Li Mei Le, Yi Jianru, Yang Yan, Zhang Xuan, Zheng Wei, Li Yu, Zhao Zhihe
a PhD Student, Department of Orthodontics, State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
b Postgraduate Student, Department of Orthodontics, State Key Laboratory of Oral Diseases, West China School and Hospital of Stomatology, Sichuan University, Chengdu, China.
Angle Orthod. 2016 Jan;86(1):66-73. doi: 10.2319/121414.1. Epub 2015 Apr 6.
To investigate the isolated and combined effects of compression and hypoxia on the osteoclastogenesis induced by periodontal ligament cells (PDLCs).
A periodontal ligament tissue model (PDLtm) was established by 3-D culturing human PDLCs on a thin sheet of poly lactic-co-glycolic acid scaffold. The PDLtm was treated with hypoxia and/or compression for 6, 24, or 72 hours. After that, a real-time polymerase chain reaction was used for gene expression analysis. The conditioned media were used for the coculture of osteoblast and osteoclast (OC) precursors; tartrate-resistant acid phosphatase staining was done to examine OC formation.
Either compression or hypoxia alone significantly up-regulated the gene expression of pro-osteoclastogenic cytokines in the PDLtm and enhanced osteoclastogenesis in the cocultures, and the combination of the two had significantly stronger effects than either stimulation alone. In addition, comparing the two stimulants, we found that the osteoclastogenic property of the PDLCs peaked earlier (at 6 hours) in the compression group than in the hypoxia group (at 24 hours).
Both compressive force and hypoxia may take part in initiating osteoclastogenesis in orthodontic tooth movement and may have combinatory effects, which could update our concepts of the mechanisms involved in the initiation of bone resorption on the pressure side of the tooth in question.
研究压缩力和低氧对牙周膜细胞(PDLCs)诱导破骨细胞生成的单独及联合作用。
通过在聚乳酸 - 乙醇酸共聚物薄片支架上三维培养人PDLCs建立牙周膜组织模型(PDLtm)。对PDLtm进行低氧和/或压缩处理6、24或72小时。之后,采用实时聚合酶链反应进行基因表达分析。将条件培养基用于成骨细胞和破骨细胞(OC)前体细胞的共培养;采用抗酒石酸酸性磷酸酶染色检测OC形成。
单独的压缩力或低氧均可显著上调PDLtm中促破骨细胞生成细胞因子的基因表达,并增强共培养中的破骨细胞生成,且二者联合作用比单独任何一种刺激的作用都显著更强。此外,比较两种刺激因素,我们发现压缩力组中PDLCs的破骨细胞生成特性在6小时时达到峰值,早于低氧组(在24小时时达到峰值)。
压缩力和低氧可能均参与正畸牙齿移动过程中破骨细胞生成启动,并可能具有联合作用,这可能会更新我们对牙齿压力侧骨吸收启动机制的认识。