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.

Highlights

  • Rheumatoid arthritis (RA) and periodontal disease (PD) are two common chronic inflammatory diseases affecting humans worldwide

  • This study revealed the presence of antibodies to 10 of the 13 tested citrullinated peptides, in RA sera [32]

  • Similar to infection with P. intermedia, inoculation with either heatkilled P. gingivalis or the purified cell membrane fraction from the same organism had no effect on either the rate or the severity of collagen-induced arthritis model (CIA). These findings indicate the requirement for live P. gingivalis, which releases bacterial factors exerting a direct or indirect effect on the host that triggers an autoimmune reaction

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Summary

Introduction

Rheumatoid arthritis (RA) and periodontal disease (PD) are two common chronic inflammatory diseases affecting humans worldwide. Such proteins are generated under physiological conditions, but the loss of tolerance in genetically susceptible individuals initiates the generation of autoantibodies against citrullinated proteins (ACPA) in the synovia and the subsequent development of RA [22,23,24]. Because the ACPA response is peptidyl citrulline-specific, host enzymes which catalyse the protein modifications that lead to the generation of citrullinated epitopes are considered highly important targets for drug development.

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