ObjectiveThis study aims to clarify the effects of diabetes mellitus (DM) on inflammatory profile during orthodontic tooth movement (OTM) and explore potential mechanisms.MethodsOTM models were established in healthy (Ctrl) and DM rats for 0, 3, 7 or 14 days. The tooth movement distance and bone structural parameters were analyzed through micro‐CT. The bone resorption activity and periodontal inflammation status were evaluated through histological staining. RNA sequencing was performed to detect differentially expressed genes in force loading‐treated periodontal ligament fibroblasts (PDLFs) with or without high glucose. The differential expression of inflammatory genes associated with NOD‐like receptor family pyrin domain containing 3 (NLRP3) between groups was tested in vitro and in vivo.ResultsDM caused remarkable reduction of alveolar bone height and density around the moved tooth, corresponding with the higher bone resorption activity and inflammatory scores of DM group. For force loading‐treated PDLFs, high glucose induced the activation of inflammatory pathways, including NLRP3. Elevated expression of NLRP3 and cascade molecules (Caspase‐1, GSDMD, and IL‐1β) were validated by RT‐qPCR, Western blot, and immunohistochemistry staining.ConclusionsDM alters the inflammatory status of periodontium and affects tissue reconstruction during OTM. NLRP3 inflammasome may involve in diabetes‐induced periodontal changes.
Cells are constantly exposed to various mechanical environments; therefore, it is important that they are able to sense and adapt to changes. It is known that the cytoskeleton plays a critical role in mediating and generating extra-and intracellular forces and that mitochondrial dynamics are crucial for maintaining energy homeostasis. Nevertheless, the mechanisms by which cells integrate mechanosensing, mechanotransduction, and metabolic reprogramming remain poorly understood. In this review, we first discuss the interaction between mitochondrial dynamics and cytoskeletal components, followed by the annotation of membranous organelles intimately related to mitochondrial dynamic events. Finally, we discuss the evidence supporting the participation of mitochondria in mechanotransduction and corresponding alterations in cellular energy conditions. Notable advances in bioenergetics and biomechanics suggest that the mechanotransduction system composed of mitochondria, the cytoskeletal system, and membranous organelles is regulated through mitochondrial dynamics, which may be a promising target for further investigation and precision therapies.
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