B 细胞特异性 Moloney MLV 插入位点 1 (Bmi-1) 是一种重要的骨质减少靶分子。本研究的目的是探讨 Bmi-1 对牙槽骨吸收的影响及其体内和体外的潜在机制。使用 Bmi-1 敲除 (Bmi-1-/-) 小鼠模型来研究 Bmi-1 对牙槽骨吸收的影响。通过微型计算机断层扫描成像、组织学和免疫组织化学染色观察 Bmi-1 对牙槽骨代谢的影响。此外，我们利用结扎诱导的实验性牙周炎模型来检查 Bmi-1 敲低 (Bmi-1±) 对炎症性牙槽骨吸收的影响。最后，我们用脂多糖（LPS）刺激人牙周膜干细胞（hPDLSC），探讨Bmi-1在成骨过程中过表达的潜在机制。与野生型小鼠相比，Bmi-1-/-小鼠表现出更多的牙槽骨通过抑制成骨来促进骨吸收，其特征是 Runt 相关转录因子 2 和 1 型胶原形成减少。此外，Bmi-1-/-小鼠牙周组织中Parkin和LC3等自噬标记物水平较低，但白介素（IL）-6和IL-1β等炎症相关因子水平较高。此外，Bmi-1 敲低加剧了结扎引起的牙槽骨丢失。在体外炎症条件下，Bmi-1过表达刺激成骨细胞分化并抑制炎症因子的产生，以及LPS刺激的hPDLSCs的自噬和凋亡。当添加自噬抑制剂3-甲基腺嘌呤（3-MA）时，Bmi-1的成骨作用进一步增强。Bmi-1通过调节自噬减轻牙槽骨吸收，表明它可能是预防牙周炎的潜在靶点牙周炎是一种慢性炎症性疾病，会导致牙周组织进行性破坏，表现为牙周袋形成、牙周附着丧失和牙槽骨吸收。目前，缺乏有效的治疗方法来再生受损的牙周组织。因此，探索牙周炎的新机制和有效的干预靶点具有重要的临床意义。 B 细胞特异性 Moloney MLV 插入位点 1 (Bmi-1) 参与细胞周期的调节、DNA 损伤修复、自噬、骨代谢、肿瘤和其他病理生理过程。自噬作为细胞内自我调节的重要机制，在牙周组织的破坏和修复中发挥着不可或缺的作用。本研究旨在探讨Bmi-1对牙周组织的作用及其内在机制。结果显示，Bmi-1 通过调节自噬来保护牙周组织，表明它可能是预防和治疗牙周炎的潜在靶点。© 2024 美国牙周病学会。

B-cell‑specific Moloney MLV insertion site-1(Bmi-1)is a crucial osteopenic target molecule. The aim of this study is to explore the effects of Bmi-1 on alveolar bone resorption and the underlying mechanisms in vitro and vivo.A Bmi-1-knockout (Bmi-1-/-) mouse model was used to investigate the effect of Bmi-1 on alveolar bone metabolism, with micro-computed tomography imaging, histology, and immunohistochemistry staining. Furthermore, we utilized a ligature-induced experimental periodontitis model to examine the impact of Bmi-1-knockdown (Bmi-1±) on inflammatory alveolar bone resorption. Finally, we stimulated human periodontal ligament stem cells (hPDLSCs) with lipopolysaccharide (LPS) to explore the potential mechanism of Bmi-1 overexpression in the process of osteogenesis.Compared with wild-type mice, Bmi-1-/- mice demonstrated more alveolar bone resorption by inhibiting osteogenesis, which was characterized by decreases in Runt-related transcription factor 2 and type 1 collagen formation. In addition, Bmi-1-/- mice had lower levels of autophagy markers such as Parkin and LC3, but higher levels of inflammation-related factors such as interleukin (IL)-6 and IL-1β in periodontal tissues. In addition, Bmi-1-knockdown aggravated ligature-induced alveolar bone loss. Under in vitro inflammatory conditions, Bmi-1 overexpression stimulated osteoblast differentiation and inhibited the production of inflammatory factors, as well as the autophagy and apoptosis in hPDLSCs stimulated with LPS. When 3-methyladenine (3-MA), an autophagy inhibitor, was added, the osteogenic effect of Bmi-1 was further enhanced.Bmi-1 alleviates alveolar bone resorption by regulating autophagy, indicating that it could be a potential target for periodontitis prevention and treatment.Periodontitis is a chronic inflammatory disease, which leads to progressive destruction of periodontal tissues, manifested as periodontal pocket formation, loss of periodontal attachment and alveolar bone resorption. Currently, there is a lack of effective treatments to regenerate damaged periodontal tissues. Therefore, it is of great clinical significance to explore new mechanisms of periodontitis and effective intervention targets. B-cell‑specific Moloney MLV insertion site-1 (Bmi-1) is involved in the regulation of the cell cycle, DNA damage repair, autophagy, bone metabolism, tumor, and other physiopathological processes. Autophagy, as an important mechanism of intracellular self-regulation, plays an indispensable role in the destruction and repair of periodontal tissues. The aim of this study was to investigate the role of Bmi-1 on periodontal tissues and its intrinsic mechanism. The results revealed that Bmi-1 regulates autophagy to protect periodontal tissues, suggesting that it may be a potential target for the prevention and treatment of periodontitis.© 2024 American Academy of Periodontology.