Abstract
ObjectivesTo determine whether serum immunity to Porphyromonas gingivalis peptidylarginine deiminase (PPAD) affects the clinical response to biological disease-modifying antirheumatic drug (bDMARD) in patients with rheumatoid arthritis (RA).MethodsIn a retrospective study, rheumatologic and periodontal conditions of 60 patients with RA who had been treated with conventional synthetic DMARD were evaluated before (baseline) and after 3 and 6 months of bDMARD therapy. After serum levels of anti-PPAD immunoglobulin G (IgG) were determined at baseline, the patients were respectively divided into two groups for high and low anti-PPAD IgG titers according to the median measurements. Genotypes at 8 functional single nucleotide polymorphisms (SNPs) related to RA were also determined.ResultsAfter 3 and 6 months of therapy, patients with low anti-PPAD IgG titers showed a significantly greater decrease in changes in the Disease Activity Score including 28 joints using C-reactive protein (DAS28-CRP) (P = 0.04 for both) and anti-cyclic citrullinated peptide (CCP) IgG levels (P = 0.03 and P = 0.04) than patients with high anti-PPAD IgG titers, although these parameter values were comparable at baseline. The anti-PPAD IgG titers were significantly positively correlated with changes in the DAS28-CRP (P = 0.01 for both) and the anti-CCP IgG levels (P = 0.02 for both) from baseline to 3 and 6 months later. A multiple regression analysis revealed a significantly positive association between the anti-PPAD IgG titers and changes in the DAS28-CRP after 6 months of bDMARD therapy (P = 0.006), after adjusting for age, gender, smoking, periodontal condition, and RA-related SNPs.ConclusionThe serum IgG levels to PPAD affect the clinical response to bDMARD in patients with RA.
Highlights
Rheumatoid arthritis (RA) is a systemic autoimmune disease that encompasses a breach of self-tolerance, chronic synovial inflammation and joint destruction [1]
After 3 and 6 months of therapy, patients with low anti-peptidylarginine deiminase (PPAD) immunoglobulin G (IgG) titers showed a significantly greater decrease in changes in the Disease Activity Score including 28 joints using C-reactive protein (DAS28-CRP) (P = 0.04 for both) and anti-cyclic citrullinated peptide (CCP) IgG levels (P = 0.03 and P = 0.04) than patients with high anti-PPAD IgG titers, these parameter values were comparable at baseline
Anti-P. gingivalis PAD Titer and biological disease-modifying antirheumatic drug (bDMARD) Response in Rheumatoid Arthritis positively correlated with changes in the DAS28-CRP (P = 0.01 for both) and the anti-CCP IgG levels (P = 0.02 for both) from baseline to 3 and 6 months later
Summary
Rheumatoid arthritis (RA) is a systemic autoimmune disease that encompasses a breach of self-tolerance, chronic synovial inflammation and joint destruction [1]. Periodontitis is a chronic inflammatory disease characterized by local inflammation and destruction of the periodontal tissue. Patients with periodontitis displayed higher serum levels of IL-6 and TNF-α than the periodontally healthy individuals [5]. A beneficial effect of treatment with inhibitors of TNF and IL-6 receptor (TNFI and IL6RI) has been suggested on periodontal inflammation as well as the rheumatologic condition in patients with RA [2,6]. These observations imply a potential non-causal association between RA and periodontitis [7]
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