• inflammation
• immune system diseases
• rheumatoid factor

With great interest, we read the work by Jenning et al, which proposed a mechanism by which Porphyromonas gingivalis (P.g.) is involved in rheumatoid arthritis (RA) progression by citrullinating and producing exogenously citrullinated human and bacterial epitopes.1 This commendable work elucidated the mechanism by which autocitrullinated prokaryotic peptidyl arginine deiminase (PPAD) mediates the inflammatory pathogenesis of RA. In particular, the authors demonstrated a correlation between anti-RA-PPAD and both anticitrullinated peptide/protein antibody (ACPA) levels and interstitial lung disease autoantigen reactivity. The study also provided evidence regarding how PPAD citrullinates the internal arginines of RA autoantigens.1 Moreover, the findings of this study suggested that the failure to clear P.g. induces bacterial citrullinated epitope-specific ACPAs, which might trigger ACPA-mediated autoimmunity.1 P.g. is the main pathogen responsible for periodontitis and has been proposed to be involved in stimulating self-reactive immune responses,2 3 which underlie the association …