BackgroundDyslipidemia increases circulating levels of oxidized low-density lipoprotein (OxLDL) and this may induce alveolar bone loss through toll-like receptor (TLR) 2 and 4. The purpose of this study was to investigate the effects of dyslipidemia on osteoclast differentiation associated with TLR2 and TLR4 in periodontal tissues using a rat dyslipidemia (apolipoprotein E deficient) model.MethodsLevels of plasma OxLDL, and the cholesterol and phospholipid profiles in plasma lipoproteins were compared between apolipoprotein E-deficient rats (16-week-old males) and wild-type (control) rats. In the periodontal tissue, we evaluated the changes in TLR2, TLR4, receptor activator of nuclear factor kappa B ligand (RANKL) and tartrate resistant acid phosphatase (TRAP) expression.ResultsApolipoprotein E-deficient rats showed higher plasma levels of OxLDL than control rats (p<0.05), with higher plasma levels of total cholesterol (p<0.05) and LDL-cholesterol (p<0.05) and lower plasma levels of high-density lipoprotein cholesterol (p<0.05). Their periodontal tissue also exhibited a higher ratio of RANKL-positive cells and a higher number of TRAP-positive osteoclasts than control rats (p<0.05). Furthermore, periodontal gene expression of TLR2, TLR4 and RANKL was higher in apolipoprotein E-deficient rats than in control rats (p<0.05).ConclusionThese findings underscore the important role for TLR2 and TLR4 in mediating the osteoclast differentiation on alveolar bone response to dyslipidemia.

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.

Amyloid-β plays a causative role in Alzheimer's disease. Occlusal disharmony causes chronic psychological stress, and psychological stress increases amyloid-β accumulation. The purpose of the present study was to investigate whether occlusal disharmony-induced psychological stress affects the accumulation of amyloid-β and its related gene expressions in the rat hippocampus. Eight-week-old male Wistar rats (n = 18) were divided into three groups of six rats each: (1) a control group that received no treatment for 8 weeks; (2) an occlusal disharmony group that underwent cutoff maxillary molar cusps for 8 weeks; and (3) a recovered group that underwent cutoff maxillary molar cusps for 4 weeks followed by recovery for 4 weeks. Occlusal disharmony increased plasma corticosterone levels in a time-dependent manner. Levels of amyloid-β 40 and 42, glucocorticoid receptor (Gr) protein, and cleaved caspase 3 (Casp3) as well as gene expressions of amyloid precursor protein, beta-secretase, Casp3, and Gr in the hippocampus in the occlusal disharmony group were significantly higher than those in the control group (P < 0.016). These findings were significantly improved by recovery of occlusion (P < 0.016). These results indicate that psychological stress induced by occlusal disharmony reversibly induces amyloid-β 40 and 42 in the rat hippocampus through the glucocorticoid signal.

HCC patients with periodontitis had higher JIS score and circulating ROS level than HCC patients without periodontitis.

Aim Reactive oxygen species (ROS) contribute to the development of periodontitis. As molecular hydrogen can act as a scavenger of ROS, we examined the effects of treatment with hydrogen‐rich water on a rat model of periodontitis. Material & Methods A ligature was placed around the maxillary molars for 4 weeks to induce periodontitis, and the animals were given drinking water with or without hydrogen‐rich water. Results The rats with periodontitis which were treated with pure water showed a time‐dependent increase in serum ROS level. Compared with the rats without periodontitis, the periodontitis‐induced rats which were given pure water also showed polymorphonuclear leucocyte infiltration and alveolar bone loss at 4 weeks. Hydrogen‐rich water intake inhibited an increase in serum ROS level and lowered expression of 8‐hydroxydeoxyguanosine and nitrotyrosine in the periodontal tissue at 4 weeks. Such conditions prevented polymorphonuclear leucocyte infiltration and osteoclast differentiation following periodontitis progression. Furthermore, inflammatory signalling pathways, such as mitogen‐activated protein kinases, were less activated in periodontal lesions from hydrogen‐rich water‐treated rats as compared with pure water‐treated rats. Conclusion Consuming hydrogen‐rich water might be beneficial in suppressing periodontitis progression by decreasing gingival oxidative stress.