Periodontitis-activated monocytes/macrophages cause aortic inflammation

• DOI: 10.1038/srep05171
• Publication Date: 2014-06-04T09:10:47Z
• Authors: Shin-ichi Miyajima; Keiko Naruse; Yasuko Kobayashi; Nobuhisa Nakamura; Toru Nishikawa; Kei Adachi; Yuki Suzuki; Takeshi Kikuchi; Akio Mitani; Makoto Mizutani; Norikazu Ohno; Toshihide Noguchi; Tatsuaki Matsubara
• Keywords: Male; 0301 basic medicine; Aortitis; Macrophages; Macrophage Activation; Atherosclerosis; Article; Monocytes; Rats; Rats, Sprague-Dawley; 03 medical and health sciences; Animals; Cytokines; Periodontitis; Cells, Cultured

A relationship between periodontal disease and atherosclerosis has been suggested by epidemiological studies. Ligature-induced experimental periodontitis is an adequate model for clinical periodontitis, which starts from plaque accumulation, followed by inflammation in the periodontal tissue. Here we have demonstrated using a ligature-induced periodontitis model that periodontitis activates monocytes/macrophages, which subsequently circulate in the blood and adhere to vascular endothelial cells without altering the serum TNF-α concentration. Adherent monocytes/macrophages induced NF-κB activation and VCAM-1 expression in the endothelium and increased the expression of the TNF-α signaling cascade in the aorta. Peripheral blood-derived mononuclear cells from rats with experimental periodontitis showed enhanced adhesion and increased NF-κB/VCAM-1 in cultured vascular endothelial cells. Our results suggest that periodontitis triggers the initial pathogenesis of atherosclerosis, inflammation of the vasculature, through activating monocytes/macrophages.