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Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
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Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
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Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients

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Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients
Journal Article

Infliximab Induced a Dissociated Response of Severe Periodontal Biomarkers in Rheumatoid Arthritis Patients

2019
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Overview
Objective: Rheumatoid arthritis and periodontal disease are associated together, but the effect of therapy provided for one disease to the second one remained under-investigated. This study investigated effect of infliximab therapy used to treat rheumatoid arthritis (RA) on various biomarkers of periodontal disease (PD) severity including serologies of Porphyromonas gingivalis and Prevotella intermedia and matrix metalloproteinase 3. Methods: Seventy nine RA patients were enrolled at the time to start infliximab therapy and the 28 joint disease activity score (DAS28), anti-cyclic citrullinated petides 2nd generation (anti-CCP2), anti-P. gingivalis antibody, and Matrix metalloproteinase 3 (MMP-3) were monitored before and at 6 months of infliximabtherapy. Joint damage and severe periodontal disease were assessed at baseline. Anti-CCP2, anti-P. gingivalis antibody, and MMP-3 weredetermined by enzyme-linked immunosorbent assay (ELISA). Results: At baseline, anti-CCP2 titers were associated with anti-P. gingivalis lipopolysaccharide (LPS)-specific antibodies titers (p < 0.05). Anti-P. gingivalis antibodies were not significantly correlated with clinical, biological, or destruction parameters of RA disease. At 6 months of infliximab therapy, MMP-3 level decreased (from 119 ± 103 ng/mL to 62.44 ± 52 ng/mL; p < 0.0001), whereas P. gingivalis antibody levels remained at the same level. DAS28 and inflammation markers C-reactive protein (CRP) and Erythrocyte sedimentation rate (ESR) also decreased significantly during infliximab therapy (p < 0.05) as anti-CCP2 levels (p < 0.001). Only high MMP-3 level at baseline was associated with infliximab efficacy (p < 0.01). Conclusion: MMP-3 level can be a useful marker of the efficacy of infliximab in RA patients. The treatment did not affect anti-P. gingivalis antibodies.