Periodontal disease may reduce the efficacy of tumor necrosis factor (TNF) inhibitor treatment in patients with rheumatoid arthritis (RA), preliminary research suggests.
The study, published in the Journal of Clinical Rheumatology, shows a significant difference in response to 6 months of infliximab (n=15), adalimumab (n=2), or etanercept (n=1) in eight patients with and 10 patients without gum disease for three measures of RA activity.
Patients with periodontal disease had no significant change from baseline on the Disease Activity Score using 28 joints (DAS28), erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP).
By contrast, compared with baseline values, patients without periodontal disease achieved a significant reduction in DAS28 score (5.5 vs 3.6), ESR (23.0 vs 11.5 mm/first hour), and CRP (7.4 vs 2.1 mg/dL).
"The possibility that a sustained gingival inflammatory state may hamper treatment response in this disease has high clinical interest because this is a treatable condition," say Eloísa Bonfá and co-authors from the Hospital das Clínicas in São Paolo, Brazil.
The team explains that periodontal disease was assessed using plaque and gingival bleeding, probing pocket depth, cementoenamel junction, and clinical attachment level. Mild-to-moderate chronic periodontal disease was diagnosed in 44% of patients and remained stable during TNF inhibitor treatment.
"Periodontal inflammation can lead to elevated levels of cytokines such as [interleukin]-1, [interleukin]-6, prostaglandin E2, and TNF, which trigger the release of CRP from the liver, thus contributing to systemic inflammation," explain the researchers.
They note that Porphyromonas gingivalis, a major pathogen of periodontal disease, has been suggested to play a role in RA onset and progression, and has even been shown to produce an enzyme that leads to citrullination of proteins targeted by antibodies involved in RA.
"Importantly, the patients evaluated herein had mild to moderate [periodontal disease], reinforcing previous observations that the association of this complication with systemic disease is not determined solely by traditional clinical signs of [periodontal disease] but also by the interaction of host immune and inflammatory mediators," the team concludes.
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