Periodontal inflammation in a rat model induced fatty liver disease through increased serum LPS.

Studies suggest a correlation between ethanol consumption and periodontal disease. We hypothesized that elevated levels of blood reactive oxygen species following ethanol consumption may increase inflammation in periodontal tissue. Rats were divided into 4 groups (6-7 rats/group). Two groups were fed an ethanol-containing liquid diet, and 2 groups were fed a pair-fed control diet. In one of each dietary group, periodontitis was ligature-induced, while the other group was left unligated. Chronic ethanol feeding alone decreased the ratio of reduced/oxidized glutathione and increased 8-hydroxydeoxy-guanosine and tumor necrosis factor (TNF)-alpha levels in the gingiva. Blood hydroperoxides were also increased. In ligature-induced periodontitis lesions, ethanol feeding enhanced polymorpho-nuclear leukocyte infiltration and TNF-alpha expression. The results suggest that chronic alcohol consumption increased periodontal inflammation, oxidative damage, and TNF-alpha production and had an additive effect on polymorphonuclear leukocyte infiltration and gingival oxidative damage, increasing the severity of periodontal inflammation in the ligature model.

Studies suggest an association between consumption of a high-cholesterol diet and periodontitis. We addressed the mechanism by which high dietary cholesterol could be detrimental to periodontal health in a rat model. Feeding a high-cholesterol diet augmented the effects of bacterial pathogens and their products (e.g., lipopolysaccharide and proteases) on production of pro-inflammatory cytokines in fibroblasts. High dietary cholesterol also increased mitochondrial 8-hydroxydeoxyguanosine in the periodontal tissues. These results suggest that excessive tissue oxidative damage induced by high dietary cholesterol could potentiate pro-inflammatory cytokine production by fibroblasts stimulated with bacterial pathogens.

In the rat model, vitamin C suppressed alveolar bone resorption, induced by high dietary cholesterol, by decreasing the oxidative damage of periodontal tissue.

No abstract