Involvement of apoptosis of cementoblast in orthodontic root resorption

压力对牙周膜的影响在正畸牙齿移动中起着至关重要的作用。然而，对PDL细胞中这种对细胞凋亡的影响和潜在的反应机制知之甚少。本研究旨在探讨压力对活性氧合酶(ROS)诱导的PDL细胞凋亡的影响，并用流式细胞仪检测压力对PDL细胞周期和细胞凋亡率的影响。体内研究显示，正畸力组末端转移酶介导的dUTP缺口末端标记(TUNEL)和caspase8阳性细胞数量增加。在我们的体外研究模型中，压力增加了G1期细胞和凋亡细胞。加力组人(H)PDL细胞内ROS水平显著升高。这些结果为压迫力诱导hPDL细胞G1期阻滞细胞凋亡提供了新的信息。

The effect of compression force on periodontal ligament (PDL) plays a critical role in orthodontic tooth movement. However, little is known about this effect on apoptosis and the underlying reactive mechanisms in PDL cells. This study focuses on the application of compression force associated with reactive oxygenspecies (ROS)-induced apoptosis in PDL cells.The cell cycle and apoptosis wereassessed in compression force-treated PDL cells using flow cytometry. In vivo study revealed an increased number of terminal transferase-mediated dUTP nick end labeling (TUNEL) and caspase 8-positive cells in the orthodontic force group. In our in vitro study model, the compression force increased the G1 phase and apoptotic cells. A large increase in the intracellular ROS levels in human (h) PDL cells was observed in the compression force group. These results provide new information on compression force-induced G1 arrestand apoptosis in hPDL cells.