Periodontal disease and sports performance: a systematic review and meta-analysis.

This systematic review and meta-analysis aimed to assess the association between athletic performance and periodontal disease (PD). Observational studies published up to April 2022 were searched in online databases (PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar). PECO statement focused on studies with professional athletes (Participants) with PD (Exposition) compared to those with healthy periodontium (Comparison) and its effects on sports performance (outcome). Searches were conducted according to the PRISMA guidelines (registration protocol: 10.17605/OSF.IO/7ADH6) and risk of bias evaluation according to the Joanna Briggs Institute checklist. A total of 793 references were retrieved, of which eight were considered eligible. Two studies did not show an association between clinical PD parameters and performance. A meta-analysis with 396 participants suggested a relationship between PD and self-reported reduction in sports performance (odds ratio [OR] = 1.55; 95% confidence interval [CI] 1.04-2.31; p = 0.03; I2 = 0%) with moderate quality of evidence accordingly GRADE analysis. Despite the differences in performance evaluations between studies, PD was associated with reduced self-reported sports performance. Additional studies assessing confounding factors and objective assessment of PD and performance are needed to clarify the real effect of both conditions.

The Relationship between Exercise and Salivary Oxidative Stress: A Systematic Review.

Salivary content has been reported as a potential biomarker for oxidative stress assessments especially in context of exercise-induced oxidative stress. This systematic review following PRISMA guidelines aimed to evaluate the effects of physical exercise and changes promoted in oxidative stress identified in saliva. METHODS: Studies published up to May 2022 were searched in online databases (PubMed, Scopus, Web of Science, The Cochrane Library, LILACS, OpenGrey, and Google Scholar). Risk of bias evaluation were performed using the Quality Assessment Tool for Before-After (Pre-Post) Studies with No Control Group. RESULTS: A total of 473 references were identified and 22 considered eligible. In this case 14 studies reported increase of antioxidant parameters in saliva while eight studies demonstrated increased lipid peroxidation after exercise. Regarding nitrite levels, two studies showed higher levels after exercise. The quality of evidence was very low due to high heterogeneity, inconsistency and indirectness among studies according Grading of Recommendations, Assessment, Development and Evaluation analysis. CONCLUSION: Increase of oxidative stress and antioxidant activity in saliva appears to be present after exercise, especially at moderate intensity. However, the wide variety of methods leads to divergent data. For precision in salivary assessments, new research with larger sample sizes and better participant matching are recommended.

Long-Term Lead Exposure Since Adolescence Causes Proteomic and Morphological Alterations in the Cerebellum Associated with Motor Deficits in Adult Rats.

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.

Spinal cord neurodegeneration after inorganic mercury long-term exposure in adult rats: Ultrastructural, proteomic and biochemical damages associated with reduced neuronal density.

Mercury chloride (HgCl2) is a chemical pollutant widely found in the environment. This form of mercury is able to promote several damages to the Central Nervous System (CNS), however the effects of HgCl2 on the spinal cord, an important pathway for the communication between the CNS and the periphery, are still poorly understood. The aim of this work was to investigate the effects of HgCl2 exposure on spinal cord of adult rats. For this, animals were exposed to a dose of 0.375 mg/kg/day, for 45 days. Then, they were euthanized, the spinal cord collected and we investigated the mercury concentrations in medullary parenchyma and the effects on oxidative biochemistry, proteomic profile and tissue structures. Our results showed that exposure to this metal promoted increased levels of Hg in the spinal cord, impaired oxidative biochemistry by triggering oxidative stress, mudulated antioxidant system proteins, energy metabolism and myelin structure; as well as caused disruption in the myelin sheath and reduction in neuronal density. Despite the low dose, we conclude that prolonged exposure to HgCl2 triggers biochemical changes and modulates the expression of several proteins, resulting in damage to the myelin sheath and reduced neuronal density in the spinal cord.

Association Between Diabetic Retinopathy and Periodontitis-A Systematic Review.

Background: Diabetic retinopathy is a common microvascular complication in diabetic patients and is considered the main cause of visual loss worldwide. Periodontitis is a chronic inflammatory condition, which compromises dental supporting tissues. The chronic bacterial challenge in periodontitis is a persistent source of inflammatory mediators that may be associated with insulin resistance, increasing the risk of complications of diabetes mellitus. This systematic review aimed to summarize the evidence in the association between diabetic retinopathy and periodontitis. Methods: This review was registered under the number CRD 42019142267. A search strategy in five electronic databases and a gray literature source was performed based on the PECO acronym. After data extraction, the qualitative synthesis and risk of bias analyses were performed using the Newcastle-Ottawa scale. The level of evidence of all studies taken together was evaluated through the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. Results: Out of the 253 citations screened, five cross-sectional studies met the eligibility criteria and were included in the qualitative analysis, in which two were judged to be of good quality, one as fair quality, and two as poor quality. Among the included studies, a significant relationship between the severity of periodontitis (CAL > 5 mm) and the severity of diabetic retinopathy (p < 0.05) was reported by four studies. Also, an association between both diseases in non-obese adults was found after adjustments [OR 2.206 (1.114-4.366); p = 0.0232). However, the analysis of evidence by GRADE assessment was rated as low. Conclusions: Although the results of individual studies suggest an association between diabetic retinopathy and periodontitis, the quality of the body of evidence was judged to be low by the GRADE approach. Further studies with larger sample sizes, adequate models of cofounders' adjustments, and prospective analysis of periodontitis and diabetes conditions ought to be conducted to clarify this association.

Alveolar bone loss induced by chronic ethanol consumption from adolescence to adulthood in Wistar rats.

Though there are literature indicating the bone loss due to alcohol consumption, studies on the association between ethanol consumption and periodontal breakdown in animals are either scarce or have provided conflicting results. Here, we investigated the effects of chronic alcohol exposure from adolescence to adulthood on the alveolar bone in rats. Wistar rats were exposed to ethanol (6.5 g/kg/day) in a solution of 22.5% (w/v) or distilled water (control) by gavage from 35 days of age (adolescent) until 90 days (adulthood). Evaluation of the bone loss was performed using scanning electronic microscopy, in which the distances between the cement-enamel junction and the alveolar bone crest from the palatal side of the first molar mandibular were measured. The measurements obtained were tabulated and analyzed using Student's t-test. Alcohol-treated group revealed greater bone loss in comparison to the control group. These findings indicate that heavy chronic alcohol exposure from adolescent to adulthood can induce alveolar bone loss in rats associated to absence of periodontitis.