Diabetes has long been considered a risk factor in implant therapy and impaired wound healing in soft and hard oral tissues. Magnesium has been proved to promote bone healing under normal conditions. Here, we elucidate the mechanism by which Mg²⁺ promotes angiogenesis and osseointegration in diabetic status. We generated a diabetic mice model and demonstrated the alveolar bone healing was compromised, with significantly decreased angiogenesis. We then developed Mg-coating implants with hydrothermal synthesis. These implants successfully improved the vascularization and osseointegration in diabetic status. Mechanically, Mg²⁺ promoted the degradation of Kelch-like ECH-associated protein 1 (Keap1) and the nucleation of nuclear factor erythroid 2-related factor 2 (Nrf2) by up-regulating the expression of sestrin 2 (SESN2) in endothelial cells, thus reducing the elevated levels of oxidative stress in mitochondria and relieving endothelial cell dysfunction under hyperglycemia. Altogether, our data suggested that Mg²⁺ promoted angiogenesis and osseointegration in diabetic mice by regulating endothelial mitochondrial metabolism.

长期以来，糖尿病一直被认为是种植体治疗和损害口腔软组织和硬组织伤口愈合的危险因素。镁已被证明在正常情况下可以促进骨骼愈合。在这里，我们阐明了 Mg²⁺ 在糖尿病状态下促进血管生成和骨整合的机制。我们生成了一个糖尿病小鼠模型，并证明肺泡骨愈合受损，血管生成显着减少。然后，我们开发了具有水热合成功能的 Mg 涂层植入物。这些植入物成功地改善了糖尿病状态下的血管形成和骨整合。在机械上，Mg²⁺ 通过上调内皮细胞中 sestrin 2 （SESN2） 的表达，促进 Kelch 样 ECH 相关蛋白 1 （Keap1） 的降解和核因子红细胞 2 相关因子 2 （Nrf2） 的成核，从而降低线粒体氧化应激水平升高，缓解高血糖下的内皮细胞功能障碍。总而言之，我们的数据表明 Mg²⁺ 通过调节内皮线粒体代谢促进糖尿病小鼠的血管生成和骨整合。