The link between periodontal disease and rheumatoid arthritis: an updated review - PubMed (original) (raw)

Review

Joanna Koziel et al. Curr Rheumatol Rep. 2014 Mar.

Abstract

Porphyromonas gingivalis is a leading pathogen in chronic periodontitis, a disease process involving progressive destruction of the tissues that support the teeth. Recently, the organism has been reported to produce a unique bacterial enzyme, P. gingivalis peptidyl-arginine deiminase (PPAD), which has the ability to convert arginine residues in proteins to citrulline. Protein citrullination alters protein structure and function; hence, PPAD may be involved in deregulation of the host's signalling network and immune evasion. Further, accumulating evidence suggests a role for autoimmunity against citrullinated proteins in the development of rheumatoid arthritis (RA). As inflammatory conditions in the lungs of cigarette smokers contribute to the breakdown of immune tolerance to citrullinated epitopes, chronic exposure to citrullinated proteins at periodontitis sites may also predispose susceptible individuals to the development of autoantibodies and the initiation of RA. In this review, we discuss evidence that PPAD may represent a mechanistic link between periodontitis and RA, diseases that are known to be significantly associated at the epidemiological level.

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Conflict of interest statement

Joanna Koziel, Piotr Mydel, and Jan Potempa declare that they have no conflict of interest.

Figures

Fig. 1

Fig. 1

A model of periodontitis-initiated pathogenesis of rheumatoid arthritis (RA) initiated by PPAD/PAD-catalysed modification of proteins in the inflamed periodontal tissue and driven by autoimmunity against citrullinated epitopes joints. Figure was created using Servier Medical Art

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