Abstract

Gingival disase and rheumatoid arthritis (RA) are linked at both the epidemiologic and pathogenesis levels. In this study, we aimed to identify environmental factors associated with RA and gingival disease and to investigate factors that protect the gingival tissue in RA patients. This retrospective study analyzed 754 RA patients with gingival disease selected from the NHANES database who completed the mobile examination center interview/examination between 1999 and 2004. Data collected included demographics, lifestyle, dietary intake, and biomarkers. The study included 173 RA patients with gingival disease. Multivariate logistic regression analysis showed that the odds of gingival disease were significantly increased with male gender. However, the odds of gingival disease was significantly decreased with increased vitamin C intake (OR = 0.996, p = 0.041), and higher serum vitamin D levels (OR = 0.979, p = 0.011). Given the significant association between the prevalence of gingival disease and RA, identification of risk factors of gingival disease will be useful as a screening tool in national health surveys to improve the management of periodontal disease in patients with RA.

Highlights

  • Rheumatoid arthritis (RA) is an autoimmune disease in which chronic synovial inflammation resulting from impaired immune homeostasis leads to joint destruction and bone erosion [1, 2]

  • Of the 31,126 participants selected from the National Health and Nutritional Examination Survey (NHANES) database who completed the mobile examination center interview/examination between 1999 and 2004, a total of 920 participants with rheumatoid arthritis were included in this study

  • Analysis of dietary characteristics showed that patients with no gingival disease had a significantly higher mean vitamin C and Beta-cryptoxanthin intake compared with patients with gingival disease

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Summary

Introduction

Rheumatoid arthritis (RA) is an autoimmune disease in which chronic synovial inflammation resulting from impaired immune homeostasis leads to joint destruction and bone erosion [1, 2]. Factors that play an important role in RA pathogenesis include tumor necrosis factor (TNF)-α, IL-6, autoreactive Th17 cells producing IL-17, and regulatory T cells (Tregs) [4,5,6]. Periodontitis with rheumatoid arthritis of synthetic disease-modifying anti-rheumatic drugs (DMARDs) to limit inflammation and slow down structural changes to the joints [7]. Based on the role played by the immune system in RA, novel therapeutic regimens are used and include propagation of Tregs, use of biologic DMARDs targeting IL-17, IL-6, and granulocyte-macrophage colonystimulating factor, TNF inhibitors, anti-CD20, and immunoproteasome inhibitors [8]

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