Abstract：
BACKGROUND: The periodontal ligament (PDL) plays an important role in orthodontic tooth movement; however, the underlying molecular mechanism remains unclear. We have previously reported that the Mohawk homeobox (Mkx), a tendon-specific transcription factor, is expressed in the PDL and regulates its homeostasis.
METHODS: In the present study, we examined the role of Mkx in orthodontic tooth movement via bone remodeling induced by mechanical stimulation in Mkx-deficient rats, which are widely used as experimental animals for orthodontic force application. Orthodontic tooth movement of the maxillary first molar was performed in 7-week-old male Mkx-deficient rats (n = 4) and wild-type Wistar rats (n = 4) using coil springs for 14 days. Hematoxylin and eosin (H&E) staining and tartrate-resistant acid phosphatase (TRAP) staining were performed to evaluate morphological changes and osteoclasts. Furthermore, changes in the expression of receptor activator nuclear factor-kappa B ligand (RANKL) were demonstrated using immunostaining.
RESULTS: The amount of tooth movement was significantly lower in Mkx-deficient rats than in wild-type rats. The number of TRAP-positive cells was suppressed in Mkx-deficient rats on the compression side.
CONCLUSIONS: Orthodontic tooth movement experiments in Mkx-deficient rats suggested that Mkx is involved in osteoclast induction at the alveolar bone surface on the compression side. This study reveals the possibility that Mkx plays a mechanosensory role in orthodontic tooth movement by inducing RANKL expression and osteoclastogenesis.
METHODS: In the present study, we examined the role of Mkx in orthodontic tooth movement via bone remodeling induced by mechanical stimulation in Mkx-deficient rats, which are widely used as experimental animals for orthodontic force application. Orthodontic tooth movement of the maxillary first molar was performed in 7-week-old male Mkx-deficient rats (n = 4) and wild-type Wistar rats (n = 4) using coil springs for 14 days. Hematoxylin and eosin (H&E) staining and tartrate-resistant acid phosphatase (TRAP) staining were performed to evaluate morphological changes and osteoclasts. Furthermore, changes in the expression of receptor activator nuclear factor-kappa B ligand (RANKL) were demonstrated using immunostaining.
RESULTS: The amount of tooth movement was significantly lower in Mkx-deficient rats than in wild-type rats. The number of TRAP-positive cells was suppressed in Mkx-deficient rats on the compression side.
CONCLUSIONS: Orthodontic tooth movement experiments in Mkx-deficient rats suggested that Mkx is involved in osteoclast induction at the alveolar bone surface on the compression side. This study reveals the possibility that Mkx plays a mechanosensory role in orthodontic tooth movement by inducing RANKL expression and osteoclastogenesis.
摘要：
背景：牙周膜（PDL）在正畸牙齿移动中起着重要作用；然而，潜在的分子机制尚不清楚.我们之前报道过，莫霍克家庭盒子(Mkx)，肌腱特异性转录因子，在PDL中表达并调节其稳态。
方法：在本研究中，我们研究了Mkx在Mkx缺陷大鼠中通过机械刺激诱导的骨重建在正畸牙齿移动中的作用，被广泛用作正畸力应用的实验动物。使用螺旋弹簧在7周龄的雄性Mkx缺陷大鼠（n=4）和野生型Wistar大鼠（n=4）中进行上颌第一磨牙的正畸移动14天。进行苏木精和伊红（H＆E）染色和抗酒石酸酸性磷酸酶（TRAP）染色以评估形态学变化和破骨细胞。此外，使用免疫染色证明了受体激活剂核因子-κB配体（RANKL）表达的变化。
结果：Mkx缺陷大鼠的牙齿移动量明显低于野生型大鼠。在压缩侧的Mkx缺陷大鼠中，TRAP阳性细胞的数量受到抑制。
结论：Mkx缺陷大鼠正畸牙齿移动实验表明，Mkx参与了压缩侧牙槽骨表面的破骨细胞诱导。这项研究揭示了Mkx通过诱导RANKL表达和破骨细胞生成在正畸牙齿移动中发挥机械感觉作用的可能性。
方法：在本研究中，我们研究了Mkx在Mkx缺陷大鼠中通过机械刺激诱导的骨重建在正畸牙齿移动中的作用，被广泛用作正畸力应用的实验动物。使用螺旋弹簧在7周龄的雄性Mkx缺陷大鼠（n=4）和野生型Wistar大鼠（n=4）中进行上颌第一磨牙的正畸移动14天。进行苏木精和伊红（H＆E）染色和抗酒石酸酸性磷酸酶（TRAP）染色以评估形态学变化和破骨细胞。此外，使用免疫染色证明了受体激活剂核因子-κB配体（RANKL）表达的变化。
结果：Mkx缺陷大鼠的牙齿移动量明显低于野生型大鼠。在压缩侧的Mkx缺陷大鼠中，TRAP阳性细胞的数量受到抑制。
结论：Mkx缺陷大鼠正畸牙齿移动实验表明，Mkx参与了压缩侧牙槽骨表面的破骨细胞诱导。这项研究揭示了Mkx通过诱导RANKL表达和破骨细胞生成在正畸牙齿移动中发挥机械感觉作用的可能性。
