The present study results link the systemic effects of induced periodontitis with changes in hepatic tissues such as microvesicular steatosis, likely caused by an increase in oxidative stress and lipid peroxidation. The findings from the present study implicate an association between a decrease of pericytes and liver disease caused by ligature-induced periodontitis in rats.

This study evaluated the nanoleakage patterns in bonded interfaces using two single-step, self-etching adhesives (Adper Prompt-AD, and One-up Bond F-OB), two two-step, self-etching primers (Clearfil SE Bond-CF, and Unifil Bond-UB), and one two-step, total-etch adhesive (Single Bond-SB). Dentin surfaces were bonded with the adhesive systems and stored in water at 37 degrees C for 1 week and 6 months. After storage periods, teeth were sectioned into 0.8 mm-thick slabs, coated with nail varnish except for the bonded interfaces, and immersed in ammoniacal AgNO(3) for 24 h. After immersion in photodeveloping solution, bonded sections were prepared and observed under a SEM using the backscattered electron mode. Undemineralized, unstained, epoxy resin-embedded sections were prepared for TEM. Nanoleakage patterns were qualitatively compared between periods. Nanoleakage was observed in all bonded specimens at both periods. CF and UB presented silver deposits predominantly restricted to the thin (0.5 microm) hybrid layer (HL) at both periods. Although no evident differences were observed in the nanoleakage pattern of UB at 7 days and 6 months, CF presented enlarged areas of silver impregnation after 6 months. SB presented accumulation of silver particles mostly within the HL at 7 days, which was intensified after 6 months. AD and OB presented massive silver accumulation within the HL and the overlying adhesive layer. No evident differences were noticed between storage periods. Silver impregnation increased for all adhesive systems from 7 days to 6 months, except for UB.

The aim of this study was to analyze the effects of chronic mild unpredictable stress (CMS) on the vasoconstrictor response and morphology of the thoracic aorta and serum lipid profiles in rats. Male Sprague-Dawley rats were submitted to CMS, which consisted of the application of different stressors for 7 days per week across 3 weeks. The rats were sacrificed 15 days after CMS exposure. CMS induced supersensitivity to the vasoconstrictor effect of phenylephrine in endothelium-intact thoracic aortic rings without changes in aortic rings without endothelium, or pre-incubated with nitric oxide (NO) synthesis inhibitor. Rats submitted to CMS showed hypertrophy of the intima and tunica media of thoracic aorta, increased serum levels of triglycerides, total cholesterol, very low-density lipoprotein cholesterol, low-density lipoprotein cholesterol and atherogenic index, without changes in high-density lipoprotein cholesterol levels, when compared with control rats. These data indicate that CMS induces physiological and morphological changes that may contribute to the development of atherosclerosis by mechanisms related to deficiency in NO production and dyslipidemia.

Experimental periodontitis caused immunohistochemistry, histopathologic, ultrastructural, oxidative, and biochemical changes in the liver of rats.

Within the limits of the present study, intermittent administration of hPTH 1-34 led to an enhanced periodontal healing process compared with non-treated animals.