Rheumatoid arthritis (RA) and adult periodontitis share common pathogenetic mechanisms and immunologic and pathological findings. One oral pathogen strongly implicated in the pathogenesis of periodontal disease, Porphyromonas gingivalis, possesses a unique microbial enzyme, peptidylarginine deiminase (PAD), the human equivalent of which has been identified as a susceptibility factor for RA. We suggest that individuals predisposed to periodontal infection are exposed to antigens generated by PAD, with de-iminated fibrin as a likely candidate, which become systemic immunogens and lead to intraarticular inflammation. PAD engendered antigens lead to production of rheumatoid factor-containing immune complexes and provoke local inflammation, both in gingiva and synovium via Fc and C5a receptors.

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Despite advances in our understanding of the inflammatory events that underlie rheumatoid arthritis (RA), which have led to targeted therapies that more effectively control the condition, the etiology of RA is not fully understood. With the discovery that serum antibodies to citrullinated peptides (ACPA) are highly specific for RA and that Porphyromonas gingivalis, the major pathogen responsible for periodontitis (PD), contains the enzyme responsible for the citrullination of peptides, a plausible explanation for observations of increased incidence and severity of PD in RA patients and an appreciation of pathogenic similarities between the two conditions has emerged. Studies of the effect of RA treatment on the severity of PD have been limited and conflicting, especially with respect to anti-TNF agents, but indicate the potential for IL-6 as a therapeutic target for both conditions. PD treatment appears to improve clinical and laboratory evidence of RA disease activity, and the response of RA to anti-TNF therapy is abrogated by the presence of PD. Thus, evaluation and treatment of PD can be recommended for all RA patients.

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