Rheumatoid Arthritis and Periodontitis: Shared Pathogenic Mechanisms and Clinical Implications: A Narrative Review

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by systemic inflammation, synovial hyperplasia, and progressive joint destruction. Periodontitis, a chronic inflammatory disease affecting the supporting structures of teeth, has been increasingly recognized as a potential contributor to RA pathogenesis. Evidence suggests that both conditions share common immunological mechanisms and microbial triggers. This review summarizes the data linking RA with periodontitis, with particular focus on shared pathogenic pathways, microbial triggers, immune system alterations, and clinical relevance. Methods: Experimental, epidemiological, and clinical studies were evaluated to explore biological and clinical links between periodontitis and RA. Special emphasis was placed on the mucosal origins of RA, bacterial-mediated citrullination, autoantibody formation, and the role of the complement system. Results: Available epidemiological data indicate that individuals with RA present higher prevalence and greater severity of periodontitis. Periodontal pathogens, such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, contribute to immune dysregulation through citrullination, and subsequent production of anti-citrullinated protein antibodies (ACPAs), a hallmark of RA. Both diseases are characterized by chronic, uncontrolled inflammation, amplified by complement activation and neutrophil hyperactivity. Clinical evidence suggests that non-surgical periodontal therapy may reduce systemic inflammatory markers and improve RA disease activity. Conclusions: The relationship between RA and periodontitis appears to be bidirectional and the recognition of this interaction supports closer collaboration between rheumatologists and dental professionals. Future studies are required to clarify causality and determine whether management strategies can influence patient outcomes.