Bernick S, Paule W, Ertl D, Nishimoto S K, Nimni M E
Department of Medicine, University of Southern California School of Medicine, Los Angeles.
J Orthop Res. 1989;7(1):1-11. doi: 10.1002/jor.1100070102.
Implantation of demineralized bone (DB) in the form of powder or intact segments in extra skeletal sites stimulates new bone formation. Urist and co-workers presented substantial evidence that there is a noncollagenous protein that has the ability to induce bone formation. One aim of this study was to trace the process of bone formation when DB, in the form of perforated rectangular plates, is implanted subcutaneously in 2-month-old rats. A second objective was to determine whether cartilage cells play a role in the formation of bone in this model. Various DB plates with 0.25 mm diameter holes were implanted subcutaneously for 1-4 weeks in rats. One week after implantation, DB plates were covered by vascularized connective tissue that invaded the perforations. Aggregates of chondrocytes were observed within the holes and on periosteal surfaces in only a few specimens. Further cartilage proliferation was not observed, and by the 2nd week there was no evidence of endochondral bone formation. Where these cartilage-like cells were present, a thin layer of mineral was deposited around them; resorption and fibrous tissue infiltration followed. This aborted form of endochondral calcification was not followed spatially by bone formation. Patent vascularized channels were invaded by alkaline phosphatase-positive mononuclear cells and fibroblasts, and became enlarged by the enzymatic action of macrophages. The next step involved the calcification of DB plates adjacent to the wide spaces. Osteoclasts now appeared leading to the resorption of this recalcified matrix. The eroded and now enlarged lacunar surfaces were lined by newly formed bone and osteoblasts. This process continued so that, at the end of 4 weeks following implantation, the original DB plates were replaced by trabecular bone. Biochemical data on calcium and alkaline phosphatase levels in the implants paralleled the morphological observations.
以粉末或完整节段形式存在的脱矿骨（DB）植入骨骼外部位可刺激新骨形成。尤里斯及其同事提供了大量证据，表明存在一种具有诱导骨形成能力的非胶原蛋白。本研究的一个目的是追踪以穿孔矩形板形式存在的DB皮下植入2月龄大鼠时的骨形成过程。第二个目的是确定软骨细胞在该模型的骨形成中是否发挥作用。将各种直径为0.25毫米的带孔DB板皮下植入大鼠体内1至4周。植入后1周，DB板被侵入穿孔的血管化结缔组织覆盖。仅在少数标本的孔内和骨膜表面观察到软骨细胞聚集。未观察到进一步的软骨增殖，到第2周时，没有软骨内成骨的证据。在这些类似软骨细胞存在的地方，它们周围沉积了一层薄薄的矿物质；随后是吸收和纤维组织浸润。这种流产形式的软骨内钙化在空间上并未伴随骨形成。有血管的通道被碱性磷酸酶阳性单核细胞和成纤维细胞侵入，并因巨噬细胞的酶促作用而扩大。下一步涉及与宽间隙相邻的DB板的钙化。现在出现了破骨细胞，导致这种重新钙化的基质被吸收。被侵蚀且现在扩大的腔隙表面衬有新形成的骨和成骨细胞。这个过程持续进行，以至于在植入后4周结束时，原来的DB板被小梁骨取代。植入物中钙和碱性磷酸酶水平的生化数据与形态学观察结果一致。
