Mechanistic Insight into Orthodontic Tooth Movement Based on Animal Studies: A Critical Review.

Mechanistic Insight into Orthodontic Tooth Movement Based on Animal Studies: A Critical Review.
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基于动物研究的正畸牙齿移动机制:综述。

DOI:
10.3390/jcm10081733
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发表时间:
2021-04-16
影响因子:
3.9
通讯作者:
Tsai A
Tsai A
中科院分区:
医学2区
文献类型:
--
作者:
Jeon HH;Teixeira H;Tsai A

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正畸牙齿移动过程中的牙槽骨重建是一个高度调节的过程,它协调破骨细胞的骨吸收和成骨细胞的新骨形成。OTM涉及的机制包括压力侧的机械感应、无菌炎症介导的破骨细胞生成和张力侧的张力诱导的成骨。几种细胞内信号通路和机械传感器包括纤毛和离子通道将机械力转化为刺激破骨细胞或成骨细胞形成的生化信号。迄今为止,许多研究都是在体外或使用人类龈沟液样本进行的。因此,使用转基因动物对研究因果关系非常有帮助。参与介导对OTM的反应的关键细胞类型包括牙周膜成纤维细胞、间充质干细胞、成骨细胞、骨细胞和破骨细胞。刺激正畸牙齿移动所需的细胞过程的细胞间信号包括核因子-κB配体受体激活剂(RANKL)、肿瘤坏死因子-α(TNF-α)、dickkopf Wnt信号通路抑制剂1(DKK 1)、硬化蛋白、转化生长因子β(TGF-β)和骨形态发生蛋白(BMP)。在这篇综述中,我们批判性地总结了目前的OTM研究,使用转基因动物模型,以提供机制的洞察OTM的细胞事件和分子调控。
Alveolar bone remodeling in orthodontic tooth movement (OTM) is a highly regulated process that coordinates bone resorption by osteoclasts and new bone formation by osteoblasts. Mechanisms involved in OTM include mechano-sensing, sterile inflammation-mediated osteoclastogenesis on the compression side and tensile force-induced osteogenesis on the tension side. Several intracellular signaling pathways and mechanosensors including the cilia and ion channels transduce mechanical force into biochemical signals that stimulate formation of osteoclasts or osteoblasts. To date, many studies were performed in vitro or using human gingival crevicular fluid samples. Thus, the use of transgenic animals is very helpful in examining a cause and effect relationship. Key cell types that participate in mediating the response to OTM include periodontal ligament fibroblasts, mesenchymal stem cells, osteoblasts, osteocytes, and osteoclasts. Intercellular signals that stimulate cellular processes needed for orthodontic tooth movement include receptor activator of nuclear factor-κB ligand (RANKL), tumor necrosis factor-α (TNF-α), dickkopf Wnt signaling pathway inhibitor 1 (DKK1), sclerostin, transforming growth factor beta (TGF-β), and bone morphogenetic proteins (BMPs). In this review, we critically summarize the current OTM studies using transgenic animal models in order to provide mechanistic insight into the cellular events and the molecular regulation of OTM.
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