Effects of periodontitis on aortic insulin resistance in an obese rat model.

The combination of obesity and its associated risk factors, such as insulin resistance and inflammation, results in the development of atherosclerosis. However, the effects of periodontitis on atherosclerosis in an obese body remain unclear. The aim of the study was to investigate the effects of ligature-induced periodontitis in Zucker fatty rats on initiation of atherosclerosis by evaluating aortic insulin resistance. Zucker fatty rats (n=24) were divided into two groups. In the periodontitis group, periodontitis was ligature-induced for 4 weeks, whereas the control group was left unligated. After the 4-week experimental period, descending aorta was used for measuring the levels of lipid deposits, immunohistochemical analysis, and evaluation of gene expression. Levels of serum C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), and insulin were also measured. Rats in the periodontitis group had significantly enhanced lipid deposits in the aorta, but not in the control group. Expression of suppressor of cytokine signaling 3, vascular cell adhesion molecule 1, reactive oxygen species, nitrotyrosine, and endothelin-1 in the periodontitis group was more intense than that in the control group. Significantly decreased levels of phosphatidylinositol 3-kinase (Pi3k) catalytic beta-polypeptide (Pi3kcb), Pi3kp85, and insulin receptor substrate 1 and 2 were observed in the periodontitis group. Levels of serum CRP and TNF-alpha were significantly increased in the periodontitis group. Under insulin-stimulated conditions, aorta in the periodontitis group altered the Akt phosphorylation. Periodontitis in obesity induced the initial stage of atherosclerosis and disturbed aortic insulin signaling.

Effects of obesity on gingival oxidative stress in a rat model.

BACKGROUND: Studies indicate a correlation between obesity and periodontitis. Oxidative stress is involved in the progression of periodontitis. The purpose of this study was to investigate the effects of obesity on gingival oxidative stress in a rat periodontitis model. METHODS: The obese Zucker rats (n = 14) and their lean littermates (n = 14) were each divided into two groups of seven rats. In one of each group, periodontitis was induced by ligature for 4 weeks, whereas the other group was left unligated. The level of 8-hydroxydeoxyguanosine and the ratio of reduced/oxidized glutathione were determined to examine gingival oxidative stress. The serum level of reactive oxygen metabolites and the gingival gene-expression pattern related to oxidative/metabolic stress, inflammation, and cell behavior were also evaluated. RESULTS: The obese rats weighed more than the lean rats at 4 weeks. Compared to lean rats, obese rats had enhanced gingival 8-hydroxydeoxyguanosine levels and a decreased ratio of reduced/oxidized glutathione in the gingival tissue, with increasing serum reactive oxygen metabolites. However, there were no significant differences in the degree of alveolar bone loss between lean and obese rats, except for teeth with and without ligatures in both rats. In addition, the periodontal lesion in obese rats showed higher 8-hydroxydeoxyguanosine levels and polymorphonuclear leukocyte infiltration than the inflamed ones in lean rats, with downregulation of multiple cytochrome P450 gene expression. CONCLUSIONS: Obesity induced gingival oxidative stress with increasing serum reactive oxygen metabolites in rats. In the periodontal lesion, gene expressions related to a capacity for xenobiotic detoxification were downregulated in the obese model.