粪肠球菌牙本质黏附及其影响因素的研究进展

谢媛; 程兴群; 李雨庆; 徐欣

doi:10.12016/j.issn.2096-1456.2024.08.009

口腔疾病防治 ›› 2024, Vol. 32 ›› Issue (8) : 632 -639. DOI: 10.12016/j.issn.2096-1456.2024.08.009

综述

粪肠球菌牙本质黏附及其影响因素的研究进展

谢媛, 程兴群, 李雨庆, 徐欣

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Research progress on the dentin adhesion of Enterococcus faecalis and its influencing factors

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摘要

粪肠球菌是难治性根尖周炎（refractory apical periodontitis，RAP）的主要致病菌，该细菌可耐受严苛环境，引发根尖周免疫炎症反应，造成根管内外持续性感染。粪肠球菌黏附于根管牙本质壁形成生物膜，其耐药和抗冲刷能力显著增强，是介导其致病的关键因素。粪肠球菌与牙本质的黏附包括非特异性和特异性黏附，后者由黏附相关毒力因子介导，主要包括肠球菌胶原结合蛋白（adhesin of collagen from enterococci，Ace）、表面蛋白（extracellular surface protein，Esp）、明胶酶（gelatinase，GelE）和丝氨酸蛋白酶（serine prtease，SprE）、菌毛以及聚集物质，且受到多个双组份系统调控。Fsr双组份系统在群体密度增加时可以促进gelE及sprE的表达，GelE进一步减少表面肠球菌胶原结合蛋白Ace，而GrvRS双组份系统则在响应血清环境时直接下调ace的表达。CroRS双组份系统及WalRK双组份系统也可能分别促进和抑制包括ace及gelE在内的多种毒力因子的表达，进而影响粪肠球菌的黏附性。此外，根管机械/化学预备、根管内环境因素等均可对粪肠球菌牙本质黏附产生影响。根管治疗中避免粪肠球菌的引入和使用干扰黏附的药物可以有效预防粪肠球菌的黏附，而多种活化荡洗方法也可以有效增加根管内粪肠球菌的清除率。针对粪肠球菌牙本质黏附关键因子与调控因素为靶点设计合理药物，有望为根管感染控制提供新的思路与手段。本文就粪肠球菌与牙本质的黏附性及其影响因素进行综述。

Abstract

Enterococcus faecalis is the main pathogen causing refractory apical periodontitis (RAP). This bacterium can tolerate harsh environments and trigger periapical immune inflammatory responses that result in persistent infection inside and outside the root canal. Adhesion to the dentin wall of root canals and the subsequent formation of biofilms significantly enhances the drug resistance and anti-erosion ability of Enterococcus faecalis, which is the key factor mediating its pathogenesis. The adhesion of Enterococcus faecalis to dentin involves non-specific adhesion and specific adhesion, and the latter is mediated by adhesion-related virulence factors, mainly including the adhesin of collagen from enterococci (Ace), extracellular surface protein (Esp), gelatinase (GelE), serine protease (SprE), endocarditis and biofilm associated pilus (Ebp) and aggregation substance (AS), which is regulated by multiple two-component systems. The two-component system Fsr can promote the expression of gelE and sprE when the cell population density increases. GelE can further reduce Ace, while the two-component system GrvRS directly downregulates ace expression in response to the serum environment. The two-component systems CroRS and WalRK may also promote and inhibit the expression of various virulence factors, including ace and gelE, thus affecting the adhesion of Enterococcus faecalis. In addition, the mechanochemical preparation and the internal environment of the root canal can also influence the adhesion of Enterococcus faecalis to dentin. Avoiding the introduction of Enterococcus faecalis and using adhesion-interfering medications during root canal treatment can effectively prevent the adhesion of Enterococcus faecalis, and a variety of activated irrigation protocols can also be effective at increasing the clearance of Enterococcus faecalis from the root canal. The design of rational drugs targeting key factors involved in and regulators of the adhesion of Enterococcus faecalis to dentin is expected to provide new ideas and strategies for root canal infection control. The present paper reviews the adhesion of Enterococcus faecalis to dentin and its influencing factors.