Periodontitis is a multifactorial inflammatory disease of tooth supporting tissues caused by oral biofilms, influenced by environmental and genetic factors, among others. Ethanol consumption has been considered a factor that enhances alveolar bone loss, especially in high doses. The present study aims to investigate the changes promoted by ethanol binge drinking per se or associated with ligature-induced periodontal breakdown on alveolar bone loss. Thirty-two Wistar rats were randomly allocated into four groups: control (C), ethanol (3g/kg/day; 3 days On-4 days Off protocol by gavage for 28 days, EtOH), experimental periodontitis (EP) and experimental periodontitis plus ethanol administration (EP+EtOH). On day 14^th, periodontitis was induced by ligatures that were placed around the lower first molars. On day 28^th, the animals were euthanized and mandibles were submitted to stereomicroscopy for exposed root area analysis and micro-computed tomography (micro-CT) for the evaluation of alveolar bone loss and microstructural parameters. The results revealed that ligature-induced alveolar bone loss is aggravated by ethanol binge drinking compared to controls (1.06 ± 0.10 vs 0.77 ± 0.04; p<0.0001). In addition, binge drinking per se altered the alveolar bone quality and density demonstrating a reduction in trabecular thickness, trabecular number parameter and bone density percentual. Periodontal disorder plus ethanol binge drinking group also demonstrated reduction of the quality of bone measured by trabecular thickness. In conclusion, intense and episodic ethanol intake decreased alveolar bone quality in all microstructural parameters analyzed which may be considered a modifying factor of periodontitis, intensifying the already installed disease.

Periodontitis is a multifactorial disease triggered by dysbiotic biofilms, involving the host's immune response, systemic and behavioral factors, including psychosocial conditions. This systematic review aimed to investigate the possible association between periodontitis and anxiety in adults. Searches were performed in PubMed, Scopus, Web of Science, Lilacs, Cochrane, and OpenGrey databases, without language restrictions, considering studies in adults (P-Participants), with (E-Exposure) and without periodontitis (C- Comparison) in an outcome of association with anxiety (O-outcome). Methodological quality assessment was carried out using the Newcastle-Ottawa protocol for case-control and cross-sectional studies, followed by an analysis of the level of evidence using the GRADE tool. Metanalysis was not performed due to several differences in methods applied by authors in primary studies. Eleven observational studies were selected according to the inclusion criteria from the total of 6,380 studies retrieved from databases. Eight studies demonstrated higher anxiety levels in subjects with periodontitis, among which only one study presented a high risk of bias. The GRADE tool revealed a low level of evidence for the anxiety outcome measured by the State-Trait Anxiety Inventory (STAI), both for case-control and cross-sectional studies. However, since anxiety may affect the quality of life of many subjects, it reinforces the need for further studies that evaluate this association for more extended periods.Clinical Trial Registration:PROSPERO-CRD42020190445.

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.