Pan Dan, Hao Yu, Tao Yuyan, Li Bolei, Cheng Lei
West China School of Stomatology (WCSS), Sichuan University, No. 14, Section 3, Renmin Nanlu, Chengdu 610041, China; West China Hospital of Stomatology, Sichuan University, Chengdu, China.
West China School of Stomatology (WCSS), Sichuan University, No. 14, Section 3, Renmin Nanlu, Chengdu 610041, China; State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu, China; Department of Stomatology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China.
Arch Oral Biol. 2025 Feb;170:106153. doi: 10.1016/j.archoralbio.2024.106153. Epub 2024 Nov 30.
This review aims to provide an overview of the role of microorganisms in the onset and progression of periapical diseases, particularly regarding their effects on bone homeostasis.
The search for this narrative review was conducted in PubMed, Web of Science and Google Scholar using relevant keywords, including checking reference lists of journal articles by hand searching.
Microorganisms directly promote osteoclasts through pathways such as nuclear factor-κB (NF-κB) and extracellular regulated protein kinases (ERK), while inhibiting osteoblasts function by interfering with the wingless-related integration site (Wnt)/β-catenin pathway in the periapical area. Moreover, microorganisms indirectly regulate periapical bone homeostasis by inducing programmed cell death and modulating the immune microenvironment through the activation of innate immunity via pattern-recognition receptors (PRRs) and subsequent cascades of responses. Among these microorganisms, Enterococcus faecalis, Porphyromonas gingivalis and Fusobacterium nucleatum play significant roles.
Microorganisms regulate pathways such as NF-ĸB and Wnt/β-catenin, as well as programmed cell death and the immune microenvironment in the periapical area, thereby disrupting bone homeostasis.
本综述旨在概述微生物在根尖周病的发生和发展中的作用，特别是它们对骨稳态的影响。
通过在PubMed、科学网和谷歌学术中使用相关关键词进行检索以撰写本叙述性综述，包括通过手工检索期刊文章的参考文献列表。
微生物通过核因子-κB（NF-κB）和细胞外调节蛋白激酶（ERK）等途径直接促进破骨细胞生成，同时通过干扰根尖周区域的无翅相关整合位点（Wnt）/β-连环蛋白途径抑制成骨细胞功能。此外，微生物通过诱导程序性细胞死亡以及通过模式识别受体（PRR）激活固有免疫并随后引发一系列反应来调节免疫微环境，从而间接调节根尖周骨稳态。在这些微生物中，粪肠球菌、牙龈卟啉单胞菌和具核梭杆菌发挥着重要作用。
微生物调节NF-κB和Wnt/β-连环蛋白等途径，以及根尖周区域的程序性细胞死亡和免疫微环境，从而破坏骨稳态。
