Orthodontic adhesives with antimicrobial and remineralizing properties may be an alternative to control white spot lesions around brackets. The aim of this study is to develop an experimental orthodontic adhesive containing boron nitride nanotubes (BNNT) and alkyl trimethyl ammonium bromide (ATAB). Methacrylate (BisGMA and TEGDMA) monomers were used to formulate the adhesives. Four experimental groups were produced with the addition of 0.1 wt.% BNNT (G_BNNT); 0.1 wt.% ATAB (G_ATAB); and 0.2 wt.% BNNT with ATAB (G_BNNT/ATAB); in the control group, no fillers were added (G_Ctrl). The degree of conversion, cytotoxicity, softening in solvent, contact angle and free surface energy, antibacterial activity, shear bond strength, and mineral deposition were evaluated. Adhesives achieved degree of conversion higher than 50% and cell viability higher than 90%. G_BNNT and G_ATAB adhesives exhibited reduced softening in solvent. Mean free surface energy was decreased in the G_BNNT adhesive. Significant reduction in bacterial growth was observed in the G_BNNT/ATAB. No statistical difference was found for shear bond strength. Mineral deposition was found in G_BNNT, G_ATAB, and G_BNNT/ATAB groups after 14 and 28 days. The addition of 0.2% BNNT/ATAB to an experimental orthodontic adhesive inhibited bacterial growth and induced mineral deposition without affecting the properties of the material.

Açaí (Euterpe oleracea Mart.) juice is rich in phenolic compounds with high antioxidant capacity. It has been observed that the use of antioxidants may be an additional strategy to nonsurgical periodontal therapy as well as to prevent alveolar bone loss. Thus, the objective of this study was to investigate the effects of açaí supplementation on experimental periodontitis in rats. Twenty male Rattus norvegicus (Wistar) rats were assigned into control, açaí, experimental periodontitis, and experimental periodontitis with açaí supplementation groups. Periodontitis was induced by placing ligatures around the lower first molars. Animals in the açaí groups received 0.01 mL/g of clarified açaí juice for 14 days by intragastric gavage. At the end of the experimental period, blood was collected to assess the reduced glutathione (GSH), Trolox equivalent antioxidant capacity (TEAC), and lipid peroxidation (TBARS) levels. Moreover, hemimandibles were analyzed by micro-computed tomography (micro-CT) for alveolar bone loss and bone quality. Açaí supplementation increased blood total antioxidant capacity and decreased lipid peroxidation. It also reduced alveolar bone loss when compared to the experimental periodontitis group. Moreover, clarified açaí per se modulated the oxidative biochemistry and bone microstructure. Thus, açaí may be considered a viable alternative for managing periodontal oxidative stress and preventing alveolar bone loss.

We aimed to investigate the effects of chronic stress (CS) on experimental periodontitis (EP) in rats. For this, 28 Wistar rats were divided into four groups: control, ligature-induced experimental periodontitis (EP), chronic stress (CS; by physical restraint model) and CS+EP (association of chronic stress and ligature-induced periodontitis). The experimental period lasted 30 days, including exposure to CS every day and ligature was performed on the 15th experimental day. After 30 days, the animals were submitted to the behavioral test of the elevated plus maze (EPM). Next, rats were euthanized for blood and mandible collection in order to evaluate the oxidative biochemistry (by nitric oxide (NO), reduced-glutathione activity (GSH), and thiobarbituric acid reactive substance levels (TBARS)) and alveolar bone characterization (by morphometric, micro-CT, and immunohistochemistry), respectively. The behavioral parameters evaluated in EPM indicated higher anxiogenic activity in the CS and CS+EP, groups, which is a behavioral reflex of CS. The results showed that CS was able to change the blood oxidative biochemistry in CS and CS+EP groups, decrease GSH activity in the blood, and increase the NO and TBARS concentrations. Thus, CS induces oxidative blood imbalance, which can potentialize or generate morphological, structural, and metabolic damages to the alveolar bone.