2019 Journal of periodontology

Effects of omega-3 fatty acids and aspirin on Porphyromonas gingivalis-induced periodontitis in rats.

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Journal of periodontology Vol. 90 (11) : 1307-1319 • Nov 2019

BACKGROUND: Periodontitis is a common chronic inflammatory disease caused by bacteria which can result in periodontal tissue inflammation, as well as alveolar bone resorption. The purpose of this study was to evaluate the effects of omega-3 fatty acids plus aspirin (ASA) on ligature-induced periodontitis in rats. METHODS: Ninety-six male Sprague-Dawley (SD) rats (age 6 weeks) were randomly divided into eight groups (n = 12 each) and had ligatures placed for 7 days, followed by daily treatment with specific drug regimens for 14 days. The rats were sacrificed 20 days after drug treatment, and their maxillary were subjected to histomorphometric analysis. RAW264.7 cells were cultured with lipopolysaccharide (LPS) or receptor activator (NF)-kappaB ligand (RANKL), and treated with various concentrations of omega-3 and ASA. Then, cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) protein expression and receptor activator of nuclear factor kappa B (RANK), tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP-9), MMP-2, and Cathepsin-K gene expression were detected. RESULTS: The administration of omega-3 fatty acids and aspirin significantly inhibited tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in serum of rats. Histomorphometric analysis showed omega-3 fatty acids plus aspirin promoted alveolar bone increase. Omega-3 fatty acids only, aspirin only, or omega-3 fatty acids plus aspirin also inhibited the protein expressions of COX-2 and iNOS in LPS-stimulated RAW264.7 cells. In addition, omega-3 combined with ASA also inhibited the RANKL-induced gene expressions of MMPs in dose-dependent manners. CONCLUSION: These results demonstrate that omega-3 fatty acids plus aspirin could decrease alveolar bone loss, while simultaneously increasing the protection against periodontal inflammation.

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