Do Thao Thi, Nguyen Vy Thuy, Nguyen Ngoc Tran Nhu, Duong Kim Tran Thien, Nguyen Tri Ta Minh, Le Duong Nguyen Thuy, Nguyen Tin Hoang
Oral Diagnosis and Periodontology Department, Faculty of Odonto-Stomatology, Can Tho University of Medicine and Pharmacy, Can Tho City, 900000, Vietnam.
Department of Physiology, Faculty of Medicine, Can Tho University of Medicine and Pharmacy, Can Tho City, 900000, Vietnam.
Clin Cosmet Investig Dent. 2024 Dec 30;16:513-531. doi: 10.2147/CCIDE.S492107. eCollection 2024.
The tight junction (TJ), a type of cell-cell junction, regulates the permeability of solutes across epithelial and endothelial cellular sheets and is believed to maintain cell polarity. However, recent studies have provided conflicting views on the roles of TJs in epithelial polarity. Membrane proteins, including occludin, claudin, and the junction adhesion molecule, have been identified as TJ components. TJs are predominantly found at the stratum granulosum and stratum corneum. Although it remains unclear whether the disruption of TJs is the cause or consequence of certain dental diseases, evidence suggests that TJ dysfunction may be a crucial factor in gingival epithelial barrier impairment and the progression of oral diseases. Bacterial infection is among the most specific factors we found that may contribute to the breakdown of the epithelial barrier formed by TJs in dental diseases. Bacteria and their products may weaken the epithelial barrier by directly destroying intercellular junctions or altering the expression of junctional proteins. Additionally, they may induce the production of inflammatory cytokines, which could lead to the downregulation of TJ proteins and, consequently, impair the epithelial barrier. This review introduces a novel perspective by exploring, for the first time, the role of TJs dysfunction in the breakdown of the oral epithelial barrier and its potential link to the progression of dental diseases such as gingivitis, periodontitis, Sjӧgren syndrome, and oral squamous cell carcinoma.
紧密连接(TJ)是一种细胞间连接,可调节溶质跨上皮细胞层和内皮细胞层的通透性,并被认为可维持细胞极性。然而,最近的研究对紧密连接在上皮极性中的作用提出了相互矛盾的观点。包括闭合蛋白、claudin和连接粘附分子在内的膜蛋白已被确定为紧密连接的组成成分。紧密连接主要存在于颗粒层和角质层。尽管目前尚不清楚紧密连接的破坏是某些牙科疾病的原因还是结果,但有证据表明,紧密连接功能障碍可能是牙龈上皮屏障受损和口腔疾病进展的关键因素。细菌感染是我们发现的最具特异性的因素之一,可能导致牙科疾病中由紧密连接形成的上皮屏障的破坏。细菌及其产物可能通过直接破坏细胞间连接或改变连接蛋白的表达来削弱上皮屏障。此外,它们可能诱导炎性细胞因子的产生,这可能导致紧密连接蛋白的下调,从而损害上皮屏障。本综述首次探讨了紧密连接功能障碍在口腔上皮屏障破坏中的作用及其与牙龈炎、牙周炎、干燥综合征和口腔鳞状细胞癌等牙科疾病进展的潜在联系,从而引入了一个新的视角。