Bone formation enhanced by implanted octacalcium phosphate involving conversion into Ca-deficient hydroxyapatite
Bone formation enhanced by implanted octacalcium phosphate involving conversion into Ca-deficient hydroxyapatite
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DOI：
10.1016/j.biomaterials.2005.12.004
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发表时间：
2006-05-01
期刊：
影响因子：
14
通讯作者：
Kamijo, R
中科院分区：
文献类型：
--
作者：
Suzuki, O;Kamakura, S;Kamijo, R
本研究旨在研究合成磷酸八钙（OCP）水解成羟基磷灰石是否影响骨形成。将小鼠骨髓基质ST-2细胞和原代颅骨成骨细胞培养在预涂有OCP或其水解的缺钙羟基磷灰石（OCP水解物; HL）的培养皿上。直到第20天测定增殖和分化的能力。将OCP和HL颗粒植入大鼠临界大小的颅骨缺损中4周和12周，然后通过组织形态计量学测量骨形成。利用X射线衍射（XRD）和傅里叶变换红外光谱（FTIR）分析了OCP的结构变化。在OCP或HL上培养的ST-2和原代成骨细胞的增殖最初受到抑制，但最终促进其向成骨细胞的分化。在骨缺损中植入OCP比HL更显著地促进骨形成，直到12周。OCP在体外和体内都有向磷灰石转化的趋势。植入OCP的转换被确定为随着植入时间的推移而逐渐推进。两者合计，这些结果表明，OCP支持同位骨形成和OCP-磷灰石转化可能参与OCP的这种刺激能力。(c)2005爱思唯尔有限公司保留所有权利。
The present study was designed to investigate whether hydrolysis of synthetic octacalcium phosphate (OCP) into hydroxyapatite affects bone formation. Mouse bone marrow stromal ST-2 cells and primary calvarial osteoblastic cells were cultured on the dishes pre-coated with OCP or its hydrolyzed Ca-deficient hydroxyapatite (OCP hydrolyzate; HL). The capacity of proliferation and differentiation was determined up to day 20. Granules of OCP and HL were implanted into critical-size rat calvaria defects for 4 and 12 weeks, and then bone formation was measured by histomorphometry. Structural changes of incubated and implanted OCP were determined by X-ray diffraction (XRD) and Fourier transform infrared spectroscopy (FTIR). The proliferation of both ST-2 and primary osteoblasts cultured on OCP or HL was initially inhibited, whereas their differentiation to osteoblasts was promoted at last. Implantation of OCP in bone defect more significantly enhanced bone formation than that of HL until 12 weeks. OCP tended to convert to apatite in vitro and in vivo. The conversion of the implanted OCP was ascertained to advance gradually with implantation periods. Taken together, these results suggest that OCP supports appositional bone formation and OCP-apatite conversion may be involved in this stimulatory capacity of OCP. (c) 2005 Elsevier Ltd. All rights reserved.