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牙周韧带中的骨硬化蛋白:生物物理力诱导牙齿移动中的稳态调节剂。

Sclerostin in periodontal ligament: Homeostatic regulator in biophysical force-induced tooth movement.

机构信息

Dental Science Research Institute, School of Dentistry, Chonnam National University, Gwangju, South Korea.

出版信息

J Clin Periodontol. 2022 Sep;49(9):932-944. doi: 10.1111/jcpe.13624. Epub 2022 Jul 4.

DOI:10.1111/jcpe.13624
PMID:35373367
Abstract

AIM

To study the role of sclerostin in periodontal ligament (PDL) as a homeostatic regulator in biophysical-force-induced tooth movement (BFTM).

MATERIALS AND METHODS

BFTM was performed in rats, followed by microarray, immunofluorescence, in situ hybridization, and real-time polymerase chain reaction for the detection and identification of the molecules. The periodontal space was analysed via micro-computed tomography. Effects on osteoclastogenesis and bone resorption were evaluated in the bone-marrow-derived cells in mice. In vitro human PDL cells were subjected to biophysical forces.

RESULTS

In the absence of BFTM, sclerostin was hardly detected in the periodontium except in the PDL and alveolar bone in the furcation region and apex of the molar roots. However, sclerostin was up-regulated in the PDL in vivo by adaptable force, which induced typical transfiguration without changes in periodontal space as well as in vitro PDL cells under compression and tension. In contrast, the sclerostin level was unaffected by heavy force, which caused severe degeneration of the PDL and narrowed periodontal space. Sclerostin inhibited osteoclastogenesis and bone resorption, which corroborates the accelerated tooth movement by the heavy force.

CONCLUSIONS

Sclerostin in PDL may be a key homeostatic molecule in the periodontium and a biological target for the therapeutic modulation of BFTM.

摘要

目的

研究骨硬化蛋白(sclerostin)在牙周韧带(PDL)作为生物物理力诱导牙齿移动(BFTM)的内稳态调节剂中的作用。

材料和方法

在大鼠中进行 BFTM,随后进行微阵列、免疫荧光、原位杂交和实时聚合酶链反应检测和鉴定分子。通过微计算机断层扫描分析牙周间隙。在小鼠的骨髓源性细胞中评估对破骨细胞生成和骨吸收的影响。体外人牙周膜细胞受到生物物理力的作用。

结果

在没有 BFTM 的情况下,除了在分叉区和磨牙根的根尖的牙周和牙槽骨中,PDL 中几乎检测不到骨硬化蛋白。然而,适应性力在体内使 PDL 中的骨硬化蛋白上调,诱导了典型的变形,而牙周间隙没有变化,体外 PDL 细胞在压缩和张力下也是如此。相比之下,重力不会影响骨硬化蛋白水平,重力会导致 PDL 严重退化和牙周间隙变窄。骨硬化蛋白抑制破骨细胞生成和骨吸收,这与重力加速牙齿移动相符。

结论

PDL 中的骨硬化蛋白可能是牙周组织中的关键内稳态分子,也是治疗调节 BFTM 的生物靶标。

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Sclerostin in periodontal ligament: Homeostatic regulator in biophysical force-induced tooth movement.牙周韧带中的骨硬化蛋白:生物物理力诱导牙齿移动中的稳态调节剂。
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