MRONJ的发病机制研究进展：从巨噬细胞极化到TGF-β信号通路的作用
Research Progress on the Pathogenesis of MRONJ: From Macrophage Polarization to the Role of the TGF-β Signaling Pathway
DOI: 10.12677/acm.2025.15102951, PDF,   
作者: 郭皓晨, 宋怡然：华北理工大学口腔医学院，河北 唐山；陈 晖*：华北理工大学附属医院口腔科，河北 唐山
关键词: 药物性颌骨坏死；巨噬细胞；TGF-β；治疗策略；Drug-Induced Jaw Necrosis； Macrophage； TGF-β； Therapeutic Strategy
摘要: 药物相关性颌骨坏死(Medication-related osteonecrosis of the jaw, MRONJ)是一种服用抗骨吸收药物(如双膦酸盐、地诺单抗)和抗血管生成药物后引发的严重并发症，其特征为颌骨区域持续暴露的坏死骨组织，伴随疼痛、感染和病理性骨折等临床症状。其发病机制涉及多个相互关联的假说，以往研究中以骨重塑抑制与炎症感染学说为主流。近年研究发现，巨噬细胞极化失衡与转化生长因子-β (TGF-β)信号通路异常也是MRONJ的核心调控环节，主导促炎的M1型巨噬细胞与主导抗炎修复的M2型巨噬细胞，它们的平衡深刻影响着炎症进展与结局，而TGF-β/Smad信号通路可以调控其极化的方向。本文综述了巨噬细胞极化与TGF-β/Smad信号通路在MRONJ中的作用与机制，并探索其在新治疗策略中的潜在应用。
Abstract: Medication-related osteonecrosis of the jaw (MRONJ) is a serious complication caused by taking anti-bone resorption drugs (such as bisphosphonates and dinozumab) and anti-angiogenesis drugs, which is characterized by continuous exposure of necrotic bone tissue in the jaw area, accompanied by clinical symptoms such as pain, infection and pathological fracture. Its pathogenesis involves many interrelated hypotheses, and the theory of bone remodeling inhibition and inflammatory infection has been the mainstream in previous studies. In recent years, it has been found that the imbalance of macrophage polarization and the abnormality of transforming growth factor-β (TGF-β) signaling pathway are also the core regulatory links of MRONJ. The balance between M1-type macrophages leading to pro-inflammation and M2-type macrophages leading to anti-inflammatory repair profoundly affects the progress and outcome of inflammation, and TGF-β/Smad signaling pathway can regulate the direction of its polarization. This paper reviews the role and mechanism of macrophage polarization and TGF-β/Smad signaling pathway in MRONJ, and explores its potential application in new therapeutic strategies.
文章引用：郭皓晨, 宋怡然, 陈晖. MRONJ的发病机制研究进展：从巨噬细胞极化到TGF-β信号通路的作用[J]. 临床医学进展, 2025, 15(10): 1824-1831. https://doi.org/10.12677/acm.2025.15102951

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