Shalish Miriam, Will Leslie A, Fukai Naomi, Hou Bo, Olsen Bjorn R
a Director of Postgraduate Program, Department of Orthodontics, Hebrew University-Hadassah School of Dental Medicine, Jerusalem, Israel.
Angle Orthod. 2014 Sep;84(5):885-90. doi: 10.2319/082313-620.1. Epub 2014 Feb 21.
To test the hypothesis that polycystin-1 (PC1) is involved in orthodontic tooth movement as a mechanical sensor.
The response to force application was compared between three mutant and four wild-type 7-week-old mice. The mutant mice were PC1/Wnt1-cre, lacking PC1 in the craniofacial region. An orthodontic closed coil spring was bonded between the incisor and the left first molar, applying 20 g of force for 4 days. Micro-computed tomography, hematoxylin and eosin staining, and tartrate-resistent acid phosphatase (TRAP) staining were used to study the differences in tooth movement among the groups.
In the wild-type mice the bonded molar moved mesially, and the periodontal ligament (PDL) was compressed in the compression side. The compression side showed a hyalinized zone, and osteoclasts were identified there using TRAP staining. In the mutant mice, the molar did not move, the incisor tipped palatally, and there was slight widening of the PDL in the tension area. Osteoclasts were not seen on the bone surface or on the compression side. Osteoclasts were only observed on the other side of the bone-in the bone marrow.
These results suggest a difference in tooth movement and osteoclast activity between PC1 mutant mice and wild-type mice in response to orthodontic force. The impaired tooth movement and the lack of osteoclasts on the bone surface in the mutant working side may be related to lack of signal from the PDL due to PC1 deficiency.
验证多囊蛋白-1(PC1)作为机械传感器参与正畸牙齿移动的假说。
比较3只突变型和4只野生型7周龄小鼠对施加力的反应。突变型小鼠为PC1/Wnt1-cre,颅面部区域缺乏PC1。在切牙与左侧第一磨牙之间粘结正畸闭合曲弹簧,施加20 g力,持续4天。采用显微计算机断层扫描、苏木精-伊红染色和抗酒石酸酸性磷酸酶(TRAP)染色研究各组牙齿移动的差异。
在野生型小鼠中,粘结的磨牙向近中移动,牙周膜(PDL)在受压侧被压缩。受压侧显示有透明化区,通过TRAP染色在该处鉴定出破骨细胞。在突变型小鼠中,磨牙未移动,切牙腭向倾斜,张力区的PDL略有增宽。在骨表面或受压侧未见破骨细胞。仅在骨髓中骨的另一侧观察到破骨细胞。
这些结果表明,PC1突变型小鼠和野生型小鼠在对正畸力的反应中,牙齿移动和破骨细胞活性存在差异。突变型工作侧牙齿移动受损以及骨表面缺乏破骨细胞可能与PC1缺乏导致的PDL信号缺失有关。