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含氟羟基磷灰石通过体外和体内抑制破骨细胞分化和功能来抑制骨吸收。

Fluorine-contained hydroxyapatite suppresses bone resorption through inhibiting osteoclasts differentiation and function in vitro and in vivo.

机构信息

State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Department of Stomotology, Sichuan Academy of Medical Science & Sichuan Provincial People's Hospital, Chengdu, China.

出版信息

Cell Prolif. 2019 May;52(3):e12613. doi: 10.1111/cpr.12613. Epub 2019 Apr 10.

DOI:10.1111/cpr.12613
PMID:30968984
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6536412/
Abstract

OBJECTIVES

Fluorine, an organic trace element, has been shown to unfavourably effect osteoclasts function at a low dose. Use of hydroxyapatite (HA) has been effective in exploring its roles in promoting bone repair. In this study, we used HA modified with fluorine to investigate whether it could influence osteoclastic activity in vitro and ovariectomy-induced osteoclasts hyperfunction in vivo.

MATERIALS AND METHODS

Fluorohydroxyapatite (FHA) was obtained and characterized by scanning electron microscope (SEM). Osteoclasts proliferation and apoptosis treated with FHA were assessed by MTT and TUNEL assay. SEM, F-actin, TRAP activity and bone resorption experiment were performed to determine the influence of FHA on osteoclasts differentiation and function. Moreover, HA and FHA were implanted into ovariectomized osteoporotic and sham surgery rats. Histology and Micro-CT were examined for further verification.

RESULTS

Fluorine released from FHA slowly and sustainably. FHA hampered osteoclasts proliferation, promoted osteoclasts apoptosis, suppressed osteoclasts differentiation and function. Experiments in vivo validated that FHA participation brought about an inhibitory effect on osteoclasts hyperfunction and less bone absorption.

CONCLUSION

The results indicated that FHA served as an efficient regulator to attenuate osteoclasts formation and function and was proposed as a candidature for bone tissue engineering applications.

摘要

目的

氟是一种有机微量元素，已被证明在低剂量下会对破骨细胞的功能产生不利影响。使用羟基磷灰石（HA）已被证明在探索其促进骨修复的作用方面是有效的。在本研究中，我们使用氟改性的 HA 来研究它是否可以影响体外破骨细胞的活性和体内去卵巢诱导的破骨细胞功能亢进。

材料和方法

通过扫描电子显微镜（SEM）获得并表征氟羟磷灰石（FHA）。通过 MTT 和 TUNEL 测定法评估 FHA 处理的破骨细胞增殖和凋亡。通过 SEM、F-肌动蛋白、TRAP 活性和骨吸收实验来确定 FHA 对破骨细胞分化和功能的影响。此外，将 HA 和 FHA 植入去卵巢骨质疏松症和假手术大鼠中。进行组织学和 Micro-CT 检查以进一步验证。

结果

FHA 缓慢而持续地释放氟。FHA 阻碍破骨细胞增殖，促进破骨细胞凋亡，抑制破骨细胞分化和功能。体内实验验证了 FHA 参与对破骨细胞功能亢进和较少的骨吸收有抑制作用。

结论

结果表明，FHA 可作为一种有效的调节剂来减弱破骨细胞的形成和功能，并被提出作为骨组织工程应用的候选物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/117c7737d4b0/CPR-52-e12613-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/f5de47666adc/CPR-52-e12613-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/ad028594d3be/CPR-52-e12613-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/5ef33b9c0429/CPR-52-e12613-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/be826fa1aa10/CPR-52-e12613-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/c099f69228e6/CPR-52-e12613-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/117c7737d4b0/CPR-52-e12613-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/f5de47666adc/CPR-52-e12613-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/ad028594d3be/CPR-52-e12613-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/5ef33b9c0429/CPR-52-e12613-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/be826fa1aa10/CPR-52-e12613-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/c099f69228e6/CPR-52-e12613-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c39/6536412/117c7737d4b0/CPR-52-e12613-g006.jpg

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