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间歇性甲状旁腺激素（PTH）可促进牙骨质生成，并减轻成牙骨质细胞中机械应变的分解代谢作用。

Intermittent parathyroid hormone (PTH) promotes cementogenesis and alleviates the catabolic effects of mechanical strain in cementoblasts.

作者信息

Li Yuyu, Hu Zhiai, Zhou Chenchen, Xu Yang, Huang Li, Wang Xin, Zou Shujuan

机构信息

Department of Orthodontics, West China Hospital of Stomatology, Sichuan University, No. 14, 3rd Section, Renmin South Road, Chengdu, 610041, China.

State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, No. 14, 3rd Section, Renmin South Road, Chengdu, 610041, China.

出版信息

BMC Cell Biol. 2017 Apr 20;18(1):19. doi: 10.1186/s12860-017-0133-0.

DOI:10.1186/s12860-017-0133-0
PMID:28427342
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5397739/
Abstract

BACKGROUND

External root resorption, commonly starting from cementum, is a severe side effect of orthodontic treatment. In this pathological process and repairing course followed, cementoblasts play a significant role. Previous studies implicated that parathyroid hormone (PTH) could act on committed osteoblast precursors to promote differentiation, and inhibit apoptosis. But little was known about the role of PTH in cementoblasts. The purpose of this study was to investigate the effects of intermittent PTH on cementoblasts and its influence after mechanical strain treatment.

RESULTS

Higher levels of cementogenesis- and differentiation-related biomarkers (bone sialoprotein (BSP), osteocalcin (OCN), Collagen type I (COL1) and Osterix (Osx)) were shown in 1-3 cycles of intermittent PTH treated groups than the control group. Additionally, intermittent PTH increased alkaline phosphatase (ALP) activity and mineralized nodules formation, as measured by ALP staining, quantitative ALP assay, Alizarin red S staining and quantitative calcium assay. The morphology of OCCM-30 cells changed after mechanical strain exertion. Expression of BSP, ALP, OCN, osteopontin (OPN) and Osx was restrained after 18 h mechanical strain. Furthermore, intermittent PTH significantly increased the expression of cementogenesis- and differentiation-related biomarkers in mechanical strain treated OCCM-30 cells.

CONCLUSIONS

Taken together, these data suggested that intermittent PTH promoted cementum formation through activating cementogenesis- and differentiation-related biomarkers, and attenuated the catabolic effects of mechanical strain in immortalized cementoblasts OCCM-30.

摘要

背景

牙根外吸收通常始于牙骨质，是正畸治疗的一种严重副作用。在这个病理过程及后续的修复过程中，成牙骨质细胞发挥着重要作用。先前的研究表明，甲状旁腺激素（PTH）可作用于定向成骨细胞前体以促进分化并抑制细胞凋亡。但关于PTH在成牙骨质细胞中的作用知之甚少。本研究的目的是探讨间歇性PTH对成牙骨质细胞的影响及其在机械牵张处理后的作用。

结果

与对照组相比，间歇性PTH处理1 - 3个周期的组中，牙骨质生成和分化相关生物标志物（骨唾液蛋白（BSP）、骨钙素（OCN）、I型胶原（COL1）和osterix（Osx））的水平更高。此外，通过ALP染色、定量ALP测定、茜素红S染色和定量钙测定发现，间歇性PTH增加了碱性磷酸酶（ALP）活性和矿化结节形成。施加机械牵张后，OCCM - 30细胞的形态发生了变化。机械牵张18小时后，BSP、ALP、OCN、骨桥蛋白（OPN）和Osx的表达受到抑制。此外，间歇性PTH显著增加了机械牵张处理的OCCM - 30细胞中牙骨质生成和分化相关生物标志物的表达。

结论

综上所述，这些数据表明，间歇性PTH通过激活牙骨质生成和分化相关生物标志物促进牙骨质形成，并减弱了永生化成牙骨质细胞OCCM - 30中机械牵张的分解代谢作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/d089f74d3286/12860_2017_133_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/f3886c9fc7da/12860_2017_133_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/3009f6f548f5/12860_2017_133_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/0418aeefcac9/12860_2017_133_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/4d35602cf0be/12860_2017_133_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/0d6bd34beda1/12860_2017_133_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/7667d9346bb7/12860_2017_133_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/d089f74d3286/12860_2017_133_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/f3886c9fc7da/12860_2017_133_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/3009f6f548f5/12860_2017_133_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/0418aeefcac9/12860_2017_133_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/4d35602cf0be/12860_2017_133_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/0d6bd34beda1/12860_2017_133_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/7667d9346bb7/12860_2017_133_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d04/5397739/d089f74d3286/12860_2017_133_Fig7_HTML.jpg

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