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维生素 D 结合蛋白并不会促进大鼠骨缺损的愈合:一项初步研究。

Vitamin-D binding protein does not enhance healing in rat bone defects: a pilot study.

机构信息

Institute of Clinical Medicine, National Yang-Ming University, No. 155, Sec. 2, Linong St., Beitou District, Taipei 11221, Taiwan, ROC.

出版信息

Clin Orthop Relat Res. 2009 Dec;467(12):3156-64. doi: 10.1007/s11999-009-0864-0. Epub 2009 May 6.

Abstract

Vitamin D-binding protein (DBP) has an anabolic effect on the skeleton and reportedly enhances bone ingrowth. We used an in vivo critical bone defect model to determine whether local administration of DBP promotes bone defect healing. We created a 5-mm segmental bone defect in the radial shaft in a rat model. Forty-eight rats were assigned to eight groups: local application of 1 microg, 5 microg, 10 microg, or 50 microg DBP (DBP-1, DBP-5, DBP-10, DBP-50), autogenous bone marrow mononuclear cells with or without 10 microg DBP (BM-DBP-10, BM), 80 microg BMP-2 delivered in gelatin sponge (BMP-2), and the sham operated group. Radiographic evaluation, histological stains, and epifluorescence microscopy were performed. Grossly, all bone gaps of the BMP-2 group were solidly bridged by callus, while all those in the sham operated group remained unhealed by 9 weeks. Only one specimen of the BM-DBP-10 and DBP-50 groups and three specimens of the BM group were solidly healed; pseudarthroses occurred in all of the other specimens. Histological study and radiographs of the specimens showed similar results. We did not observe the enhanced bone healing reported in a previous study.

摘要

维生素 D 结合蛋白 (DBP) 对骨骼具有合成代谢作用,据报道可促进骨内生长。我们使用体内临界骨缺损模型来确定 DBP 的局部给药是否促进骨缺损愈合。我们在大鼠模型中创建了桡骨干 5 毫米节段性骨缺损。将 48 只大鼠分为 8 组:局部应用 1μg、5μg、10μg 或 50μg DBP(DBP-1、DBP-5、DBP-10、DBP-50)、自体骨髓单个核细胞加或不加 10μg DBP(BM-DBP-10、BM)、80μg BMP-2 包埋在明胶海绵中(BMP-2)和假手术组。进行放射学评估、组织学染色和荧光显微镜检查。大体上,BMP-2 组的所有骨间隙均被骨痂牢固桥接,而假手术组的所有骨间隙在 9 周时仍未愈合。只有 BM-DBP-10 和 DBP-50 组的一个标本和 BM 组的三个标本被牢固愈合;所有其他标本均发生假关节。标本的组织学研究和 X 线片显示出相似的结果。我们没有观察到先前研究中报道的增强骨愈合。

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