Anti‐Neutrophil Cytoplasmic Autoantibodies: A Renewed Paradigm in Periodontal Disease Pathogenesis?

In the past, various models including the autoimmunity model have been proposed to explain the pathogenesis of periodontal diseases. The aim of this review is to introduce the pathogenic role of anti‐neutrophil cytoplasmic autoantibodies (ANCAs) in various autoimmune diseases and compare these condi...

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Bibliographic Details
Published in:Journal of periodontology (1970) 2006-08, Vol.77 (8), p.1304-1313
Main Authors: Sharma, C.G. Dileep, Pradeep, A.R.
Format: Article
Language:English
Subjects:
Antibodies, Antineutrophil Cytoplasmic - immunology
Antigens, Bacterial
Apoptosis
Autoantibodies
Autoimmune Diseases - immunology
Dentistry
Humans
neutrophils
Neutrophils - enzymology
Neutrophils - immunology
Neutrophils - metabolism
Periodontal Diseases - immunology
periodontal diseases/pathogenesis
Reactive Oxygen Species - metabolism
Superantigens
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Summary:In the past, various models including the autoimmunity model have been proposed to explain the pathogenesis of periodontal diseases. The aim of this review is to introduce the pathogenic role of anti‐neutrophil cytoplasmic autoantibodies (ANCAs) in various autoimmune diseases and compare these conditions with periodontal disease to elucidate common pathogenic mechanisms. Also, a novel model to explain the pathogenesis of periodontal disease based on the concept of ANCA‐associated autoimmunity is proposed. This encompasses a wide array of biochemical mediators that range from direct and indirect initiators of ANCA production and eventual release of proinflammatory mediators and free radicals, all of which have been implicated in periodontal tissue destruction in the past. In addition, specific links between the typical ANCA‐associated diseases and periodontal disease are discussed. Finally, a new paradigm in the periodontal disease‐associated destruction is proposed that includes the currently accepted mechanism, namely, the genetic‐microbial‐host interactions.
ISSN:0022-3492
1943-3670
DOI:10.1902/jop.2006.050308