Classification of periodontal diseases: an unstable past with a relatively stable future

1) Introduction

Our basic understanding of periodontal disease and the concepts of etiopathogenesis have evolved and substantially changed during past centuries. The initial classification systems were based upon clinical features of the diseases (1870–1920), then came the concepts of classical pathology (1920–1970), and presently we are following the infectious etiology of the diseases (1970–present) 1.Most important landmark in our current understanding of periodontal diseases was work done by Lӧe et al. 2 on natural history of periodontal diseases where they observed the progression of periodontal diseases naturally without interfering. Their observations showed that natural history of periodontal disease, in some but not all patients, results in tooth loss. In the following sections we shall study why many classification systems were proposed, their drawbacks and finally the classification system that we are presently following.

Although in all standard books, the classification of periodontal diseases is one of the initial chapters of the book, but it is my personal opinion that due to complexities involved in understanding the past and the present of classification systems readers should first read about gingival and periodontal diseases and then should read in detail the classification of periodontal diseases.

2) Why do we need a classification system?

Classification of diseases is done to simplify our understanding regarding different diseases in a particular medical or dental field. Generally diseases are classified according to their etiology into different classes like inflammatory, congenital, genetic, neoplastic, acquired etc. Disease names which last with “itis” have inflammatory etiology, for example periodontitis. Classification of diseases also helps us to communicate, for example if i say a patient is suffering from generalized aggressive periodontitis, you shall have an idea about all the clinical signs and symptoms of the disease. So, half of our job is done. Now we can elaborate the disease by going into detailed clinical and radiographic examination of the patient and describe how this condition is manifested in this particular patient. Classification also helps us to formulate the treatment plan, predict the outcome of treatment as well as to educate the patient about disease.

3) Historical background:

The initial workers on periodontal diseases did not specify any particular terminology for these conditions until Fauchard (1723), who used term “scurvy of the gums” for the first time 3. Since then researchers have introduced names for diseases of the periodontium on the basis of etiologic factors, pathologic changes or clinical manifestations. For the ease of understanding let us divide the classification systems proposed on the basis of dominant paradigms,

4) Classification of periodontal diseases based on the clinical features paradigm (1870 to 1920):

These were initial classification systems proposed solely on the basis of clinical features of the disease. At that time there was a little knowledge about the etiopathogenesis of the diseases. Many researchers at that time proposed that these diseases are caused by local factors 4-8 while others believed that systemic factors were responsible for the diseases 9-12. Some researchers suggested that local factors are responsible for the diseases but in some cases systemic factors also play an important role 13-15.

During this time period due to relatively few publications and lack of appropriate interactions between different schools of thoughts, researchers individually put forward their point of view regarding classification of periodontal diseases. G. V. Black (1886) 16, based on his understanding of clinical features of different periodontal diseases published following classification,

G. V. Black classification of periodontal diseases:

Constitutional gingivitis

Painful form of gingivitis

Simple gingivitis

Calcic inflammation of the peridental membrane

Phagedenic pericementitis

Constitutional gingivitis:

These included scurvy, mercurial gingivitis and potassium iodide gingivitis.

Painful form of gingivitis:

This condition is presently known as necrotizing ulcerative gingivitis (NUG) which is a painful condition with necrosis of gingiva and tooth supporting structures.

Simple gingivitis:

This term was used to describe the condition where local deposits caused inflammation of periodontal membrane.

Calcic inflammation of the peridental membrane:

In this condition the calculus deposition was associated with an even or generalized pattern of destruction of alveolar bone which progressed through long duration of time.

Phagedenic pericementitis:

This condition shared many features same as Calcic inflammation of the peridental membrane except that the calculus deposition was less and there was irregular pattern of alveolar bone destruction.

5) Classification of periodontal diseases based on classical pathology paradigm (1920-1970):

This paradigm was dominated by pathology of the disease process. Almost all the classification systems given during this period used terms like atrophic, degenerative, dystrophic etc. These classification systems were based on the ‘principles of general pathology’ as presented by Orban et al. 17

The first widely accepted classification system was given by Gottlieb who classified periodontal diseases into four types 18-20 :

Gottlieb’s classification of periodontal diseases:


Alveolar atrophy or diffuse atrophy


Occlusal trauma

The term Schmutz-Pyorrhӧe was used to describe periodontal condition that was caused due to accumulation of deposits on the teeth leading to inflammation, shallow pockets, and resorption of the alveolar crest. Alveolar atrophy or diffuse atrophy was described as a noninflammatory disease in which minimal local factors i.e. deposites were present on the teeth, deep pockets were seen in later stages with loosening of teeth and eventually leading to tooth loss. Paradental-Pyorrhӧe was characterized by irregularly distributed pockets varying from shallow to extremely deep. The disease process in this case may have started as Schmutz-Pyorrhӧe or as diffuse atrophy. The fourth condition described was occlusal trauma in which there was alveolar bone resorption and tooth mobility due to increased occlusal physical overload.

Orban’s classification of periodontal diseases

Orban in 1942 proposed a classification based on classical pathology paradigm 21.  This classification was accepted by American Academy of Periodontology (AAP) and gained wide acceptance. In this classification periodontitis was classified into two categories simplex and complex. Periodontitis simplex was secondary to gingivitis and characterized by bone loss, pockets, abscess formation and calculus deposits. Complex was secondary to periodontosis, having similar aetiological factors to periodontitis and little or no calculus and was considered as degenerative disease.

Orban’s classification of periodontal diseases


I. Gingivitis (little or no pocket formation: can include ulcerative form Vincent’s)

  1. Local (calculus, food impaction, irritating restorations, drug action, etc.).
  2. Systemic
    • Pregnancy
    • Diabetes and other endocrine dysfunctions
    • Tuberculosis
    • Syphilis
    • Nutritional disturbances
    • Drug action
    • Allergy
    • Hereditary
    • Idiopathic

II. Periodontitis

Simplex (secondary to gingivitis).

Complex ( secondary to periodontosis).


Periodontosis (as a rule attacks young girls and older men; often caries immunity

A. Systemic disturbances

  1. Diabetes
  2. Endocrine dysfunctions
  3. Blood dyscrasias
  4. Nutritional disturbances
  5. Nervous disorders
  6. Infectious diseases (acute & chronic)

B. Hereditary

C. Idiopathic


Periodontal Atrophy (Recession, no inflammation, no pockets; osteoporosis.)

  1. Local trauma (e.g., from toothbrush)
  2. Presenile
  3. Senile
  4. Disuse
  5. Following inflammation
  6. Idiopathic


Gingival Hypertrophy

  1. Chronic irritation (see inflammation)
  2. Drug action (e.g.. Dilantin sodium)
  3. Idiopathic (e.g.. g-ingivoma, elephantiasis. fibromatosis)


I. Periodontal Traumatism

A. Occlusal trauma

Based on classical pathology paradigm many classifications were given during this time period. These include classification by Fish 1944 22, Goldman et al. 1956 23, Goldman & Cohen 1968 24, Grant et al. 1968 25.

6) Classification systems based on Infection/host response paradigm (1970–present):

This paradigm stated with the classical ‘experimental gingivitis’ studies published by Harald Löe and his colleagues from 1965 to 1968 26-29. Their research work showed that host response in an important factor in determining the disease progression and its outcome. Along with this research done on neutrophils from juvenile periodontitis (periodontosis) cases showed their defective chemotactic and phagocytic functions which supported this concept 30-31.

Page and Schroeder in 1982 proposed a new classification system which was based on Infection/host response paradigm. In this classification five distinctly different forms of periodontitis were described. It is important to discuss this classification as the American Academy of Periodontology (AAP) in 1986 adopted a new classification which incorporated these groups.

Page and Schroeder classification of periodontal diseases

Prepubertal periodontitis       



Juvenile periodontitis

Rapidly progressing periodontitis

Adult type periodontitis

Acute necrotizing ulcerative gingivo-periodontitis.

Prepubertal periodontitis:

This type of periodontitis was described as a condition that occurs during or immediately after eruption of primary teeth. Two forms were described in this condition localized and generalized forms. In generalized form acute inflammation is present with proliferation and clefting of gingival margin. Genetic predisposition is present in most of patients. Neutrophils and monocytes from peripheral blood demonstrate defective function and peripheral white blood cell count is markedly elevated. Periodontitis may be refractory to antibiotic treatment. All primary teeth were affected but permanent teeth may or may not be affected.

In localized form it was described that only some teeth are affected with destruction not as rapid as in generalized form.  Gingival tissue may or may not exhibit inflammation. Functional defects are present in peripheral neutrophils and monocytes. Disease can be treated with root curettage and antibiotic therapy.

Juvenile periodontitis:

This condition was described as of circumpubertal origin where diagnosis was usually made at age beyond puberty.  Lesions are primarily around permanent first molars and/or incisors with usually symmetrical distribution. The disease is 4 times more prevalent in females as compared to males. Clinically gingiva appears completely normal with minimal local factors. X-linked dominant or recessive genetic trait is present. Majority of patients with this condition have neutrophil and monocytes function defects.

Juvenile Periodontitis 

A classical Juvenile Periodontitis case showing clinically healthy gingiva with minimal inflammation and little or no local factors

Juvenile Periodontitis

 Clinical examination shows deep periodontal pockets ranging from 8-12 mm with respect to 1st molars in all four quadrants

Pocket depth measurement

Radiograph showing bone loss with respect to 1st molar


Rapidly progressing periodontitis:

This condition was described as generalized, affecting most of the teeth with age of onset between puberty and 35 years. The periodontal destruction is rapid which gradually slows down spontaneously. In active disease the gingiva is acutely inflamed with marginal proliferation whereas in inactive disease gingiva may appear completely normal. Most of the patients have neutrophil and monocyte function defects.  Most of the patients respond appropriately to the treatment but small number of patients are refractory to treatment.

Rapidly progressing periodontitis

A 32 years old female patient with rapidly progressive periodontitis where disease is in inactive phase

Rapidly progressive periodontitis

Periodontal probing demonstrating deep periodontal pockets

Periodontal probing

Radiograph showing generalized alveolar bone loss


Adult periodontitis:

Here the age of onset of the disease was described as usually 30 to 35 years and older. Incisors and molars are more severely affected as compared to rest of dentition. The accumulation of plaque is consistent with periodontal destruction. Neutrophil and monocytes function defects are not usually present. Pattern of bone destruction is highly variable. Acute inflammation of gingiva is not usually present with gingiva being more fibrotic and thickened. Disease is usually treatable by routine non-surgical and surgical periodontal therapy.

Acute necrotizing ulcerative gingivo-periodontitis:

This was described as an acute infective condition characterized by deep craters in interdental bone either in localized regions or throughout the mouth. Mouth of the patient is foul smelling. This condition is usually seen in malnutritioned or immunocompomised patients. A pseodomembrane is seen on the lesion made up of necrotic tissue and bacteria.

7) American Academy of Periodontology classification systems:

Based on classification given by Page and Schroeder (1982), American Academy of Periodontology in 1986 adopted a new classification system. Further, (AAP) at World Workshop in Clinical Periodontics at Princeton in 1989 amended the classification system with few refinements 32.

AAP periodontal disease classification systems 1986 and 1989



I. Juvenile Periodontitis

A. Prepubertal

B. Localized juvenile periodontitis

C. Generalized juvenile periodontitis

II. Adult Periodontitis

III. Necrotizing Ulcerative Gingivo-Periodontitis

IV. Refractory Periodontitis

I. Early-Onset Periodontitis

A. Prepubertal periodontitis

1. Localized

2. Generalized

B. Juvenile periodontitis

1. Localized

2. Generalized

C. Rapidly progressive periodontitis

II. Adult Periodontitis

III. Necrotizing Ulcerative Periodontitis

IV. Refractory Periodontitis

V. Periodontitis Associated with Systemic Disease


1989 AAP classification of periodontal diseases was based upon following factors,

  1. Presence ⁄ absence of clinically detectable inflammation.
  2. Extent and pattern of attachment loss.
  3. Patient’s age at onset.
  4. Rate of progression.
  5. Presence ⁄ absence of miscellaneous signs and symptoms, including pain, ulceration and amount of observable plaque and calculus.

Drawbacks of AAP 1989 classification system:

  1. One major drawback of this classification was that it heavily depended upon the age of the patient 33-35.
  2. Classification did not include a gingivitis or gingival disease category.
  3. There was considerable overlap between different categories within the classification system. Some cases were difficult to place in one category as they possessed some features of other category also. Especially, ‘Rapidly Progressive Periodontitis’ was a heterogeneous category.
  4. Different forms of periodontitis proposed in the classification shared many microbiologic and host response features, which suggested extensive overlap and heterogeneity among the categories 36.
  5. The refractory periodontitis was also a heterogeneous category as the criteria for this condition was difficult to relate clinically while placing the patient in this category.

As a result of these drawbacks Ranney in 1989 proposed a different classification and he suggested that “refractory periodontitis” category should be eliminated 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 37-38.

American Academy of Periodontology (AAP) world workshop 1999 Classification of Periodontal Diseases and Conditions:

In 1999 an international workshop for classification of periodontal diseases and conditions was held at Oak Brook (Illinois, USA) in which a group of internationally acknowledged experts produced a generally accepted and scientifically founded classification of periodontal diseases. This classification was quite different from earlier classifications as it addressed wide variety of periodontal diseases and conditions. This classification is very complete, detailed and complex. The simplified classification is as follows,

I. Gingival diseases

A. Plaque induced

B. Non-plaque induced

II. Chronic periodontitis

A. Localized

B. Generalized

III. Aggressive periodontitis

A. Localized

B. Generalized

IV. Periodontitis as a manifestation of systemic disease

V. Necrotizing periodontal diseases

VI. Abscesses of the periodontium

VII. Periodontitis associated with endodontic lesions

VIII. Developmental or acquired deformities and conditions.

The detailed classification is as follows: 


AAP world workshop 1999 Classification of Periodontal Diseases and Conditions

AAP world workshop 1999 Classification of Periodontal Diseases and Conditions

Highlights of new classification system:

Addition of a gingival disease component

This is an important change in new classification of periodontal diseases and conditions. Gingivitis is commonly attributed to plaque accumulation but many other conditions also have gingivitis as one of the clinical features. So, in new classification we have two categories,

Dental plaque-induced gingival diseases: These include plaque induced gingivitis and systemic conditions as well as endocrinal conditions which exacerbate plaque-associated gingivitis. Systemic diseases such as diabetes and leukemia can exacerbate plaque-associated gingivitis. Endocrine changes (puberty, pregnancy), medications (nifedipine, cyclosporine and phenytoin) and malnutrition (vitamin C deficiency) add a component to plaque induced gingivitis.

Non-plaque-induced gingival lesions: In this category we have Mucocutaneous disorders (e.g., lichen planus, pemphigoid), allergic reactions (e.g., restorative materials, toothpastes, gum), trauma (chemical, physical or thermal) as well as disorders of genetic origin such as hereditary gingival fibromatosis. The gingivitis in these conditions cannot be attributed to plaque accumulation so these are categorized as Non-plaque-induced gingival lesions.

Replacement of “Early-Onset Periodontitis” with “Aggressive Periodontitis”:

In 1989 classification early onset periodontitis category consisted of patients having significant attachment loss in the presence of little local factors (plaque and calculus) and age less than 35 years. Although it is a fact that this condition is commonly found in people under 35 years of age, but it may also affect older patients. So, a new term “aggressive periodontitis” was introduced for this condition because earlier term was too restrictive. The diagnosis of aggressive periodontitis is made on the basis of clinical presentation, radiographic features, rapid duration of disease progression and possible familial aggregation in an otherwise healthy patient. Other factors include elevated levels of putative periodontal pathogens such as Actinobacillus actinomycetemcomitans or Porphyromonas gingivalis. Abnormalities in neutrophil and monocytic functions can also be demonstrated in these patients. Hyper-responsive macrophage phenotype, including elevated levels of PGE2 and IL-1β are usually present. Disease was categorized as localized if ≤30% teeth were involved and generalized if >30% teeth were involved and severity was classified on the basis of clinical attachment loss (CAL) as slight (1-2 mm CAL), moderate (3-4 mm CAL) or severe (> 5 mm CAL).

Replacement of “Adult Periodontitis” with “Chronic Periodontitis”:

Adult periodontitis category in 1989 classification was designated for patients more that 35 yrs of age having slow rate of disease progression and periodontal destruction consistent with presence of local factors. Although these cases are common at age 35 yrs or more but this condition can be seen in adolescents and even in the primary dentition of children. Another drawback here was age at which a patient presents for treatment does not necessarily reflect the age at which the disease began. So, to overcome these difficulties a new term “Chronic Periodontitis” was given to categorize these patients. Disease was categorized as localized if ≤30% teeth were involved and generalized if >30% teeth were involved and severity was classified on the basis of clinical attachment loss (CAL) as slight (1-2 mm CAL), moderate (3-4 mm CAL) or severe (> 5 mm CAL). Periods of disease progression and regression may occur in random manner in this condition.

Elimination of the ‘Prepubertal Periodontitis’ category:

It was difficult to categorize prepubertal periodontitis as a single entity as some of the severe cases of periodontitis in children were attributed to systemic diseases and some may occur without any modifying factors 40-41. In fact beginning of chronic periodontitis has been suggested to start in childhood. So, this category was discontinued in new classification.

Discontinuation of term “Refractory Periodontitis”:

As our present knowledge about pathogenesis of periodontal diseases suggests that there are many factors that affect the disease progression and its response to treatment, category “Refractory Periodontitis” was eliminated from new classification as a separate entity. Factors like extent of disease prior to therapy, type of therapy provided (nonsurgical vs. surgical, with or without antibiotics, etc.), tooth type and furcation involvement, species and strains of microflora, degree of host response (particularly immune response), and whether the patient smokes make it difficult to classify a patient as refractory periodontitis patient. So, based on these factors this category was discontinued.

Replacement of “Necrotizing Ulcerative Periodontitis” with “Necrotizing Periodontal Diseases”:

Another important change was Replacement of “Necrotizing Ulcerative Periodontitis” with “Necrotizing Periodontal Diseases”. Necrotizing ulcerative gingivitis (NUG) and necrotizing ulcerative periodontitis (NUP) were clinically distinguishable disease entities but it was unclear that whether they were part of the same disease process or were two distinct diseases. So, a new term “Necrotizing Periodontal Diseases” was used for these conditions.

Addition of “Periodontal Abscesses” and “Periodontitis Associated with Endodontic Lesions” as new entities:

These conditions were added in the classification system as such without any change in their definitions. Periodontitis associated with endodontic lesions indicate periodontic-endodontic lesions in which there is both a periodontic and an endodontic component.

Addition of new category “developmental and acquired deformities and conditions”:

These are conditions which influence the course of the disease and may dramatically affect the results of treatment. So, it was felt that these acquired deformities and conditions should be should be added in the classification as a separate category.

Critical analysis of AAP 1999 classification system:

An important observation that we make in new classification system is that it appears complicated and too comprehensive, particularly from the clinical aspect. It may be difficult to remember details of classification. But on the other hand earlier simpler classification systems were not able to clearly classify some patients which was their major drawback. However, it must be clear that the recent classification system is also not ideal classification and in future it may be subjected to amendments but till date it is one of the most scientifically sound and widely accepted classification of periodontal diseases and conditions.

8) Conclusion:

As the title of this topic states “an unstable past with a relatively stable future”, due to complexities involved in categorization of periodontal diseases the classifications given in past were subjected to criticism and were amended or new classifications were proposed. The present classification system (AAP world workshop 1999 classification) we are following is based on our knowledge of infection and host response. This is a scientifically sound and well accepted system but it does not mean that it is perfect. In future our research is focused at molecular and genetic mechanisms of pathogenesis of periodontal diseases which may further provide us with new knowledge and a new way of understanding and hence classifying periodontal diseases and conditions.


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