Junctional epithelium (JE) attaching to the enamel surface seals gaps around the teeth, functioning as the first line of gingival defense. Runt-related transcription factor 2 (Runx2) plays a role in epithelial cell fate, and the deficiency of Runx2 in JE causes periodontal destruction, while its effect on the barrier function of JE remains largely unexplored. In the present study, hematoxylin–eosin (H&E) staining revealed the morphological differences of JE between wild-type (WT) and Runx2 conditional knockout (cKO) mice. We speculated that these changes were related to the down-regulation of E-cadherin (E-cad), junctional adhesion molecule 1 (JAM1), and integrin β6 (ITGB6) in JE. Moreover, immunohistochemistry (IHC) was conducted to assess the expressions of these proteins. To verify the relationship between Runx2 and the three above-mentioned proteins, human gingival epithelial cells (HGEs) were cultured for in vitro experiment. The expression of Runx2 in HEGs was depleted by lentivirus. Quantitative real-time PCR (qRT-PCR) and Western blotting analysis were adopted to analyze the differences in mRNA and protein expressions. Taken together, Runx2 played a crucial role in maintaining the structure and function integrality of JE via regulating the expressions of E-cad and JAM1.

附着在牙釉质表面的接合上皮 (JE) 密封牙齿周围的间隙，作为牙龈防御的第一道防线。Runt 相关转录因子 2 ( Runx2 ) 在上皮细胞命运中发挥作用，JE中Runx2的缺乏会导致牙周破坏，而其对 JE 屏障功能的影响在很大程度上仍有待探索。在本研究中，苏木精-伊红 (H&E) 染色揭示了野生型 (WT) 和Runx2之间 JE 的形态差异条件敲除 (cKO) 小鼠。我们推测这些变化与乙脑中 E-钙粘蛋白 (E-cad)、连接粘附分子 1 (JAM1) 和整合素 β6 (ITGB6) 的下调有关。此外，进行免疫组织化学 (IHC) 以评估这些蛋白质的表达。为了验证Runx2与上述三种蛋白之间的关系，培养人牙龈上皮细胞（HGEs）进行体外实验。Runx2在 HEG 中的表达被慢病毒耗尽。采用定量实时PCR（qRT-PCR）和蛋白质印迹分析来分析mRNA和蛋白质表达的差异。合起来，Runx2 通过调节 E-cad 和 JAM1 的表达，在维持 JE 的结构和功能完整性方面发挥了关键作用。