Porphyromonas gingivalis and rheumatoid arthritis

<jats:sec> <jats:title>Purpose of review</jats:title> <jats:p>To explore the pathogenic association between periodontal disease and rheumatoid arthritis focusing on the role of <jats:italic toggle="yes">Porphyromonas gingivalis</jats:italic>.</jats:p> </jats:sec> <jats:sec> <jats:title>Recent findings</jats:title> <jats:p>In the last decades our knowledge about the pathogenesis of rheumatoid arthritis substantially changed. Several evidences demonstrated that the initial production of autoantibodies is not localized in the joint, rather in other immunological-active sites. A central role seems to be played by periodontal disease, in particular because of the ability of <jats:italic toggle="yes">P. gingivalis</jats:italic> to induce citrullination, the posttranslational modification leading to the production of anticitrullinated protein/peptide antibodies, the most sensitive and specific rheumatoid arthritis biomarker.</jats:p> </jats:sec> <jats:sec> <jats:title>Summary</jats:title> <jats:p>The pathogenic role of <jats:italic toggle="yes">P. gingivalis</jats:italic> has been demonstrated in mouse models in which arthritis was either triggered or worsened in infected animals. <jats:italic toggle="yes">P. gingivalis</jats:italic> showed its detrimental role not only by inducing citrullination but also by means of other key mechanisms including induction of NETosis, osteoclastogenesis, and Th17 proinflammatory response leading to bone damage and systemic inflammation.</jats:p> </jats:sec>