Selective COX-2 inhibitor and omega-3 fatty acid in experimental periodontitis
Objectives: The present study was planned to evaluate the individual and combined effects of selective cyclooxygenase-2 (COX-2) inhibitor; celecoxib, and omega-3 fatty acid on the gingival tissue levels of prostaglandin E2 (PGE2), prostaglandin F2a(PGF2a), leukotriene B4 (LTB4), and platelet activating factor (PAF) in endotoxin-induced periodontitis in rats. Methods: Experimental periodontitis was induced by repeated injection of E. coli endotoxin (LPS). Forty-four adult male Sprague-Dawley rats were divided into 5 study groups as follows; saline control, LPS, celecoxib, omega-3 fatty acid and combination groups. Celecoxib and omega-3 fatty acid was given either as a single agent or as a combination therapy for 15 days. On day 15, the rats were sacrificed and the gingival tissue samples were analyzed for PGE2, PGF2a, LTB4 and PAF levels by enzyme immunoassay. The defleshed jaws were analyzed morphometrically for alveolar bone loss. Data were evaluated statistically by using parametric tests. Results: LPS injection resulted in significantly more bone loss than the saline controls (P<0.05) and significant elevations in the gingival tissue levels of all the analyzed mediators except PGF2a. Individual administration of celecoxib revealed significant reductions in PGE2 and PAF levels (P<0.05), while omega-3 fatty acid provided significant reduction in PGE2, PGF2a and LTB4 levels in comparison to the LPS group (P<0.05). Combined administration of celecoxib and omega-3 fatty acid exhibited significantly lower values than those of the LPS group in all the analyzed mediators (P<0.05), which approximated to the levels in the saline control group (P>0.05). Conclusion: The present study indicate that celecoxib and omega-3 fatty acid, when used individually show a rather partial effect on the control of the analyzed mediators, but when combined they show a synergic effect and provide significant reductions in the gingival tissue levels of PGE2, PGF2a, LTB4, and PAF in LPS-induced experimental periodontitis.