Runx2条件性敲除小鼠釉质缺陷的部分挽救

该研究旨在探讨外源性Runx2过表达对小鼠成釉细胞Runx2敲除导致的釉质缺陷的挽救作用。采用免疫组化验证Runx2在Runx2条件性敲除且人源性Runx2过表达小鼠成釉细胞中的表达。HE染色观察成熟期成釉细胞形态及釉质基质蛋白残余。用体视显微镜和扫描电镜观察小鼠牙齿表面形态和釉柱结构。结果显示,RUNX2蛋白在出生后10天龄Tg;cKO小鼠成熟早期成釉细胞中成功表达。15天龄Tg;cKO小鼠与cKO小鼠相比,成熟晚期成釉细胞形态及排列未见明显改善,但釉质基质蛋白残余量明显减少。3月龄Tg;cKO小鼠与cKO小鼠相比,釉质磨耗减轻,釉柱间孔隙减少,釉柱排列更规则。该研究结果表明,人源性Runx2过表达可部分挽救小鼠成釉细胞Runx2敲除导致的釉质缺陷。

Partial Rescue of Enamel Defects in Runx2 Conditional Knockout Mice

This study aimed to explore the rescue effect of exogenous Runx2 overexpression on enamel defects caused by Runx2 knockout in mouse ameloblasts.Immunohistochemistry was used to detect the expression of Runx2 in ameloblasts of Tg;cKO mice.HE staining was used to observe the morphology of mature ameloblasts and the residual enamel matrix protein.A stereoscopic?microscope and scanning electron microscope were used to observe the tooth surface morphology and enamel rod structure.The results showed that RUNX2 protein was successfully expressed in early maturation stage ameloblasts in Tg;cKO mice on postnatal day 10.Compared with cKO mice,Tg;cKO mice showed no significant improvement in the morphology and arrangement of late maturation stage ameloblasts on postnatal day 15,but the residual amount of enamel matrix protein was significantly reduced.Compared with cKO mice,the 3-month-old Tg;cKO mice had less enamel abrasion,reduced pores between enamel rods,and more regular enamel rods.This study demonstrated that human-derived Runx2 overexpression could partially rescue the enamel defect caused by Runx2 knockout in mouse ameloblasts.