The association between periodontitis (PD) and rheumatoid arthritis (RA) has been linked to autoantibodies. In recent years, Arg-gingipain (Rgp) triggered myeloperoxidase (MPO) release, which mediates protein carbamylation to form anti-carbamylated proteins (anti-CarP), perpetuating RA progression has gained interest. This study assessed the association between Rgp with MPO and anti-CarP in pre-clinical RA (preRA), early RA (eRA), and established RA (RA) participants with PD.
Methods
A total of 108 participants were categorized into preRA, eRA, RA, and nonRA controls with and without PD. Periodontal and rheumatological parameters were assessed. Rgp-B gene expression from subgingival plaque and MPO and anti-CarP in saliva and serum were assessed. Data were analyzed with SPSS Version 26.
Results
Rgp-B gene expressions were similar across PD groups. In eRA-PD, serum and saliva MPO and saliva anti-CarP levels were highest; strong correlations were present between rgp-B with clinical attachment loss (CAL) (r = 0.783), salivary MPO with visible plaque index (VPI) (r = 0.667), and gingival bleeding index (GBI) (r = 0.767), and salivary anti-CarP with CAL (r = 0.667) and GBI (r = 0.850). Strong positive correlations were detected between salivary MPO and anti-CarP in preRA-PD (r = 0.903), eRA-PD (r = 0.783), RA-PD (r = 0.726), and nonRA-PD (r = 0.470).
Conclusion
Rgp-B gene expression was associated with PD status. Periodontal inflammation, particularly in early RA, was linked to elevated MPO and anti-CarP levels, suggesting that local inflammation may amplify immune responses via MPO-mediated carbamylation. These associations highlight the clinical relevance of periodontal assessment and management in RA patients and at-risk individuals.
