occur as more information is acquired.’ (AAP Consensus
Report 1989 ) As a consequence of these problems, the 1989 classification was criticized
shortly after it was published and a different system was proposed by Ranney
8. Need for assumptions concerning previous disease progression,
9. The necessity for detailed information on the quality of treatment provided previously
and the patient response to this therapy
10. The apparent lack of a consistent basis for classification
MERITS : Other important features included the acknowledgment that some forms of
periodontitis could be significantly modified by host factors (i.e. the category of ‘Periodontitis
Associated with Systemic Disease’) and still other forms did not appear to respond well to
conventional therapy (i.e. the ‘Refractory Periodontitis’ category).
Provided that the relevant information is available, as many as possible additional secondary
descriptors should be used to further define the clinical situation. These include distribution
within the dentition, rate of progression, response to treatment, relation to systemic diseases,
microbiological characteristics, ethnic group and other factors.
GENCO 1990
I. Periodontitis In Adults
II. Periodontitis In Juveniles
A. Localized Form
B. Generalized Form
III. Periodontitis With Systemic Involvement

12. A. Primary Neutrophil Involvement Disorders
B. Secondary/Associated Neutrophil Impairment
C. Other Systemic Diseases
IV. Miscellaneous Conditions
Shortcomings:
 Onset, duration of diseases not considered
 Gingival diseases not considered
RANNEY, 1993
Gingivitis
Gingivitis, Plaque Bacterial
Non - Aggravated
Systemically Aggravated
Related To Sex Hormones
Related To Drugs
Related To Systemic Diseases
Necrotising Ulcerative Gingivitis
Systemic Determinants Unknown
Related To HIV
Gingivitis, Non-Plaque
Associated With Skin Disease
Allergic
Infectious
Periodontitis
Adult Periodontitis
Non-Aggravated
Systemically Aggravated
Neutropenia

13. Leukemias
Lazy Leukocyte Syndrome
AIDS
Diabetes Mellitus
Crohn’s Disease
Addison’s Disease
Early Onset Periodontitis
Localised Early Onset Periodontitis
Neutrophil Abnormality
Generalised Early Onset Periodontitis
Neutrophil Abnormality
Immunodeficient
Early Onset Periodonttis Related To Systemic Disease
Leucocyte Adhesion Deficiency
Hypophosphatasia
Papillon-Lefevre Syndrome
Neutropenias
Leukemias
Chediak Higashi Syndrome
AIDS
Diabetes Mellitus Type I
Trisomy 21
Histiocytosis X
Ehlers-Danlos Syndrome(Type VIII)
Early Onset Periodontitis,Systemic Determinants
Unknown
Necrotising Ulcerative Periodontitis

14. Systemic Determinants Unknown
Related To HIV
Related To Nutrition
Periodontal Abscess
Shortcomings: Lengthy
Changes in Ranney’s classification:
 He suggested elimination of the ‘Refractory Periodontitis’ category since it was a
heterogeneous group and it was impossible to standardize the treatment that necessarily
would have to be given prior to making the diagnosis.
 In addition, he recommended elimination of the ‘Periodontitis Associated with Systemic
Disease’ category since expression of all forms of periodontitis can be modified by some
systemic diseases or abnormalities, it is probably better to consider them in that specific
context, rather than treating them as a unique category.
CLASSIFICATION OF PERIODONTAL DISEASES AMERICAN ACADEMY OF
PERIODONTOLOGY 1999
Problems, inconsistencies, and deficiencies associated with the 1989 classification led many
clinicians and investigators to call for a revision of the currently used system. This resulted in a
1999 international workshop on the classification of periodontal diseases. There were six major
problems with the 1989 classification that needed to be addressed:
 It did not include a gingivitis or gingival disease category.
 The periodontitis categories had nonvalidated age dependent criteria.
 There was extensive crossover in rates of progression of the different categories of
periodontitis. ‘Rapidly Progressive Periodontitis’ was a heterogeneous category.
 There was extensive overlap in the clinical characteristics of the different categories of
periodontitis.
 ‘Refractory Periodontitis’ was a heterogeneous category.
 ‘Prepubertal Periodontitis’ was a heterogeneous category.
GINGIVAL DISEASES
Dental plaque induced
Non plaque induced

15. CHRONIC PERIODONTITIS
Localised
Generalised
AGGRESSIVE PERIODONTITIS
Localised
Generalised
PERIODONTITIS AS MANIFESTATION SYSTEMIC DISEASES
Associated with hematological disorders
Associated with genetic disorders
Not otherwise specified
NECROTIZING PERIODONTAL DISEASES
Necrotizing Ulcerative gingivitis
Necrotizing Ulcerative periodontitis
ABSCESSES OF THE PERIODONTIUM
Gingival abscess
Periodontal abscess
Periocoronal abscess
PERIODONTITIS ASSOCIATED WITH ENDODONTIC LESIONS
Endodontic –periodontal lesion
Periodontal – endodontic lesion
Combined lesion
DEVELOPMENTAL OR ACQUIRED DEFORMITIES OR CONDITION
Localized tooth related
Mucogingival deformities around teeth
Mucogingival deformities in edentulous area
Occlusal trauma
Changes In The Classification System For Periodontal Diseases As Compared To 1989
Classification
1. Addition of a Section on "Gingival Diseases"

16. As mentioned above, the 1989 classification did not include a section on gingival diseases.
This has been remedied by the development of a detailed classification of gingival diseases
and lesions that are either dental plaque-induced or not primarily associated with dental
plaque. An important feature of the section on dental plaque-induced diseases is
acknowledgment that the clinical expression of gingivitis can be substantially modified by:
1) systemic factors such as perturbations in the endocrine system,
2) medications, and
3) malnutrition
The section on non-plaque induced gingival lesions includes a wide range of disorders that
affect the gingiva. Many of these disorders are frequently encountered in clinical practice.
2. Replacement of "Adult Periodontitis" With "Chronic Periodontitis"
From the outset, the term "Adult Periodontitis" created a diagnostic dilemma for
clinicians. Epidemiologic data and clinical experience suggest that the form of
periodontitis commonly found in adults can also be seen in adolescents. If this is true,
how can non-adults (e.g.adolescents) with this type of periodontitis be said to have "adult
periodontitis?"Clearly, the age-dependent nature of the adult periodontitis designation
created problems. Therefore, workshop participants concluded that it would be more
accurate to adopt a nonspecific term such as "Chronic Periodontitis" to characterize this
constellation of destructive periodontal diseases.
A great deal of discussion centered around what words should be used to replace the
Adult Periodontitis term. Substitute terminology such as "Periodontitis-Common Form"
and "Type II Periodontitis" were considered and eventually rejected by the majority of
the group. The term "Chronic Periodontitis" was criticized by some participants, since
"chronic" might be interpreted as "noncurable" by some people. Nevertheless, "Chronic
Periodontitis" was eventually agreed upon as long as it was understood that it did not
imply that this disease was nonresponsive to treatment. Traditionally, this form of
periodontitis has been characterized as a slowly progressive disease Indeed, data from
many sources confirm that patients with this form of periodontitis usually exhibit slow
rates of progression. However, there are also data indicating that some patients may
experience short periods of rapid progression. Therefore, workshop participants
concluded that rates of progression should not be used to exclude people from receiving
the diagnosis of chronic Periodontitis
3. Replacement of "Early-Onset Periodontitis" With "Aggressive Periodontitis"
The term "Early-Onset Periodontitis" (EOP) was used in the 1989 AAP and 1993
European classifications as a collective designation for a group of dissimilar destructive
periodontal diseases that affected young patients (i.e., prepubertal, juvenile, and rapidly

17. progressive periodontitis). It was logically assumed that these diseases all had an early
onset because they affected young people. Unfortunately, the "early onset "designation
implies that one has temporal knowledge of when the disease started. However, in
clinical practice and most other situations this is rarely the case. In addition, there is
considerable uncertainty about arbitrarily setting an upper age limit for patients with so
called early-onset periodontitis. For example, how does one classify the type of
periodontal disease in a 21-year-old patient with the classical incisor-first molar pattern
of Localized Juvenile Periodontitis (LJP)? Since the patient is not a juvenile, should the
age of the patient be ignored and the disease classified as LJP anyway? This type of
problem stems from the age dependent nature of the 1989 classification system. A similar
problem arises when the 1989 classification is applied to a 21-year-old patient with
generalized periodontal destruction. Does such a patient have "Rapidly Progressing
Periodontitis" (RPP) or "Generalized Juvenile Periodontitis" (GJP)? It can be argued that
neither designation is acceptable. The diagnosis of RPP may not be appropriate since the
rate of progression is not known, and the GJP designation is unacceptable because the
patient is no longer a juvenile. Because of these problems, workshop participants decided
that it was wise to discard classification terminologies that were age-dependent or
required knowledge of rates of progression. Accordingly, highly destructive forms of
periodontitis formerly considered under the umbrella of "Early-Onset Periodontitis" were
renamed using the term "Aggressive Periodontitis." In general, patients who meet the
clinical criteria for LJP or GJP are now said to have "Localized Aggressive Periodontitis"
or "Generalized Aggressive Periodontitis," respectively.
In the consensus report for "Aggressive Periodontitis", workshop participants
have listed some characteristics that should be helpful in distinguishing between localized
and generalized forms of this group of periodontal diseases. Since these features have not
been universally used in the older literature to place patients in the LJP or GJP categories,
it would be inappropriate to assume that there will be a consistent one-to-one relationship
in transferring information from the old classification system to the new. For example,
some patients formerly classified as having GJP in the older literature might
appropriately be placed in either the Chronic Periodontitis or Generalized Aggressive
Periodontitis categories in the new classification system, depending on a variety of
primary and secondary characteristics
The Rapidly Progressive Periodontitis (RPP) designation has been discarded.
Patients who were formerly classified as having RPP will, depending on a variety of
other clinical criteria, be assigned to either the "Generalized Aggressive Periodontitis" or
"Chronic Periodontitis" categories. It should be emphasized that patients with rapidly
progressive forms of periodontitis exist. They do not, however, represent a homogeneous
group. The 1989 classification contained a category termed "Prepubertal Periodontitis"
which had localized and generalized forms. The category was originally developed to
accomodate those rare situations in which children with primary teeth had severe

18. periodontal destruction. It is now known that most of the patients who have been given
the diagnosis of generalized pre-pubertal periodontitis actually had one of a variety of
systemic conditions that interfere with resistance to bacterial infections. Such conditions
include leukocyte adherence deficiency, congenital primary immunodeficiency,
hypophosphatasia, chronic neutrophil defects or cyclic neutropenia. Under the new
classification system, such patients would be placed under the heading of "Periodontitis
as a Manifestation of Systemic Diseases".
Workshop participants agreed that prepubescent children who have periodontal
destruction without any modifying systemic conditions would, depending on a variety of
secondary features, fit under the categories of "Chronic Periodontitis" or "Aggressive
Periodontitis" in the new classification. The idea that periodontitis has its beginnings in
childhood is supported by retrospective epidemiologic data suggesting that localized
radiographic bone loss can be detected around the primary dentition of some children. In
addition, generalized periodontitis has also been reported in young children without any
detectable underlying systemic disease.
The concept that periodontitis develops at an early age is strengthened by data from many
epidemiologic studies demonstrating that periodontal attachment loss can be found
around the permanent teeth of adolescents
4. Elimination of a Separate Disease Category for "Refractory Periodontitis"
In the 1989 classification, a separate disease category was devoted to Refractory
Periodontitis. This heterogeneous group of periodontal diseases refers to instances in
which there is a continuing progression of periodontitis in spite of excellent patient
compliance and the provision of periodontal therapy that succeeds in most patients.
Because of the diversity of clinical conditions and treatments under which periodontal
therapy fails to arrest the progression of periodontitis, workshop participants were of the
opinion that "Refractory Periodontitis" is not a single disease entity. Indeed, it was
considered possible that a small percentage of cases of all forms of periodontitis might be
non responsive to treatment. Therefore the group concluded that, rather than a single
disease category, the "refractory" designation could be applied to all forms of
periodontitis in the new classification system (e.g., refractory chronic periodontitis,
refractory aggressive periodontitis, etc. It is recommended that future studies of these
patients describe as fully as possible the population under investigation to minimize
heterogeneity of the study sample.
5. Clarification of the Designation "Periodontitis as a Manifestation of Systemic
Diseases"
In the 1989 classification, one of the disease categories was "Periodontitis Associated
With Systemic Disease." In general, this category has been retained in the new

19. classification since it is clear that destructive periodontal disease can be a manifestation
of certain systemic diseases. The Consensus Report for this portion of the workshop
contains of list of systemic diseases in which periodontitis is a frequent manifestation. It
should be noted that diabetes mellitus is not on this list. In the collective view of
workshop participants, diabetes can be a significant modifier of all forms of periodontitis
but there are insufficient data to conclude that there is a specific diabetes mellitus-
associated form of periodontitis. For example, the presence of uncontrolled diabetes
mellitus can alter the clinical course and expression of chronic and aggressive forms of
periodontitis. Similarly, the new classification does not contain a separate disease
category for the effects of cigarette smoking on periodontitis. Smoking was considered to
be a significant modifier of multiple forms of periodontitis. One of the apparent
inconsistencies in the new system is inclusion in the "Dental Plaque-Induced Gingival
Diseases" portion of the classification a list of gingival diseases that can be modified by
systemic factors. On this list is "diabetes mellitus-associated gingivitis." How can one
justify inclusion of a diabetes mellitus-associated gingivitis category and purposely
exclude a parallel periodontitis category? The reason for this decision was that plaque-
induced gingivitis was considered a single entity by the work-shop participants. This is
not the case for periodontitis, where there are clearly different clinical forms. It would
have been possible to include in the new classification additional subcategories such as
"diabetes mellitus-associated chronic periodontitis" and "diabetes mellitus-associated
aggressive periodontitis."
However, the group decided that this would be unnecessarily complicated and not yet
justified by supporting data.
6. Replacement of "Necrotizing Ulcerative Periodontitis" With "Necrotizing
Periodontal Diseases"
Workshop participants acknowledged that necrotizing ulcerative gingivitis (NUG) and
necrotizing ulcerative periodontitis (NUP) are clinically identifiable conditions. However,
the group was less certain about the relationship between NUG and NUP. Are these
clinical conditions part of a single disease process or are they truly separate diseases?
Since there are insufficient data to resolve these issues, the group decided to place
both clinical conditions under the single category of "Necrotizing Periodontal Diseases."
If future studies show that NUG and NUP are fundamentally different diseases, then they
can be separated in subsequent revisions of the classification. One of the potential
problems with inclusion of "Necrotizing Periodontal Diseases" as a separate category is
that both NUG and NUP might be manifestations of underlying systemic problems such
as HIV infection. If this is true, then it might be more appropriate to place these
conditions under manifestations of systemic diseases. The reason that this was not done is
that there are many factors, other than systemic diseases, that appear to predispose to the

20. development of NUG or NUP such as emotional stress and cigarette smoking. Since our
understanding of these clinical conditions is far from complete, it was concluded that for
the time being they should be included under a single and separate category in the new
classification.
7. Addition of a Category on "Periodontal Abscess"
The 1989 classification did not include a section on periodontal abscesses. This has been
remedied by the addition of a simple classification primarily based on location (i.e.,
gingival, periodontal, pericoronal) of these commonly encountered lesions. It could be
argued that periodontal abscesses are part of the clinical course of many forms of
periodontitis and formation of a separate disease category is not justified. However, in the
view of workshop participants, since periodontal abscesses present special diagnostic and
treatment challenges they deserve to be classified apart from other periodontal diseases.
8. Addition of a Category on "Periodontic-Endodontic Lesions"
The 1989 classification did not include a section on the connection between periodontitis
and endodontic lesions. Therefore a simple classification dealing with this area has been
added.
9. Addition of a Category on "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.
DEMERITS: (go thru them as they were taken from some random notes)
 Complex classification as over 100 disease categories are listed
 Certain factors mentioned on “modifying factors” are infact not………….???
 Diabetes was not included as diabetes associated periodontitis but was included as
diabetes associated gingivitis
 Developmental/ acquired deformities – difficult to include them. Inappropriate to include
it

21.  Removal of localized juvenile periodontitis – retrograde step, since it was the most well
defined of all periodontal diseases and with a large body of research
 No separate category like “historical/ previous disease”
And so no explanation on periodontal destruction that took place earlier and whether it is
in progress during presentation
 To some clinicians, selection of the term ‘chronic’ as a replacement for ‘adult’ to
describe the most common form of periodontitis may seem inappropriate since it might
be interpreted to mean that the disease is permanent or incurable
 Why could modern classifications of periodontal diseases not be based on the
microbiological features of these infections, or on the genetic factors that seem to control
the clinical expression of these diseases?
 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 host-modifying 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
MERITS:
 A badly needed gingivitis or gingival disease category was added.
 In addition, the heterogeneous disease categories of prepubertal, refractory and rapidly
progressive periodontitis were eliminated as distinct or stand-alone entities. The
‘refractory’ designation remains in the new classification, but not as a single entity.
Conceptually, all forms of periodontitis can be unresponsive to treatment.
 Furthermore, the troublesome criteria of age and rate of progression were removed as a
basis for classifying different forms of periodontitis.
 The reasons for these changes were not arbitrary, but were based on available data and
the current understanding of the nature of periodontal infections.
 Elimination of the categories of ‘Refractory Periodontitis’ and ‘Rapidly Progressive
Periodontitis’ was badly needed because of their extraordinary heterogeneity.
 In addition, elimination of the ‘Prepubertal Periodontitis’ category was important since
existing data do not support the notion that it is a single entity.

22. CONCLUSION
In the past 130years classification systems for periodontal diseases have evolved based on the
understanding of the nature of these diseases at the time the classifications were proposed.
Although classification systems for periodontal diseases currently in use are
firmly based on, and dominated by, the Infection/Host Response paradigm, some features of the
older paradigms are still valid and have been retained. 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. Since it is probable that essentially all dentists and
periodontists in the world are convinced that most periodontal diseases are infections, it is
unlikely that the Infection/Host Response paradigm will be replaced in the near future.
Diagnosis is defined as the act of identifying a disease from its signs and symptoms, whereas
classification is defined as the act or method of distribution into groups.
CRITICAL EVALUATION :
During the 1950s and 1960s the importance of dental plaque as the major etiologic factor for

23. periodontal diseases became more and more evident. The ultimate proof of the association
between plaque and gingival inflammation was shown by Loe and coworkers in their
experimental gingivitis
The influence of this way of thinking was clearly evident during the 1966 Workshop in
Periodontics when the entity periodontosis was revisited. In the committee report
it was concluded: Evidence to support the conventional concept of periodontosis is
unsubstantiated. It was the consensus of the section that the term periodontosis is ambiguous and
that the term should be eliminated from periodontal nomenclature. Nevertheless, the committee
is aware that some evidence exists to indicate that a clinical entity different from adult
periodontitis may occur in adolescents and young adults.
Although, in my opinion, the conclusion there is insufficient knowledge to separate truly
different diseases (disease heterogeneity) from differences in the presentation ⁄ severity of the
same disease (phenotypic variation) from the European Workshop on Periodontology in 1993
still holds true today, it was concluded in the 1996 World Workshop in Periodontics that there
was a clear need for a revised classification system for periodontal diseases. This resulted in a
new classification which was agreed upon at the International Workshop for a Classification of
Periodontal Diseases and Conditions in 1999
The concept of essentialism and nominanlism was given by Scadding in 1996. The essentialistic
idea implies the real existence of a disease. Thus the doctor’s skills consist in identifying the
causal disease and then prescribing the appropriate treatment. The counterpart of essentialism is
nominalism, which implies that a disease name is just a name given to a group of subjects who
share a group of well defined signs and symptoms. Ideally, a nominalistic disease definition
describes a set of criteria that are fulfilled by all persons said to have the disease, but not fulfilled
by persons that are considered free from the disease. This set of criteria is dependent on the level
of knowledge of a given disease. For example, if the etiology is known, e.g. cholera, then the key
criterion for the disease is the presence of Vibrio cholerae. However, for many diseases the
etiology is complex or not known, and consequently a large number of diseases are defined as
syndromes.