Omega-3 fatty acid Administration and Serum IL-1beta, Osteocalcin, CRP Levels

Objective: This study was planned to evaluate effects of therapeutic and prophylactic + therapeutic administration of omega-3 fatty acid on serum levels of interleukin 1-beta (IL-1beta), osteocalcin (OC), and C-reactive protein (CRP) in experimental periodontitis. Methods: Experimental periodontitis was induced by repeated injection of Escherichia coli lipopolysaccharide (LPS). Thirty-eight adult male Sprague-Dawley rats were divided into 4 study groups as follows; saline controls, LPS, therapeutic omega-3 fatty acid (TO3) and prophylactic + therapeutic omega-3 fatty acid (P+TO3) groups. In TO3 group, omega-3 fatty acid was given to rats having experimental periodontitis for 15 days. In P+TO3 group, omega-3 fatty acid was started 15 days before induction of experimental periodontitis and was continued for another 15 days. On day 15 after induction of periodontitis, serum samples were obtained and rats were sacrificed. Serum samples were analyzed for IL-1beta, OC, and CRP concentrations by enzyme-linked immunosorbent assay. Defleshed jaws were analyzed morphometrically for alveolar bone loss. Data were evaluated statistically by non-parametric tests. Results: LPS injection resulted in significant amount of bone loss (P<0.05). Neither therapeutic nor prophylactic + therapeutic administration of omega-3 fatty acid with the doses and duration of therapy used in this study was effective in preventing endotoxin-induced alveolar bone loss. Therapeutic and prophylactic + therapeutic administration of omega-3 fatty acid revealed significantly higher IL-1beta and OC levels than LPS group (P<0.05). There were no significant differences in serum CRP levels. Conclusions: Omega-3 fatty acid administration does not seem to affect circulating levels of CRP. The significantly increased serum OC level observed in both treatment regimens of omega-3 fatty acid might have an effect in increasing bone remodeling and thereby inhibit progression of alveolar bone resorption. However the significant increase in serum IL-1beta may counteract this mechanism by promoting osteoclast activity resulting in no observable change in bone loss.