Periodontal bacteria and the rheumatoid arthritis-related antigen RA-A47: the cross-reactivity potential

摘要

Purpose of review The purpose of this review is to evaluate the mechanisms that underlie the association between periodontal pathogens and rheumatoid arthritis (RA). Recent findings This review focuses on the cross-reactivity hypothesis as a mechanism that might contribute to explain the pathologic evolution of periodontal infections from periodontitis to RA. The scientific rationale is that immune reactions following infection by periodontal bacteria might cross-react with RA autoantigens, in this way eventually leading to autoimmunity. Using the rheumatoid antigen associated with RA-A47 arthritis as an antigen model and analyzing five periodontal bacteria (eg, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Treponema denticola, Tannerella forsythia and Prevotella intermedia), an extremely varied pattern of peptide sharing was found. In the context of the cross-reactivity hypothesis, the data allow us to glimpse the possibility of distinguishing the periodontal bacteria capable of attacking the periodontal tissue from those that are additionally equipped with a rheumatologic potential by virtue of the sharing of peptide sequences with RA antigens.