Tooth germ injury can lead to abnormal tooth development and even tooth loss, affecting various aspects of the stomatognathic system including form, function, and appearance. However, the research about tooth germ injury model on cellular and molecule mechanism of tooth germ repair is still very limited. Therefore, it is of great importance for the prevention and treatment of tooth germ injury to study the important mechanism of tooth germ repair by a tooth germ injury model. Here, we constructed a Tg(dlx2b:Dendra2-NTR) transgenic line that labeled tooth germ specifically. Taking advantage of the NTR/Mtz system, the dlx2b⁺ tooth germ cells were depleted by Mtz effectively. The process of tooth germ repair was evaluated by antibody staining, in situ hybridization, EdU staining and alizarin red staining. The severely injured tooth germ was repaired in several days after Mtz treatment was stopped. In the early stage of tooth germ repair, the expression of phosphorylated 4E-BP1 was increased, indicating that mTORC1 is activated. Inhibition of mTORC1 signaling in vitro or knockdown of mTORC1 signaling in vivo could inhibit the repair of injured tooth germ. Normally, mouse incisors were repaired after damage, but inhibition/promotion of mTORC1 signaling inhibited/promoted this repair progress. Overall, we are the first to construct a stable and repeatable repair model of severe tooth germ injury, and our results reveal that mTORC1 signaling plays a crucial role during tooth germ repair, providing a potential target for clinical treatment of tooth germ injury.

牙胚损伤可导致牙齿发育异常甚至牙齿脱落，影响口颌系统的各个方面，包括形态、功能和外观。然而，牙胚损伤模型对牙胚修复的细胞分子机制的研究还很有限。因此，通过牙胚损伤模型研究牙胚修复的重要机制，对于牙胚损伤的防治具有重要意义。在这里，我们构建了一个专门标记牙胚的Tg(dlx2b:Dendra2-NTR)转基因品系。利用 NTR/Mtz 系统，dlx2b ⁺Mtz 有效地耗尽了牙齿生殖细胞。通过抗体染色、原位杂交、EdU染色和茜素红染色评价牙胚修复过程。严重受伤的牙胚在停止 Mtz 治疗后的几天内得到修复。在牙胚修复早期，磷酸化的4E-BP1表达增加，表明mTORC1被激活。在体外抑制 mTORC1 信号或在体内敲低 mTORC1 信号可抑制受损牙胚的修复。正常情况下，小鼠门牙在损伤后得到修复，但抑制/促进 mTORC1 信号转导抑制/促进了这一修复进程。总的来说，我们率先构建了一个稳定的、可重复的严重牙胚损伤修复模型，