Institute of Biomedicine, School of Medicine, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
Department of Clinical Pathology and Forensic Medicine, School of Medicine, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
J Oral Pathol Med. 2019 Sep;48(8):735-744. doi: 10.1111/jop.12917. Epub 2019 Jul 4.
Oral lichen planus (OLP) is a chronic T-cell-mediated inflammatory disease, which is associated with increased risk of developing oral squamous cell carcinoma. Epithelial-to-mesenchymal transition is a physiological phenomenon occurring during growth and organogenesis, but it has also an important role in tumorigenesis. In the present work, we studied the expression of known epithelial-to-mesenchymal transition markers in oral lichen planus.
In total, 54 oral lichen planus and 22 control samples were analyzed for epithelial-to-mesenchymal transition markers. Samples were immunohistochemically stained for claudin-1, claudin-4 and claudin-7, cadherin-1 (E-cadherin), Twist-related protein 1 (TWIST1) and zinc finger E-box-binding homeobox 1 (ZEB1).
The expression of claudin-1, claudin-4 and E-cadherin was significantly weaker in oral lichen planus epithelium compared to controls (P < 0.001). The quantity of claudin-7-expressing cells (P < 0.001) and claudin-7 staining intensity (P < 0.05) in the stroma was greater in lichen planus than in control samples. TWIST1 and ZEB1 stainings were negative in the epithelium in both lichen planus and controls. The number of TWIST1-expressing cells in the stroma was higher in lichen planus than in controls (P < 0.001). There was a statistically significant difference in ZEB1 staining intensity in the stroma between lichen planus and control samples (P < 0.05).
The data indicate that the expression of claudin-1, claudin-4 and E-cadherin is decreased in oral lichen planus. This may lead to disturbance in epithelial tight junctions, cell-cell connections and epithelial permeability, contributing to oral lichen planus pathogenesis. Based on the present study, the role of TWIST1 and ZEB1 in oral lichen planus remains unclear.
口腔扁平苔藓（OLP）是一种慢性 T 细胞介导的炎症性疾病，其发生口腔鳞状细胞癌的风险增加。上皮-间充质转化是一种发生在生长和器官发生过程中的生理现象，但它在肿瘤发生中也起着重要作用。在本工作中，我们研究了口腔扁平苔藓中已知的上皮-间充质转化标志物的表达。
共分析了 54 例口腔扁平苔藓和 22 例对照样本的上皮-间充质转化标志物。采用免疫组织化学法检测 claudin-1、claudin-4 和 claudin-7、钙黏蛋白 1（E-钙黏蛋白）、Twist 相关蛋白 1（TWIST1）和锌指 E 盒结合同源框 1（ZEB1）的表达。
与对照组相比，口腔扁平苔藓上皮中 claudin-1、claudin-4 和 E-钙黏蛋白的表达明显减弱（P<0.001）。在基质中，claudin-7 表达细胞的数量（P<0.001）和 claudin-7 染色强度（P<0.05）在扁平苔藓中大于对照组。上皮中 TWIST1 和 ZEB1 染色均为阴性。在基质中，TWIST1 表达细胞的数量在扁平苔藓中高于对照组（P<0.001）。扁平苔藓和对照组之间基质中 ZEB1 染色强度有统计学差异（P<0.05）。
数据表明，口腔扁平苔藓中 claudin-1、claudin-4 和 E-钙黏蛋白的表达减少。这可能导致上皮紧密连接、细胞-细胞连接和上皮通透性紊乱，有助于口腔扁平苔藓的发病机制。基于本研究，TWIST1 和 ZEB1 在口腔扁平苔藓中的作用尚不清楚。
