牙周炎是一种慢性炎症性疾病，其特征是牙槽骨进行性破坏。牙槽骨破坏最关键的机制是骨稳态失衡，其中成骨细胞介导的骨基质合成在调节骨稳态中发挥着重要作用。调节性细胞死亡在炎症微环境和骨稳态调节中发挥重要作用。慢性炎症、氧化应激等因素可直接参与线粒体和死亡受体介导的信号通路，调节B细胞淋巴瘤2（Bcl-2）家族蛋白和半胱氨酸天冬氨酸特异性蛋白酶（caspase）活性，从而影响成骨细胞细胞凋亡和牙槽骨稳态。慢性炎症和细胞损伤通过RIPK1/RIPK3/MLKL信号通路诱导成骨细胞坏死性凋亡，加剧炎症反应并加速牙槽骨破坏。病原微生物和细胞损伤等刺激也可能激活caspase-1依赖性或独立信号通路和gasdermin D (GSDMD)家族蛋白，促进成骨细胞焦亡并释放促炎细胞因子以介导牙槽骨损伤。牙周炎中的铁过载和脂质过氧化可引发成骨细胞铁死亡，影响其存活和功能，最终导致骨稳态失衡。本文重点探讨牙周病通过调节性细胞死亡影响骨稳态的机制，旨在为牙周炎和牙槽骨稳态失衡的治疗提供研究证据。

Periodontitis is a chronic inflammatory disease characterized by progressive destruction of alveolar bone. The most critical mechanism underlying alveolar bone destruction is the imbalance of bone homeostasis, where osteoblast-mediated bone matrix synthesis plays an important role in regulating bone homeostasis. Regulatory cell death is instrumental in both the inflammatory microenvironment and the regulation of bone homeostasis. Chronic inflammation, oxidative stress, and other factors can be directly involved in mitochondrial and death receptor-mediated signaling pathways, modulating B-cell lymphoma 2 (Bcl-2) family proteins and cysteine aspartic acid specific protease (caspase) activity, thereby affecting osteoblast apoptosis and alveolar bone homeostasis. Chronic inflammation and cellular damage induce osteoblast necroptosis via the RIPK1/RIPK3/MLKL signaling pathway, exacerbating the inflammatory response and accelerating alveolar bone destruction. Stimuli such as pathogenic microorganisms and cellular injury may also activate caspase-1-dependent or independent signaling pathways and gasdermin D (GSDMD) family proteins, promoting osteoblast pyroptosis and releasing pro-inflammatory cytokines to mediate alveolar bone damage. Iron overload and lipid peroxidation in periodontitis can trigger ferroptosis in osteoblasts, impacting their survival and function, ultimately leading to bone homeostasis imbalance. This article focuses on the mechanism of periodontal disease affecting bone homeostasis through regulatory cell death, aiming to provide research evidence for the treatment of periodontitis and alveolar bone homeostasis imbalance.