A15193 Activated TLR4 /NF-KB associated signal transduction molecules may accelerate the progression of atherosclerosis

Abstract

Objectives: Recently concern about possible links between periodontal disease and atherosclerotic vascular disease has intensified investigation into possible association. Periodontitis could elicite endothelial dysfunction by increased serum inflammatory cytokine, which could play a vital role in accelerating the progression of atherosclerosis. The activation of TLR4 and NF-κB signaling pathways may be involved in the bacteria-mediated a chronic inflammatory response. The aim of this study was to demonstrate that periodontal pathogens infection accelerate atherosclerosis in the animal model. Methods: 36 age- and sex-matched New Zealand White rabbits were randomly divided into the control group and the experimental groups,12 rabbits maintained on a normal diet as a model for the control group, and 24 rabbits maintained on a diet consisting of 0.5% fat for 14 weeks to induce the accumulation of lipid deposits in the aorta as a model for atherogenesis and One-half of the animals received silk ligatures around their mandibular premolars followed by an application of periodontal pathogens to induce atherogenesis and periodontitis. Animals were sacrificed after 14 weeks. Periodontal disease severity was by direct visualization of bone loss. The data of 36 rabbits was compared between the control group and the experimental groups. Results: the levels of expression of TLR4/NF-κB in atherosclerotic lesions were increased compared with the control group. Conclusion: The activation of TLR4/NF-κB signaling pathways may be involved in the bacteria-mediated chronic inflammatory response