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间歇性甲状旁腺激素[1-34]增强颞下颌关节髁突软骨的软骨生成。

Intermittent Parathyroid Hormone [1-34] Augments Chondrogenesis of the Mandibular Condylar Cartilage of the Temporomandibular Joint.

机构信息

Division of Orthodontics, University of Connecticut Health Center, Farmington, CT, USA.

UCONN School of Engineering, University of Connecticut, Storrs, CT, USA.

出版信息

Cartilage. 2021 Oct;12(4):475-483. doi: 10.1177/1947603519833146. Epub 2019 Mar 22.

DOI:10.1177/1947603519833146
PMID:30897936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8461153/
Abstract

OBJECTIVE

To characterize the long-term effects of intermittent parathyroid hormone (I-PTH) on the mandibular condylar cartilage (MCC) and subchondral bone of the temporomandibular joint, and

MATERIALS AND METHODS

For the experiments, sixteen 10-week-old mice were divided into 2 groups: (1) I-PTH ( = 8)-subcutaneous daily injection of PTH; (2) control group ( = 8)-subcutaneous daily injection of saline solution. Experiments were carried out for 4 weeks. Mice were injected with calcein, alizarin complexone, and cell proliferation marker before euthanasia. For the experiments, primary chondrocyte cultures from the MCC of eight 10-week-old mice were treated with I-PTH for 14 days.

RESULTS

There was a significant increase in bone volume, tissue density, mineral deposition, osteoclastic activity, cell proliferation in the cartilage, and cartilage thickness in the I-PTH-treated mice when compared with the control group. In addition, immunohistochemistry in cartilage revealed that I-PTH administration led to an increase in expression of vascular endothelial growth factor and to a decreased expression of sclerostin, matrix metallopeptidase 13, and aggreganase-1 (ADAM-TS4). Quantitative polymerase chain reaction analysis of the I-PTH-treated chondrocytes revealed significantly decreased relative expression of collagen type X (), alkaline phosphatase (), and Indian Hedgehog () and remarkable increased expression of , fibroblast growth factor 2 (), and proteoglycan 4 ().

CONCLUSION

I-PTH administration causes anabolic effects at the subchondral region of the mandibular condyle while triggers anabolic and protective effects at the MCC.

摘要

目的

描述甲状旁腺激素(I-PTH)间歇性作用对颞下颌关节髁突软骨(MCC)和软骨下骨的长期影响,

材料和方法

在实验中,将 16 只 10 周龄的小鼠分为 2 组:(1)I-PTH(n=8)-每日皮下注射 PTH;(2)对照组(n=8)-每日皮下注射生理盐水。实验进行了 4 周。在安乐死前,用钙黄绿素、茜素复合物和细胞增殖标志物对小鼠进行注射。在实验中,来自 8 只 10 周龄小鼠 MCC 的原代软骨细胞用 I-PTH 处理 14 天。

结果

与对照组相比,I-PTH 处理组的骨体积、组织密度、矿化沉积、破骨细胞活性、软骨细胞增殖和软骨厚度均显著增加。此外,软骨的免疫组织化学显示,I-PTH 给药导致血管内皮生长因子表达增加,骨硬化蛋白、基质金属蛋白酶 13 和聚集酶-1(ADAM-TS4)表达减少。I-PTH 处理的软骨细胞的定量聚合酶链反应分析显示,胶原类型 X()、碱性磷酸酶()和印度刺猬()的相对表达显著降低,而 、成纤维细胞生长因子 2()和蛋白聚糖 4()的表达显著增加。

结论

I-PTH 给药对下颌髁突软骨下区域有合成作用,同时对 MCC 有合成和保护作用。

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本文引用的文献

1
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Orthod Craniofac Res. 2017 Jun;20 Suppl 1:162-166. doi: 10.1111/ocr.12157.
2
PTH [1-34] induced differentiation and mineralization of mandibular condylar cartilage.PTH [1-34] 诱导下颌髁突软骨的分化和矿化。
Sci Rep. 2017 Jun 12;7(1):3226. doi: 10.1038/s41598-017-03428-y.
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Expression of hypoxia inducible factor-2 alpha in overloaded- stress induced destruction of mandibular condylar chondrocytes.缺氧诱导因子-2α在负荷过重应激诱导的下颌髁突软骨细胞破坏中的表达
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T cells, osteoblasts, and osteocytes: interacting lineages key for the bone anabolic and catabolic activities of parathyroid hormone.T细胞、成骨细胞和骨细胞:甲状旁腺激素骨合成与分解代谢活动的关键相互作用谱系
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Enhancement of Lumbar Fusion and Alleviation of Adjacent Segment Disc Degeneration by Intermittent PTH(1-34) in Ovariectomized Rats.间歇性甲状旁腺激素(1-34)对去卵巢大鼠腰椎融合的增强作用及相邻节段椎间盘退变的缓解作用
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Parathyroid hormone: anabolic and catabolic actions on the skeleton.甲状旁腺激素:对骨骼的合成代谢和分解代谢作用
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Response of knee fibrocartilage to joint destabilization.膝部纤维软骨对关节不稳定的反应。
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Lubricin protects the temporomandibular joint surfaces from degeneration.润滑素可保护颞下颌关节表面免于退变。
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Vasodilation to PTH (1-84) in bone arteries is dependent upon the vascular endothelium and is mediated partially via VEGF signaling.骨动脉中甲状旁腺激素 (1-84) 的血管舒张依赖于血管内皮细胞,并部分通过 VEGF 信号转导介导。
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