Cyclical tensile force on periodontal ligament cells inhibits osteoclastogenesis through OPG induction
Cyclical tensile force on periodontal ligament cells inhibits osteoclastogenesis through OPG induction
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DOI：
10.1177/154405910608500512
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发表时间：
2006-05-01
影响因子：
7.6
通讯作者：
Mitani, H
中科院分区：
文献类型：
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作者：
Kanzaki, H;Chiba, M;Mitani, H
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。咬合负荷抑制萎缩性牙槽骨吸收。此前，我们发现对 PDL 细胞的持续压缩力会诱导破骨细胞生成支持活性，并上调 RANKL。我们假设，与压缩不同，周期性张力通过上调 TGFbeta 上调 PDL 细胞中的 OPG 表达，并且不会诱导破骨细胞生成支持活性。 PDL 细胞在体外受到循环拉力的机械刺激。经受周期性张力的PDL细胞的条件培养基抑制破骨细胞生成。周期性张力不仅上调 PDL 细胞中 RANKL mRNA 的表达，而且上调 PDL 细胞中 OPG mRNA 的表达。张力也会上调 PDL 细胞中 TGF-β 的表达。在周期性张力刺激下，给予TGF-β中和抗体以剂量依赖性方式抑制OPG上调。此外，使用TGF-β中和抗体可以部分恢复PDL细胞条件培养基在周期性张力下的破骨细胞生成抑制作用。总之，张力通过 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。
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 upregulates OPG expression in PDL cells via TGFbeta 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 upregulation 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.