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牙周膜细胞上的周期性拉伸力通过诱导骨保护素抑制破骨细胞生成。

Cyclical tensile force on periodontal ligament cells inhibits osteoclastogenesis through OPG induction.

作者信息

Kanzaki H, Chiba M, Sato A, Miyagawa A, Arai K, Nukatsuka S, Mitani H

机构信息

Division of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University, Sendai, Japan.

出版信息

J Dent Res. 2006 May;85(5):457-62. doi: 10.1177/154405910608500512.

DOI:10.1177/154405910608500512
PMID:16632761
Abstract

The periodontal ligament (PDL) maintains homeostasis of periodontal tissue under mechanical tensile-loading caused by mastication. Occlusal load inhibits atrophic alveolar bone resorption. Previously, we discovered that continuous compressive force on PDL cells induced osteoclastogenesis-supporting activity, with up-regulation of RANKL. We hypothesized that, unlike compression, cyclical tensile force up-regulates OPG expression in PDL cells via TGF-beta up-regulation, and does not induce osteoclastogenesis-supporting activity. PDL cells were mechanically stimulated by cyclical tensile force in vitro. The conditioned media of PDL cells that had been subjected to cyclical tensile force inhibited osteoclastogenesis. Cyclical tensile force up-regulated not only RANKL mRNA expression, but also OPG mRNA expression in PDL cells. Tensile force up-regulated TGF-beta expression in PDL cells as well. Administration of neutralizing antibodies to TGF-beta inhibited OPG up-regulation under cyclical tensile-force stimulation in a dose-dependent manner. Additionally, the osteoclastogenesis-inhibitory effect of the conditioned media of PDL cells under cyclical tensile force was partially rescued by the administration of TGF-beta neutralizing antibodies. In conclusion, tensile force inhibited the osteoclastogenesis-supporting activity of PDL cells by inducing the up-regulation of OPG via TGF-beta stimulation.

摘要

牙周韧带（PDL）在咀嚼引起的机械拉伸负荷下维持牙周组织的稳态。咬合负荷可抑制萎缩性牙槽骨吸收。此前，我们发现对PDL细胞持续施加压缩力会诱导破骨细胞生成支持活性，并上调RANKL。我们推测，与压缩力不同，周期性拉伸力通过上调TGF-β来上调PDL细胞中OPG的表达，且不会诱导破骨细胞生成支持活性。在体外对PDL细胞施加周期性拉伸力进行机械刺激。经历周期性拉伸力的PDL细胞的条件培养基可抑制破骨细胞生成。周期性拉伸力不仅上调了PDL细胞中RANKL mRNA的表达，还上调了OPG mRNA的表达。拉伸力也上调了PDL细胞中TGF-β的表达。给予TGF-β中和抗体以剂量依赖性方式抑制了周期性拉伸力刺激下OPG的上调。此外，给予TGF-β中和抗体可部分挽救周期性拉伸力作用下PDL细胞条件培养基的破骨细胞生成抑制作用。总之，拉伸力通过TGF-β刺激诱导OPG上调，从而抑制PDL细胞的破骨细胞生成支持活性。

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