Background: Regular physical activity boosts several physical capacities and reduces many inflammatory markers of several diseases. In this sense, periodontal disease is a multifactorial inflammatory disease of tooth supporting tissues that has been claimed to trigger processes of systemic alterations. The aim of this systematic review and meta-analysis was to assess the effects of physical activity on periodontal disease. Methods: Observational studies published until August 2018 were searched in online databases (PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar) after developing a PECO statement that focused on the comparison between adults that followed a routine of exercises or presented a sedentary lifestyle and its effects on periodontal disease. Searching and data extraction were conducted by following PRISMA guidelines. Registration protocol: CRD42016049661. Quality assessment and risk of bias were analyzed by following Fowkes and Fulton protocol. Results: A total of 512 references were retrieved, while only seven were considered eligible. Two meta-analysis involving the prevalence of periodontal disease and unadjusted/adjusted Odds ratio were performed. One of studies did not find association between clinical periodontal parameters and physical activity. Six articles suggested an association between periodontal disease and regular practice of physical activity since a reduction of periodontal prevalence was observed. Moderate level of evidence was demonstrated on GRADE analysis. Conclusion: Physical activity was associated as a potential tool for reduction of periodontal disease prevalence. The frequency of physical activity is directly related to a low occurrence of periodontitis. However, it is important that further investigations evaluate the effects of other exercise variables, such as volume and intensity, on the periodontal disease prevalence.

This systematic review aims to investigate the association between psychological stress and periodontitis through analysis of cortisol levels and periodontal clinical parameters. This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guide and based on PECO (Participants, Exposure, Comparators, Outcomes) question and registered at PROSPERO under the code CRD42017076670. As eligibility criteria, observational studies performed in adult humans presenting periodontitis (P), which evaluated patients exposed (E) and nonexposed to psychological stress (C) and to verify the association between this type of stress and periodontitis (O) were included. The searches were performed until March 2018. The following databases were used: PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar. After searches, the duplicate results were removed. The remaining citations were selected according to eligibility criteria in two phases. In the first phase, the title/abstract was evaluated. In the second phase, the articles were chosen previously were assessed by full text. After selection, the studies were submitted to data extraction and risk of bias evaluation by Fowkes and Fulton. A total of 1,386 citations were retrieved. After duplicates removal and selection process, three articles were selected by full text. Among them, two articles reported a positive association between psychological stress and periodontitis. All articles were classified as low risk of bias. Even though two articles highlighted an association between psychological stress and the presence of a possible modulatory pattern of cortisol levels in clinical parameters of periodontitis, more studies are necessary to elucidate this question.

Periodontitis is an inflammatory disease of dental supporting tissues (gingiva, periodontal ligament, and bone) and it has been suggested as a possible etiology for rheumatoid arthritis (RA). In this systematic review, we aim to verify if periodontitis represents a risk factor for RA. Electronic databases were consulted until March 2018 considering eligibility criteria focusing on: (P, participants) adults; (E, exposure) with periodontitis; (C, comparison) without periodontitis; and (O, outcome) development of RA. Quality assessment of studies and risk-of-bias evaluation were also performed. To undertake a quantitative analysis, the number of persons with RA and a total number of participants for the case group (with periodontitis) and control group (without periodontitis) were used to calculate the odds ratio (OR) with a 95% confidence interval (CI). A total of 3888 articles were identified, and nine studies were considered eligible. Seven of 9 articles suggested an association among diseases by the common pro-inflammatory profiles. The pooled analysis of 3 articles showed a higher RA prevalence for persons with periodontitis ( n = 1177) than controls ( n = 254) (OR 1.97; CI 1.68–2.31; p < 0.00001). However, considerable heterogeneity among studies was verified (I2 = 96%, p < 0.00001). Periodontitis may represent a risk factor for RA by heredity, bacterial infection, and the pro-inflammatory profile shared between both diseases. Although most of the elective studies report an association between periodontitis and RA, the quantitative analysis showed a high heterogeneity, leading to the need for further studies.

Lead (Pb) is an environmental contaminant that presents a high risk for human health. We aimed to investigate the possible alterations triggered by the exposure to Pb acetate for a long period in motor performance and the possible relationship with biochemical, proteomic and morphological alterations in the cerebellum of rats. Male Wistar rats were exposed for 55 days, at 50 mg/Kg of Pb acetate, and the control animals received distilled water. Open field (OF) and rotarod tests; biochemistry parameters (MDA and nitrite); staining/immunostaining of Purkinje cells (PC), mature neurons (MN), myelin sheath (MS) and synaptic vesicles (SYN) and proteomic profile were analyzed. Pb deposition on the cerebellum area and this study drove to exploratory and locomotion deficits and a decrease in the number of PC, MN, SYN and MS staining/immunostaining. The levels of MDA and nitrite remained unchanged. The proteomic profile showed alterations in proteins responsible for neurotransmitters release, as well as receptor function and second messengers signaling, and also proteins involved in the process of apoptosis. Thus, we conclude that the long-term exposure to low Pb dose promoted locomotion and histological tracings, associated with alterations in the process of cell signaling, as well as death by apoptosis.

Background: An amount of cognition decline is normal with aging; however, intrinsic and extrinsic risk factors may exacerbate it, affecting social and occupational tasks. Masticatory dysfunction (MD), as a general term, refers to an impairment in the masticatory function triggered by a structural factor, such as tooth loss; functional factors, such as weaker bite force or a poorer masticatory performance; or both factors. MD acting as a source of chronic stress, promotes functional and morphological changes on the hippocampus, a brain area crucial for learning and memory abilities. This study aimed to synthesize evidence on the association between MD and cognitive deficit (CD), and demonstrate whether might be adequately considered as a risk factor. Methods: Observational studies were screened in seven online databases; the search strategy (PECO) was focused in observational studies with humans as a population (P), presenting groups exposed (E), and non-exposed (C) to tooth loss, in which cognition parameters were measured and compared between groups (O). The final selection included only those studies comparing the effect in cognition between subjects having ≥20 remaining teeth and <20 remaining teeth, considering the latter as a structural factor triggering MD by the literature. Searching and data extraction were conducted following PRISMA guidelines. Qualitative and risk of bias evaluations were performed. The meta-analysis (MA) was constructed including the odds ratio (OR) and its 95% confidence interval (CI) comparing two groups—with/without MD. The level of evidence was rated by Grading Recommendations Assessment, Development and Evaluation (GRADE) approach. Results: In total, 5,666 citations were identified, 14 accomplished our eligibility criteria, and nine were include in the MA. The MA demonstrates that individuals with MD had 46% higher chance to presented CD (OR 2.24 [1.73, 2.90], p < 0.00001, I 2 = 46%). The level of evidence was rated as low by GRADE. Conclusion: Despite the low certainty in evidence, according to our MA, MD is positively associated with increased risk of CD. However, more studies including other factors underlying MD and similar measurements should be conducted to obtain a strong estimate of the risk.

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Background 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. Materials and methods 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. Results 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. Conclusions 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.