The release of fluoride from restorative materials (Vitremer, Ketac-Fil, Fuji II LC and Freedom) was evaluated during two 15-day periods, before and after a topical application of acidulated phosphate fluoride gel (APF). For each material, 6 specimens were made, which were immersed in 2 ml of deionized water. The fluoride concentration dosages in the solutions were read at intervals of 24 hours for 15 days. After this period, the specimens of each material received treatment with APF gel for 4 minutes and the fluoride released was analyzed at 24-hour intervals during the following 15 days. The analysis of variance and the Tukey test (p < 0.05) showed that the total mean fluoride released during the initial 15 days was greater for Vitremer and Ketac-Fil and lower for Fuji II LC and Freedom; and in the final 15 days there was a difference in release readings, with the greatest value for Vitremer, followed by Fuji II LC, Ketac-Fil and Freedom. The comparison of the results between the 1st day and the 16th day (after gel application) showed a greater fluoride release on the 16th day for Vitremer, Fuji II LC and Freedom and was equal for Ketac-Fil. Although all the materials evaluated gained fluoride with the application of APF, the data suggest that the resin-modified ionomers are more efficient in releasing fluoride to the medium than the other materials.

This study aimed to investigate in vitro and in vivo the influence of hyperglycemic condition on biocompatibility and biomineralization of gray mineral trioxide aggregate (GMTA) and white mineral trioxide aggregate (WMTA). For the in vitro study, fibroblast‐like cells L929 were cultured under high or normal glucose concentration to investigate the effects of both MTA's on cell proliferation and inflammatory cytokines production IL‐1β, IL‐6, and TNF‐α. For the in vivo study, polyethylene tubes containing MTA materials and empty tubes were implanted into dorsal connective tissues of Wistar rats previously assigned normal and hyperglycemic. After 7 and 30 days, the tubes with surrounding tissues were removed and subjected to histological, fluorescence and immunohistochemical analyzes of IL‐1β, IL‐6, and TNF‐α. In vitro study showed that, under high glucose condition, GMTA reduced cell proliferation and IL‐6 production compared with WMTA. Moreover, in vivo study revealed that hyperglycemic condition did not modify the inflammatory response and cytokines production in the tissue close to both materials. Independently of hyperglycemic status, mineralized areas were observed with both materials, but the fluorescence intensity of WMTA was diminished on 14 days in hyperglycemic animals. It is possible to conclude that GMTA was able to inhibit the proliferation rate and IL‐6 production under high glucose concentration in vitro. Furthermore, cytokines production and inflammatory response were not upregulated in hyperglycemic animals; however, a decrease in the calcium deposition was observed in presence of WMTA, suggesting a delay in the mineralization process.

The incidence of cardiovascular disease has increased in the general population, and cardiac damage is indicated as one important cause of mortality. In addition, pollution and metal exposure have increased in recent years. For this reason, toxic effects of metals, such as nickel, and their relation to cardiac damage should be urgently established. Although free radical-mediated cellular damage and reactive oxygen species have been theorized as contributing to the nickel mechanism of toxicity, recent investigations have established that free radicals may be important contributors to cardiac dysfunction. However, there is little information on the effect of nickel exposure on markers of oxidative stress in cardiac tissue. Nickel exposure (Ni 2C 100 mg L ¡ 1 from NiSO 4 ) signi cantly increased lipoperoxide and total lipid concentrations in cardiac tissue. We also observed increased serum levels of cholesterol (59%), lactate dehydrogenase (LDH-64%), and alanine transaminase (ALT-30%) in study animals. The biochemical parameters recovered to the control values with tocopherol intake (0.2 mg 200 g ¡ 1 ). Vitamin E alone signi cantly decreased the lipoperoxide concentration and increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in the heart. Since no alterations were observed in catalase and GSH-Px activities by nickel exposure while SOD activities were decreased, we conclude that superoxide radical (O 2 ¡ ) generated by nickel exposure is of primary importance in the pathogenesis of cardiac damage. Tocopherol, by its antioxidant activity, decreased the toxic effects of nickel exposure on heart of rats.

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