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• Occlusal interference induces oxidative stress in the masseter muscle. • UCP3 regulates redox status in occlusal abnormally related masseter muscle. • Oxidative stress links occlusal interference to masticatory dysfunction. To determine whether occlusal alteration contributes to masticatory muscle damage by inducing oxidative stress. Thirty Sprague-Dawley rats were randomly divided into six groups, including occlusal interference groups (3 days, 7 days, 14 days, 21 days, and removal for 3 days) and a sham group. A rat experimental model of occlusal interference was generated by a 0.6-mm unilateral bite-raise. The rats were euthanised for evaluation of histologic changes in the masseter muscles using haematoxylin-eosin staining. To further investigate the role of oxidative stress and uncoupling protein (UCP3) in the development of occlusal dysfunction-induced masseter damage, levels of UCP3 protein were measured by western blot analysis. Compared with the sham group, the connective tissue of the masseter muscle was extended partially and inflammatory cells appeared following the induction of malocclusion. With respect to the oxidative stress markers, there were increases in malondialdehyde (MDA) content but decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities; furthermore, the expression of UCP3 was upregulated. After eliminating the occlusal interference for 3 days, the degree of inflammation was substantially alleviated, the MDA content decreased, and SOD and GPX activities increased. The expression of UCP3 decreased. Occlusal interference induces oxidative stress in the masseter muscle, regulated by UCP3. Overall, these findings have significant implications for the understanding of how occlusal dysfunction causes muscle fatigue and pain. [ABSTRACT FROM AUTHOR]

Objective To assess the association between interleukin gene polymorphism and recurrent aphthous stomatitis (RAS). Designs Two electronic databases, PubMed and Embase, were utilized to assemble potentially relevant studies meeting the inclusion criteria. A meta-analysis was conducted using Revman 5.3 software (London, UK), and the pooled odds ratio (OR) and 95% confidence interval (CI) were then used to evaluate the strength of the relationship between the gene polymorphisms of IL-1beta(−511C/T), IL-1beta(+3954C/T), IL-6(−174G/C) and IL-10(−1082G/A) and the risk of RAS. Results Ten studies were included in the final meta-analysis, with 884 cases and 1104 controls participating. The results demonstrated that the polymorphism of IL-1beta(−511C/T) significantly increased the probability of the development of RAS in Europeans. (T vs . C: OR = 1.35, 95%CI = 1.09–1.67; CC vs . CT + TT: OR = 1.77, 95%CI = 1.24–2.53; CC vs . TT: OR = 1.86, 95%CI = 1.18–2.95). Furthermore, the C allele in IL-1beta(+3954C/T) was determined to be related to the risk of RAS in Americans (C vs . T: OR = 1.52, 95%CI = 1.07–2.17) and the presence of the C gene was considered a risk variant (CC + CT vs . TT: OR = 1.46, 95%CI = 1.01–2.11), but no relationship was found between the polymorphism of IL-10(−1082G/A) and the risk of RAS. Conclusions The meta-analysis suggested that the mutation of IL-1beta(−511C/T) in Europe and IL-1beta(+3954C/T) in America tend to increase the risk of RAS, but the polymorphism of IL-10(−1082G/A) appears to have no association with RAS risk in America. Further study is required to confirm the above conclusions. [ABSTRACT FROM AUTHOR]