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1
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. [email protected].
2
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
3
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. [email protected].
1
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. [email protected].
2
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China.
3
Department of Periodontics, the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310009, China. [email protected].
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.
牙周病是以牙槽骨渐进性破坏为特征的慢性炎症性疾病。牙槽骨破坏最关键的机制是骨稳态失衡，而成骨细胞介导的骨基质合成在骨稳态调节中发挥重要作用。调节性细胞死亡在炎性微环境和骨稳态调控中发挥重要作用。慢性炎症、氧化应激等因素可直接参与线粒体、死亡受体介导的信号通路，调节B淋巴细胞瘤蛋白2（Bcl-2）家族蛋白和胱天蛋白酶（caspase）活性，影响成骨细胞凋亡，从而影响牙槽骨稳态；慢性炎症与细胞损伤可经由RIPK1/RIPK3/MLKL信号通路诱发成骨细胞坏死性凋亡，从而加剧炎症反应并加速牙槽骨破坏；病原微生物、细胞损伤等刺激可通过caspase-1依赖或非依赖性信号通路及消皮素D（GSDMD）家族蛋白活化，促进成骨细胞焦亡，并释放促炎性细胞因子，介导牙槽骨破坏；牙周病中铁过载和脂质过氧化可诱发成骨细胞铁死亡，影响成骨细胞的存活和功能，从而导致骨稳态失衡。本综述围绕牙周病通过调节性细胞死亡影响骨稳态的机制，以期探讨调控牙周病患者牙槽骨稳态失衡的对策。.
