Characterization of matrix-induced osteogenesis in rat calvarial bone defects: II. Origins of bone-forming cells
Characterization of matrix-induced osteogenesis in rat calvarial bone defects: II. Origins of bone-forming cells
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DOI：
10.1007/s002239900737
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发表时间：
1999-12-01
影响因子：
4.2
通讯作者：
Glimcher, MJ
中科院分区：
文献类型：
--
作者：
Wang, J;Glimcher, MJ
利用两种分离脱矿骨基质（DBM）植入物与宿主骨的实验模型，鉴定骨形成细胞在大鼠颅骨缺损修复中的来源。将大鼠DBM， Gdn-HCl提取的不溶性DBM残渣和Gdn-HCl提取的不溶性DBM，再加入透析后的Gdn-HCl提取物，植入两种模型，阻止相邻宿主骨细胞参与修复。此外，硬脑膜和覆盖颅骨缺损的皮下组织中的细胞局部用h -3胸腺嘧啶标记，以确定这些细胞被刺激分裂并分化成成骨细胞的来源。对这些缺损模型愈合过程中发生的时间事件的组织学研究，结合3h -胸腺嘧啶标记表明，DBM诱导的成骨细胞最初来自硬脑膜未分化的间充质干细胞，后来由覆盖缺损的结缔组织中的细胞增强，而不是来自圆形缺损周围的颅骨细胞。通过DBM和提取Gdn-HCl后DBM的重组组分刺激硬脑膜和皮下组织细胞增殖并主要分化为成骨细胞，在很小程度上分化为成软骨细胞。gdn - hcl萃取的不溶性DBM不能诱导成骨或软骨。这些结果表明，需要细胞因子或其他因子存在于DBM中，以诱导来自硬脑膜和其上结缔组织的骨形成细胞来修复颅骨缺损。
Two experimental models that separated demineralized bone matrix (DBM) implants from the host bone were utilized to identify the origins of bone-forming cells in the repair of calvarial defects in rats. Rat DBM, Guanadine HCl (Gdn-HCl) extracted insoluble residue of DBM, and Gdn-HCl extracted insoluble DBM to which the dialyzed Gdn-HCl extract was added back, were implanted in the two models which prevented cells of the adjacent host bone from participating in the repair. in addition, cells in the dura and in the subcutaneous tissue overlying the calvarial defect were locally labeled with H-3-thymidine to identify the origins of those cells that were stimulated to divide and differentiate to osteoblasts. Histological studies of the temporal events that occurred during the healing process in these defect models, combined with 3H-thymidine labeling demonstrated that the osteoblasts induced by DBM were initially derived from undifferentiated mesenchymal stem cells of the dura and later augmented by cells in the overlying connective tissue covering the defect, and not from cells in the cranial bone surrounding the circular defect. The cells of both dura and subcutaneous tissue were stimulated to proliferate and differentiate principally to osteoblasts and to a very much lesser extent to chondroblasts by DBM and by reconstituted components of DBM after Gdn-HCl extraction. Gdn-HCl-extracted insoluble DBM failed to induce bone or cartilage. These results indicate that the cytokines or other factors present in DBM are required to induce bone-forming cells derived from the dura and the overlying connective tissue for the repair of the calvarial defect.