Oral bacterium P. gingivalis has been well-documented as a mediator of periodontal disease. Furthermore, hosts harboring this pathogen have been shown to have greater risk for rheumatoid arthritis. Researchers are elucidating the mechanisms by which P. gingivalis contributes to the pathogenesis of arthritic and their related disorders. Upregulation of intestinal lipopolysaccharides and subsequent inflammation, as well as citrullination of alpha-enolase, which shares homology with human tissue α-enolase, are described mechanisms of autoimmunity.
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