Jia Yibing, Li Zili, Huang Pengjie, Wang Yan, Yang Bo
Hospital of Stomatology, Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, China.
Front Cell Infect Microbiol. 2025 Aug 11;15:1634909. doi: 10.3389/fcimb.2025.1634909. eCollection 2025.
Periodontitis is a global inflammatory oral disease, and plaque-induced host excessive immune response is recognized as a major cause of its pathogenesis. In recent years, the relevance of mitochondrial dysfunction to periodontitis has been increasingly investigated, particularly with respect to macrophages, the key immune cells in the periodontal immune microenvironment. Mitochondrial dysfunction drives macrophage M1 polarization and osteoclast differentiation through mechanisms such as metabolic reprogramming, reactive oxygen species release, abnormal mitophagy, abnormal mitochondrial biogenesis and damaged mitochondrial dynamic. In addition, mitochondrial transfer in the periodontitis setting has been reported in several researches. In this review, we highlight the impact of mitochondrial dysfunction on macrophages in the periodontitis setting and summarize emerging therapeutic strategies for targeting mitochondria in periodontitis, including antioxidants, modulators of metabolic reprogramming, nanomaterials and photodynamic therapy.
牙周炎是一种全球性的炎症性口腔疾病，菌斑诱导的宿主过度免疫反应被认为是其发病机制的主要原因。近年来，线粒体功能障碍与牙周炎的相关性受到越来越多的研究，特别是关于巨噬细胞，这是牙周免疫微环境中的关键免疫细胞。线粒体功能障碍通过代谢重编程、活性氧释放、异常线粒体自噬、异常线粒体生物合成和受损的线粒体动力学等机制驱动巨噬细胞M1极化和破骨细胞分化。此外，多项研究报道了牙周炎情况下的线粒体转移。在这篇综述中，我们强调了线粒体功能障碍对牙周炎情况下巨噬细胞的影响，并总结了针对牙周炎中线粒体的新兴治疗策略，包括抗氧化剂、代谢重编程调节剂、纳米材料和光动力疗法。
