Periodontopathic bacteria in rheumatoid arthritis pathogenesis: bridging clinical associations to molecular mechanisms

Periodontitis (PD) is a chronic inflammatory disease linked to microbial dysbiosis, while rheumatoid arthritis (RA) is an autoimmune disorder characterized by anti-citrullinated protein antibodies (ACPA). Despite their distinct etiologies, a clinical and serological association between PD and RA has been observed. Oral microorganisms, especially <i>Porphyromonas gingivalis</i> (<i>P. gingivalis</i>), may contribute to RA onset or progression through dissemination to joints or systemic inflammation. This review explores a: the role of oral microbiota and immune responses in RA b; clinical pathogenic pathways from oral pathogens to the joints c; mechanistic studies on the impact of periodontal pathogens on RA; and d. preventive and therapeutic strategies. <i>P. gingivalis</i> and other periodontal pathogens have been detected in synovial tissues and fluids of RA patients. Microbiome analyses show a more diverse oral microbiota with elevated periodontal disease-associated bacteria in RA patients. Studies demonstrate that <i>P. gingivalis</i> can induce citrullination, autoantibody production, and inflammation, exacerbating joint damage. Future research should investigate the impact of periodontal therapy and RA treatments on the oral microbiota, while large-scale clinical trials are needed to validate the causal relationship between periodontal pathogens and RA.