Kaabi Hassan Hamed, Alsoghier Abdullah Mohamed, Alredah Islam Abdulrahim, Alqahtani Rayan Mohammed, Alsanie Ibrahim Suliman, Balto Hanan Abdulgafour
Department of Oral Medicine and Diagnostic Sciences, College of Dentistry, King Saud University, Riyadh, Saudi Arabia.
Central Research Laboratory, Medical Research Unit on Experimental Animals, King Saud University.
Acta Odontol Scand. 2025 May 13;84:226-231. doi: 10.2340/aos.v84.43564.
Little was found on the association between diabetes and its effect on epithelial intercellular adhesion. However, no study reported the association between hyperglycemia and E-cadherin-mediated cell adhesion in tongue epithelium. This study aimed to explore the potential impacts of hyperglycemia on the epithelial E-cadherin expression in the tongue's epithelial tissue in streptozotocin (STZ)-induced diabetic rats.
Twelve male Wistar albino rats were randomly allocated into control and STZ-induced diabetic groups. At the 5-week post-STZ injection, rats were euthanized, and the tongues were harvested and preserved in formalin. Epithelial thickness was assessed using hematoxylin and eosin (H&E) staining, while immunohistochemistry (IHC) was employed to analyze the expression of E-cadherin. Statistical analysis was performed using unpaired t-tests and two-proportion Z-tests, with a significance level determined at p < 0.05.
The results showed a significant reduction in epithelial thickness in the dorsal tongue of STZ-diabetic rats compared to the control group (p = 0.0173). Additionally, E-cadherin expression in the dorsal tongue epithelium was markedly weaker in the diabetic group than in the control (p < 0.0001).
This exploratory study is the first to report that hyperglycemia reduces E-cadherin expression in the dorsal tongue epithelium, possibly contributing to oral epithelial alterations observed in diabetes. These findings not only highlight the potential diagnostic value of E-cadherin as a biomarker for oral complications in diabetic patients but also provide a foundation for future translational and clinical studies exploring therapeutic interventions targeting epithelial integrity in diabetes.
关于糖尿病及其对上皮细胞间黏附的影响，相关研究较少。然而，尚无研究报道高血糖与舌上皮中E-钙黏蛋白介导的细胞黏附之间的关联。本研究旨在探讨高血糖对链脲佐菌素（STZ）诱导的糖尿病大鼠舌上皮组织中上皮E-钙黏蛋白表达的潜在影响。
将12只雄性Wistar白化大鼠随机分为对照组和STZ诱导的糖尿病组。在注射STZ后5周，对大鼠实施安乐死，采集舌头并保存在福尔马林中。使用苏木精和伊红（H&E）染色评估上皮厚度，同时采用免疫组织化学（IHC）分析E-钙黏蛋白的表达。采用非配对t检验和双比例Z检验进行统计分析，显著性水平设定为p < 0.05。
结果显示，与对照组相比，STZ糖尿病大鼠舌背上皮厚度显著降低（p = 0.0173）。此外，糖尿病组舌背上皮中E-钙黏蛋白的表达明显弱于对照组（p < 0.0001）。
这项探索性研究首次报道高血糖会降低舌背上皮中E-钙黏蛋白的表达，这可能是糖尿病患者口腔上皮改变的原因之一。这些发现不仅突出了E-钙黏蛋白作为糖尿病患者口腔并发症生物标志物的潜在诊断价值，还为未来探索针对糖尿病上皮完整性的治疗干预措施的转化和临床研究奠定了基础。
