Immune crosstalk between periodontitis and rheumatoid arthritis: oral microbiota as a trigger of autoimmunity

Background. Rheumatoid arthritis (RA) and periodontitis are chronic inflammatory diseases that share multiple pathogenic mechanisms, including activation of pro-inflammatory cytokines, immune cell infiltration, microbial dysbiosis, and destruction of connective and bone tissues. Growing evidence suggests that periodontitis may act not only as a comorbid condition but also as a potential trigger in the development of RA, particularly through the involvement of Porphyromonas gingivalis. Purpose – to summarize current data on the pathogenetic link between RA and periodontitis, with a focus on the role of the oral microbiota in the development of autoimmune processes. Materials and Methods. A content analysis of publications from PubMed, Clinical Key, Cochrane Library, EBSCO, and Google Scholar databases was conducted. Sources that highlighted the association between RA and periodontitis in accordance with the principles of evidence-based medicine were selected. The review was prepared following the PRISMA guidelines. Results. Porphyromonas gingivalis is a bacterium that expresses the enzyme peptidylarginine deiminase (PPAD), which can citrullinate host proteins. These modified proteins are recognized by the immune system as foreign, leading to the production of specific autoantibodies against citrullinated proteins. High levels of such antibodies (anti-citrullinated protein antibodies, ACPA) are frequently detected in RA patients and are associated with more severe disease. Citrullinated proteins and the PPAD enzyme itself are found in the periodontal tissues of patients with periodontitis. In addition, Aggregatibacter actinomycetemcomitans promotes excessive citrullination via neutrophil activation and the release of neutrophil extracellular traps (NETs), further contributing to the generation of autoantigens. RA patients exhibit significant alterations in oral microbiota composition – an increased prevalence of P.gingivalis, Tannerella forsythia, and Treponema denticola, along with a decrease in commensal bacteria such as Streptococcus and Actinomyces. These microbiota shifts may precede the clinical onset of arthritis, indicating potential prognostic value. Conclusions. The presence of periodontitis, particularly involving P.gingivalis, may contribute to the development of autoimmune responses characteristic of RA. The oral microbiota plays a critical role in breaking immune tolerance, highlighting the need for an integrated medical-dental approach in managing patients with inflammatory diseases. Oral microbiota analysis may serve as a promising tool for early diagnosis, monitoring, and prevention of rheumatoid arthritis, especially in genetically predisposed individuals.