4.6 Article

Rheumatoid arthritis and salivary biomarkers of periodontal disease

Journal

JOURNAL OF CLINICAL PERIODONTOLOGY
Volume 37, Issue 12, Pages 1068-1074

Publisher

WILEY
DOI: 10.1111/j.1600-051X.2010.01625.x

Keywords

biological markers; inflammation; interleukin-1 beta; matrix metalloproteinase (MMP); periodontal disease; rheumatoid arthritis; saliva; salivary biomarkers; tumour necrosis factor (TNF)-alpha

Funding

  1. National Institute of Health, Bethesda, Maryland [P20 RR020145, M01-RR02602]
  2. University of Kentucky General Clinical Research Core

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P>Aim To test the hypothesis that rheumatoid arthritis (RA) influenced levels of salivary biomarkers of periodontal disease. Methods Medical assessments, periodontal examinations and pain ratings were obtained from 35 RA, 35 chronic periodontitis and 35 age- and gender-matched healthy controls in a cross-sectional, case-controlled study. Unstimulated whole saliva samples were analysed for interleukin-1 beta (IL-1 beta), matrix metalloproteinase-8 (MMP-8) and tumour necrosis factor-alpha (TNF-alpha) concentrations. Results The arthritis and healthy groups had significantly less oral disease than the periodontitis group (P < 0.0001), with the arthritis group having significantly more sites bleeding on probing (BOP) than matched controls (P=0.012). Salivary levels of MMP-8 and IL-1 beta were significantly elevated in the periodontal disease group (P < 0.002), and IL-1 beta was the only biomarker with significantly higher levels in the arthritis group compared with controls (P=0.002). Arthritis patients receiving anti-TNF-alpha antibody therapy had significantly lower IL-1 beta and TNF-alpha levels compared with arthritis patients not on anti-TNF-alpha therapy (P=0.016, 0.024) and healthy controls (P < 0.001, P=0.011), respectively. Conclusion RA patients have higher levels of periodontal inflammation than healthy controls, i.e., an increased BOP. Systemic inflammation appears to influence levels of select salivary biomarkers of periodontal disease, and anti-TNF-alpha antibody-based disease-modifying therapy significantly lowers salivary IL-1 beta and TNF-alpha levels in RA.

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