This study aims to evaluate if ligature-induced periodontitis can potentiates the deleterious effects of immobilization in the skeletal striated muscle, contributing to the development of muscle atrophy due to disuse. Forty Wistar rats were divided into four groups: (1) Control Group (CG), (2) Periodontal Disease (PDG), (3) Immobilized (IG), and (4) Immobilized with Periodontal Disease (IPDG). Periodontal disease was induced for 30 days, with ligature method, and the immobilization was performed with cast bandage for 15 days. Prior to euthanasia, nociceptive threshold and muscular grasping force were evaluated. Afterwards, the soleus muscle was dissected and processed for sarcomere counting and morphological/morphometric analysis. For data analysis, was used the one-way ANOVA and post-test Tukey (p < 0.05). The IG and IPDG presented lower muscle weight, lower muscular grip strength, and less number of sarcomeres compared to CG. The PDG showed reduction of muscle strength and nociceptive threshold after 15 days of periodontal disease and increased connective tissue compared to CG. The IPDG presented lower muscle length and nociceptive threshold. The IG presented reduction in cross-sectional area and smaller diameter, increase in the number of nuclei and a nucleus/fiber ratio, decrease in the number of capillaries and capillary/fiber ratio, with increase in connective tissue. The IPDG had increased nucleus/fiber ratio, decreased capillaries, and increased connective tissue when compared to the IG. The IPDG presented greater muscle tissue degeneration and increased inflammatory cells compared to the other groups. Ligature-induced periodontitis potentiated the deleterious effects of immobilization of the skeletal striated muscle.
Introduction: It is possible that physical activity protects the periodontium by mitigating excessive inflammatory response of the individual. There is some evidence from longitudinal studies and a prospective study demonstrating that physically active adults have experienced a decrease in the risk of periodontitis. To date no study has jointly explored the relationship of physical activity and periodontitis using inflammatory biomarkers. Objective: In this regard, the objective was to assess the bone tissue behavior of rats with experimental periodontitis subjected to aquatic exercise. Methods: Twenty-four male Wistar rats were divided into four groups: 1) without periodontitis and without exercise (CS); 2) without periodontitis and with exercise (CE); 3) with periodontitis and without exercise (DPS); 4) with periodontitis and with exercise (DPE). The animals from groups CE and DPE had swimming sessions for four weeks and the DPS and DPE groups were subjected to ligature-induced periodontitis. After 30 days the animals were sacrificed, and had their right and left hemimandibles removed for radiographic and histological analysis. The data obtained were analyzed and evaluated through ANOVA and Tukey tests. Results: Bone loss in the animals from the DPE group was found to be significantly lower (61.7 ± 2.2; p <0.05) than in those from the DPS group (84.5 ± 1.2; p <0.05), while in terms of the number of osteoblasts (DPS=11.0 ± 1.4; DPE=10.7 ± 5.2) and osteocytes (DPS=17.3 ± 3.1; DPE=19.0 ± 4.4), there was no significant decrease (p <0.05) in the groups subjected to experimental periodontitis, regardless of physical exercise. Conclusion: Physical exercise was found to have a protective effect in relation to bone height and did not influence bone density. Level of evidence II; Therapeutic studies - investigation of treatment results.
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