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本文引用的文献

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The role of hypoxia in orthodontic tooth movement.缺氧在正畸牙齿移动中的作用。
Int J Dent. 2013;2013:841840. doi: 10.1155/2013/841840. Epub 2013 Oct 21.
2
The osteogenic differentiation of PDLSCs is mediated through MEK/ERK and p38 MAPK signalling under hypoxia.缺氧条件下,PDLSCs 的成骨分化是通过 MEK/ERK 和 p38 MAPK 信号通路介导的。
Arch Oral Biol. 2013 Oct;58(10):1357-68. doi: 10.1016/j.archoralbio.2013.03.011. Epub 2013 Jun 24.
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Analysis of time-course gene expression profiles of a periodontal ligament tissue model under compression.分析受压牙周膜组织模型的时程基因表达谱。
Arch Oral Biol. 2013 May;58(5):511-22. doi: 10.1016/j.archoralbio.2012.10.006. Epub 2012 Oct 30.
4
Effects of vascular endothelial cells on osteogenic differentiation of noncontact co-cultured periodontal ligament stem cells under hypoxia.缺氧环境下血管内皮细胞对非接触共培养牙周膜干细胞成骨分化的影响。
J Periodontal Res. 2013 Feb;48(1):52-65. doi: 10.1111/j.1600-0765.2012.01503.x. Epub 2012 Aug 21.
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Osteoclast formation in mouse co-cultures.小鼠共培养体系中破骨细胞的形成。
Methods Mol Biol. 2012;816:177-86. doi: 10.1007/978-1-61779-415-5_12.
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Rat osteoblast cultures.大鼠成骨细胞培养物。
Methods Mol Biol. 2012;816:31-41. doi: 10.1007/978-1-61779-415-5_3.
7
The effect of antioxidants on the production of pro-inflammatory cytokines and orthodontic tooth movement.抗氧化剂对促炎细胞因子产生和正畸牙齿移动的影响。
Mol Cells. 2011 Aug;32(2):189-96. doi: 10.1007/s10059-011-0071-1. Epub 2011 May 12.
8
Hypoxia inducible factor-1α directly induces the expression of receptor activator of nuclear factor-κB ligand in periodontal ligament fibroblasts.缺氧诱导因子-1α 直接诱导核因子-κB 受体激活剂配体在牙周膜成纤维细胞中的表达。
Mol Cells. 2011 Jun;31(6):573-8. doi: 10.1007/s10059-011-1055-x. Epub 2011 Apr 20.
9
Expression of osteoclastogenesis inducers in a tissue model of periodontal ligament under compression.在受压牙周韧带组织模型中破骨细胞诱导剂的表达。
J Dent Res. 2011 Jan;90(1):115-20. doi: 10.1177/0022034510385237. Epub 2010 Oct 12.
10
Effects of HSP70 on the compression force-induced TNF-α and RANKL expression in human periodontal ligament cells.HSP70 对压应力诱导的人牙周膜细胞 TNF-α 和 RANKL 表达的影响。
Inflamm Res. 2011 Feb;60(2):187-94. doi: 10.1007/s00011-010-0253-x.

压缩和缺氧在牙周膜细胞诱导破骨细胞生成过程中发挥独立作用,同时具有联合效应。

Compression and hypoxia play independent roles while having combinative effects in the osteoclastogenesis induced by periodontal ligament cells.

作者信息

Li Mei Le, Yi Jianru, Yang Yan, Zhang Xuan, Zheng Wei, Li Yu, Zhao Zhihe

机构信息

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.

出版信息

Angle Orthod. 2016 Jan;86(1):66-73. doi: 10.2319/121414.1. Epub 2015 Apr 6.

DOI:10.2319/121414.1
PMID:25844508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8603963/
Abstract

OBJECTIVE

To investigate the isolated and combined effects of compression and hypoxia on the osteoclastogenesis induced by periodontal ligament cells (PDLCs).

MATERIALS AND METHODS

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.

RESULTS

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).

CONCLUSIONS

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.

摘要

目的

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。

材料与方法

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。

结果

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)。

结论

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。