Can periodontopathic bacteria induce the cytokines production that cause atherosclerosis in ApoE knockout mice ?

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Circulatory disorders such as atherosclerosis involve very complex factors such as hyperlipidemia, obesity, smoking, and genetic factors. It has been clarified in recent years that microbial infections invades the vascular endothelial cells, and triggers atherosclerosis at the invasion site. In consequence, atherosclerosis has been considered to relate a microbial infection-induced inflammatory disorder. Epidemiological studies have shown the relationship between periodontal disease and ischemic arterial disease. Postulated mechanisms to link periodontal disease-associated biofilm and vascular disease are shown in many research groups. We detected periodontopathic Treponema denticola in samples of atherosclerosis lesions. We extracted DNA from embedded arterial disease samples and investigated the presence of T.denticola 16S rRNA in 6 aneurysm lesions. When the samples were stained with specific anti-T.denticola antibody, we observed aggregated antigenic particles reacting with the antibody in and around foam cells in aneurysms. In cooperation with a heart surgery center, we extracted DNA from plaque samples from coronary arterial walls at the sites of arterosclerosis lesions, and investigated the presence of specific DNA of Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Campylobacter rectus and T.denticola. We concluded that detections of P.gingivalis and Crectus from coronary disease sites were closely related with their infections in periodontal sites. We demonstrated that the cells of T. denticola produced IL-8, and ICAM-1 from human umbilical vein epithelial cells. These findings suggest that periodontopathic bacterial affect the cytokine network that plays a significant role to control homeostasis results in the trigger or relates to inflammatory responses.