The Israeli National Center for Trauma & Emergency Medicine Research, Gertner Institute, Tel Hashomer, Israel.
Department of Endodontics, Rambam Health Care Campus, Haifa, Israel.
Int Endod J. 2024 Dec;57(12):1727-1744. doi: 10.1111/iej.14132. Epub 2024 Sep 18.
Root resorption consists of complex, multistep processes that involve cell signalling caused by inflammation and stromal cells, which promotes the secretion of receptor activator of nuclear factor κB ligand/ macrophage-colony stimulating factor (RANKL/M-CSF) resulting in a resorptive process.
The aim of this narrative review was to analyse the literature related to root resorption resulting from microbial infection and to comparing it with non-microbial infection.
An electronic literature search was performed using the PubMed database and applying keywords of articles published in English. Eligible papers were reviewed to reveal the descriptions of bone and root resorption processes. The abstracts were searched manually to identify articles about infection-stimulating bone and root resorption.
Three main types of root resorption were identified, two associated with primary bacterial infection and one secondary to bacterial infection. These include external inflammatory resorption, internal inflammatory resorption and external cervical (invasive) resorption.
The magnitude of cytokine involvement that promotes resorption and M-CSF/RANKL production depends on multiple factors, including pathogen virulence, site of infection and host genetic factors that activate the inflammation at the infection site. Two mechanisms activate the resorption mechanisms-the canonical and non-canonical pathways that can activate clastic cells independently of the RANKL/RANK canonical pathways.
Two pathways of root resorption co-exist in the body. When resorption is caused by infection, chronic inflammation due to bacterial infection prolongs the secretions of pro-inflammatory cytokines that intensify root and bone resorption. The second pathway is bacterial independent of the non-infection root resorption that is part of the wound healing process, which is limited in time due to its innate ability.
根吸收由涉及由炎症和基质细胞引起的细胞信号的复杂、多步骤过程组成,这促进了核因子 κB 配体/巨噬细胞集落刺激因子(RANKL/M-CSF)受体激活剂的分泌,从而导致吸收过程。
本叙述性综述的目的是分析与微生物感染引起的根吸收相关的文献,并将其与非微生物感染进行比较。
使用 PubMed 数据库进行电子文献检索,并应用发表在英文文章中的关键词。对合格的论文进行了综述,以揭示骨和根吸收过程的描述。手动搜索摘要以确定关于感染刺激骨和根吸收的文章。
确定了三种主要类型的根吸收,两种与原发性细菌感染有关,一种与细菌感染后有关。这些包括外部炎症性吸收、内部炎症性吸收和外部颈(侵袭性)吸收。
促进吸收和 M-CSF/RANKL 产生的细胞因子参与程度取决于多种因素,包括病原体毒力、感染部位和宿主遗传因素,这些因素可激活感染部位的炎症。两种机制激活吸收机制——经典和非经典途径,可独立于 RANKL/RANK 经典途径激活破骨细胞。
两种根吸收途径共存于体内。当吸收由感染引起时,由于细菌感染引起的慢性炎症会延长促炎细胞因子的分泌,从而加剧根和骨吸收。第二种途径是独立于感染的非感染性根吸收,它是伤口愈合过程的一部分,由于其内在能力,时间有限。