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Periodontitis

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(Carranza et al. 2006, Flemmig 1999)

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By periodontitis is understood an inflammatory disease of the dental support tissue, which is caused by specific microorganisms or a group of specific microorganisms. The result is progressive destruction of the periodontium, which consists of periodontal membrane with fibers, alveolar bone and root cementum.
It differs clinically from gingivitis in the presence of bone loss, which does not occur with gingivitis. The primary clinical signs of periodontitis comprise clinical loss of attachment, loss of alveolar bone, periodontal pockets and gingival inflammation. In addition, there is gingival enlargement or recession, gingival bleeding on probing, and increased mobility, tooth movement or tooth loss (Flemmig 1999).

According to the 1999 classification of periodontal diseases, three forms of periodontitis are distinguished:
  • Chronic periodontitis
  • Aggressive periodontitis
  • Periodontitis as a manifestation of systemic diseases
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Chronic periodontitis

The following characteristics apply for chronic periodontitis:
  • Prevalence in adults but can also occur in children
  • Degree of tissue destruction correlates with local factors
  • Associated with a variable microbiological pattern
  • Subgingival calculus can be found regularly
  • Slow to moderate progression with possible periods of rapid progression
  • Can be modified by or associated with the following diseases:
    • Systemic diseases such as diabetes mellitus or HIV
    • Local predisposition
    • Environmental factors such as smoking or stress
Chronic periodontitis can further be divided into a generalized and local form. Mild and moderate forms are distinguished from severe chronic periodontitis.
In the local form, fewer than 30% of sites are affected; in the generalized form, more than 30% of sites are affected.
The disease is mild when the clinical loss of attachment is 1-2 mm and moderate with clinical loss of attachment of 3-4 mm. Severe disease is present when the clinical loss of attachment is over 5 mm.

Aggressive periodontitis

The following characteristics apply for aggressive periodontitis:
  • Otherwise clinically healthy patient
  • Rapid loss of attachment and bone
  • The severity of the disease does not correlate with the volume of microorganisms present
  • Increased familial incidence
The following are found frequently but are not always present:
  • Affected sites are infected with Aggregatibacter actinomycetemcomitans
  • Abnormal phagocyte function
  • Over-reactive macrophages, which produce increased quantities of prostaglandin E2 (PGE2) and interleukin-1β
  • The disease is self-limiting in some cases.
Aggressive periodontitis can be divided into a localized and a generalized form.

Localized aggressive periodontitis

  • Starts at puberty
  • Disease at the first molar or canine with loss of attachment in at least two remaining teeth, one of which is the first molar
  • Strong serum antibody reaction to infectious agents

Generalized aggressive periodontitis

  • Usually affects persons under 30 years (exceptions are possible)
  • Generalized loss of attachment affects the first molars and canines and at least three other teeth.
  • Episodic destruction of the periodontium
  • Weak serum antibody reaction to infectious agents

Periodontitis as a manifestation of systemic diseases

Periodontitis can develop with the following systemic diseases:

Disease/syndrome Tissue, cell or biochemical defect Periodontal status Inheritance
Connective tissue diseases  
Ehlers-Danlos syndrome  
Type IV Collagen type III Weak tissue and aggressive periodontitis Autosomal recessive or autosomal dominant
Type VII Procollagen peptidase Weak tissue and aggressive periodontitis Autosomal recessive or autosomal dominant
Type IX Collagen Weak tissue and aggressive periodontitis X-linked
Mucopolysaccharidosis Proteoglycans Gingival hypertrophy  
Mannosidosis Mannose Gingival hypertrophy  
Familial fibromatosis Collagen Gingival hypertrophy  
 
Metabolic disorders  
Acatalasia Catalase Gingival necrosis and aggressive periodontitis Autosomal recessive
Hypophosphatasia Alkaline phosphatase Weakly mineralized bone and cementum and aggressive periodontitis Autosomal recessive (autosomal dominant?)
 
Leukocyte malfunction  
Chédiak-Higashi syndrome Neutrophil Aggressive periodontitis Autosomal recessive
Chronic neutropenia Neutrophil Aggressive periodontitis Autosomal dominant
Cyclical neutropenia Neutrophil Aggressive periodontitis Autosomal dominant
Leukocyte adhesion deficiency Neutrophil Aggressive periodontitis Autosomal dominant
 
Skin defects  
Papillon-Lefèvre syndrome Keratin or epithelium Aggressive periodontitis Autosomal recessive
 
Chromosomal malfunction  
Trisomy 21 Various biochemical chronic inflammatory periodontitis, Aggressive periodontitis  
(after Aldred and Bartold 1998)


sources

  • Aldred, M. J.; Bartold, P. M. (1998): Genetic disorders of the gingivae and periodontium. In: Periodontol. 2000 18, S. 7–20
  • Carranza, Fermin A.; Newman, Michael G.; Takei, Henry H.; Klokkevold, Perry R. (2006): Carranza's clinical periodontology. 10th ed. St. Louis, Mo.: Saunders Elsevier
  • Flemmig, T. F. (1999): Periodontitis. In: Ann. Periodontol. 4 (1), S. 32–38. DOI: 10.1902/annals.1999.4.1.32