线粒体功能障碍在牙周炎发生、发展及治疗中作用的研究进展

Research progress on the role of mitochondrial dysfunction in the occurrence,progression and treatment of periodontitis

牙周炎是全球范围内的高发性疾病,牙周组织破坏的主要原因是细菌介导的免疫炎症反应。近年来,越来越多的研究表明线粒体功能障碍与牙周炎发生、发展之间存在相关性。本文从氧化应激、炎症反应和线粒体稳态调控三个角度对线粒体功能障碍在牙周炎发生、发展中的作用及相关治疗的研究进展进行综述。线粒体是细胞活性氧的主要来源和攻击靶点;线粒体功能障碍会产生大量活性氧,加剧牙周局部的氧化应激,造成细胞毒性和组织损伤;线粒体也是细胞炎症反应的中心,线粒体功能障碍引发的炎症正反馈效应可能解释了牙周炎迁延不愈的特点;仿生材料负载药物的方式在恢复线粒体功能、控制牙周炎发展以及促进牙周组织再生上具有潜在价值。然而,线粒体功能障碍在牙周炎发生、发展中的关键作用位点仍不十分清楚,改善线粒体功能在牙周治疗中尚处于实验阶段。未来可重点关注线粒体功能障碍对牙周组织细胞的影响,探究其在牙周炎发生、发展中的具体作用机制,以期为牙周炎的治疗提供新思路。

Periodontitis is a widespread disease worldwide,with the primary cause of tissue loss being an immune inflammatory response mediated by bacteria.Increasing evidence has revealed a significant correlation between mitochondrial dysfunction and the occurrence and progression of periodontitis.This paper provides a review of current research on the role of mitochondrial dysfunction in the occurrence and development of periodontitis and related therapies from the perspectives of oxidative stress,inflammatory responses,and the regulation of mitochondrial homeostasis.Mitochondria are the main source and target of cellular reactive oxygen species.Mitochondrial dysfunction can generate large amounts of reactive oxygen species,exacerbating local oxidative stress in periodontal tissues and causing cell toxicity and tissue damage.Mitochondria are also the center of cellular inflammatory responses,and the positive feedback loop of inflammation induced by mitochondrial dysfunction may explain the persistent and unresolved nature of periodontitis.Biomaterials loaded with pharmacological agents show potential in restoring mitochondrial function,controlling the development of periodontitis,and promoting periodontal tissue regeneration.However,the key sites of mitochondrial dysfunction in the occurrence and development of periodontitis are not yet fully understood,and the improvement of mitochondrial function in periodontal therapy is still in the experimental stage.Future research efforts should focus on the effect of mitochondrial dysfunction on periodontal cells and explore its specific mechanism in the occurrence and progression of periodontitis in order to provide new insights into the treatment of periodontitis.