To investigate the possible link between Porphyromonas gingivalis infection and rheumatoid arthritis (RA), according to antibody profile, genetic and environmental factors, and RA severity.
For assessing P gingivalis infection, serum levels of antibodies directed against P gingivalis lipopolysaccharide were measured in 694 patients with early RA who were not exposed to steroids or disease-modifying antirheumatic drugs. Anti-P gingivalis antibody titers were compared between patients with early RA and various control groups, and according to various patient characteristics.
Anti-P gingivalis antibody titers did not significantly differ between patients with RA and controls and did not significantly differ with anti-citrullinated protein antibody (ACPA), rheumatoid factor (RF), or HLA shared epitope status. Anti-P gingivalis antibody titers were significantly higher among patients who had never smoked compared to patients who had ever smoked (P = 0.0049). Among nonsmokers, high anti-P gingivalis antibody levels were associated with a higher prevalence of erosive change (47.5% versus 33.3% with modified Sharp/van der Heijde score erosion subscale ≥1; P = 0.0135).
In this large early RA cohort, we did not detect any association of anti-P gingivalis antibodies with RA or with ACPA status. These results suggest that the association of periodontitis and RA could be linked to bacterial species other than P gingivalis or to a mechanism other than citrullination. Nevertheless, we found higher anti-P gingivalis antibody titers in nonsmokers. In addition, in this population of nonsmokers, high anti-P gingivalis antibody titers were associated with more severe disease. We hypothesize that the role of tobacco in RA pathogenesis is so high that the effect of P gingivalis could be revealed only in a population not exposed to tobacco.