Periodontitis: Classification

Periodontitis (inflammation of the periodontium) is one of the periodontal diseases (diseases of the periodontium). Their classification, established by the International Workshop for a Classification of Periodontal Diseases and Conditions in 1999, is still valid. The very comprehensive classification, which, incidentally, does not follow the ICD code (ICD:, English : International Statistical Classification of Diseases and Related Health Problems) of the WHO, makes the following classification of periodontal diseases:

I. Gingival diseases

Since pathologic (diseased) processes of the gingiva (the gums) initially proceed without involvement of the periodontium (tooth-supporting apparatus) or without loss of attachment (loss of the periodontal supporting apparatus due to periodontal inflammation), they are not discussed further here.

II Chronic periodontitis (CP)

An infectious disease of the periodontium, it is associated with the formation of gingival pockets and/or gingival recession (receding gums). It is predominantly slow and results in progressive (progressive) attachment loss as well as degradation of the alveolar bone (arcuate bone portion of the upper and lower jaws where the tooth compartments (alveoli) are located) surrounding the tooth. This most common form of periodontitis is often diagnosed in adulthood, but it can occur in all age groups, even in the first dentition (milk teeth). Prevalence and severity increase with age. Etiologically (causally), biofilm (plaque, bacterial plaque) and calculus (subgingival tartar adhering below the gingival margin) play an important role as local irritation factors; pathogenesis and thus progression are determined by host reactivity. Host reactivity, in turn, is influenced by specific risk factors. The formerly used term “adult periodontitis” (periodontitis in adults) has been replaced by “chronic periodontitis”. Furthermore, the term “marginal (superficial) periodontitis” (periodontitis affecting the marginal (superficial) periodontium) was dropped. Chronic periodontitis is further subdivided according to extent and severity into:

II.1. localized – less than 30% of the tooth surfaces are affected.

II.2. Generalized – more than 30% of the tooth surfaces are affected.

  • Mild – 1 to 2 mm of clinical attachment loss (CAL: distance between the enamel-cement interface and the bottom of the gingival pocket)).
  • Moderate – 3 to 4 mm CAL
  • Heavy – from 5 mm CAL

III Aggressive periodontitis (AP)

The term replaces the formerly common “Early Onset / Early-onset Periodontitis” and “Juvenile Periodontitis” (“Periodontitis in the adolescent”) or “Rapidly progressive periodontitis”. Aggressive periodontitis predominantly shows clearly recognizable, specific clinical findings with regard to the interactions taking place between host and bacteria. Noticeable are:

  • Rapidly progressive tissue destruction (tissue destruction).
  • Clinical inconspicuousness
  • Familial clustering.

Other characteristics, but not consistently, may include:

  • Disproportion between the amount of biofilm and the extent of tissue destruction.
  • Increased number of Actinobacillus actinomycetemcomitans, sometimes Porphyromonas gingivalis.
  • Abnormal phagocyte function
  • Hyperresponsive macrophage phenotype with increased PGE2 and IL-1 ß production.
  • U. U. self-limiting tissue destruction.

Like chronic periodontitis, the aggressive form can be further divided into:

III.1. localized

III.2. generalized

IV. Periodontitis as a manifestation of systemic disease (PS)

This includes the influence of general diseases with established evidence that entail disturbances in defense mechanisms and connective tissue metabolism and, through these modifications, increase the individual risk of periodontitis without triggering specific periodontitis.IV.1. associated with hematological disorders – acquired neutropenia (decrease of neutrophil granulocytes in blood), leukemia (blood cancer), others.

IV.2. Associated with genetic disorders – Familial or cyclic neutropenia, trisomy 21 (Down syndrome), Papillon-Lefèvre syndrome, leucocyte adhesion deficiency syndrome (LADS), Chediak-Higashi syndrome, histiocytosis syndrome, glycogen storage syndrome, infantile genetic agranulocytosis, Cohen syndrome, Ehlers-Danlos syndrome, hypophosphatasia, other

IV.3 Not otherwise specified – e.g., estrogen deficiency or osteoporosis.

V. Necrotizing periodontal disease (NP)

V.1. necrotizing ulcerative gingivitis (NUG).

V.2. necrotizing ulcerative periodontitis (NUP).

Representing different stages of the same infection, in NUG it is limited to the gingiva, but in NUP it affects the entire periodontium. A reduced systemic immune defense seems to be related. Stress, malnutrition, smoking and HIV infection are discussed as predisposing factors. An accumulation of NUP is found in systemic diseases such as HIV, severe nutritional deficiencies and immunosuppression. Characteristics include:

  • NUG: Gingival necrosis – absent interdental papillae; association with fusiform bacteria (Prevotelle intermedia) and spirochetes.
  • NUP: not only necrosis of the gingiva, but also of the desmodont (root membrane; connective tissue of the periodontium) and alveolar bone.
  • Gingival hemorrhage (bleeding gums).
  • Pain

Other diagnostic criteria may include:

VI. abscesses of the periodontium

Abscesses are purulent (purulent) infections of the periodontium and are classified according to their localization:

VI.1. gingival abscess – localized to the gingiva (gingival margin or interdental papilla).

VI.2. periodontal abscess – localized in the gingival pocket, with destruction of the alveolar bone and ligament (elastic fibrous apparatus between bone and tooth root)

VI.3. pericoronary abscess – localized to the tissue around a partially erupted (partially erupted) tooth crown.

Accompanying symptoms in varying combinations may include:

  • Swelling
  • Pain
  • Color change
  • Tooth mobility
  • Tooth extrusion (displacement of the tooth from the tooth socket).
  • Suppuration (pus secretion)
  • Fever
  • Reactive lymphadenitis (inflammation of the lymph nodes)
  • Radiological lightening of the alveolar bone.

VII Periodontitis associated with endodontic lesions

While periodontitis associated with biofilm (plaque, bacterial plaque) originates marginally (at the gingival margin) and progresses apically (toward the root apex), endodontic processes (triggered by pathologic processes of the tooth interior) may invade the desmodont (periodontium) from apically (from the root apex) and via lateral canals and ascend marginally or coronally (toward the tooth crown). VII.1 Combined periodontal-endodontic lesions – This describes situations where periodontal and endodontic lesions – also known as paro-endo lesions for short – are present in combination. These may develop independently or may be the cause or result of the other situation.

VIII Developmental or acquired deformities and conditions

This includes locally predisposing factors originating from tooth morphology or mucosal condition that may have a pathologic effect on the integrity of the gingiva or periodontium, thus favoring the onset of periodontal disease: VIII.1. factors favoring plaque retention:

  • Dental anatomy
  • Restorations/Apparatus
  • Root fractures (root fractures)
  • Cervical root resorptions and cementations.

VIII.2. mucogingival conditions near the teeth:

  • Recessions (localization of the gingival margin apical (rootward) of the enamel-cement interface).
  • Absence of keratinized gingiva (gums).
  • Shortened attached mucosa
  • Localization of the frenulum of the lip/tongue.
  • Gingival enlargements – e.g. gingival overgrowth, irregular gingival margin, pseudo-pockets.
  • Abnormal color

VIII.3. mucosal changes on edentulous alveolar ridges.