Nilsson O S, Urist M R, Dawson E G, Schmalzried T P, Finerman G A
J Bone Joint Surg Br. 1986 Aug;68(4):635-42. doi: 10.1302/0301-620X.68B4.3733844.
In dogs, resection of a length of the ulna equal to twice the diameter of the mid-shaft leaves a defect which consistently fails to unite. In response to an implant of 100 mg of bovine bone morphogenetic protein (BMP), the defect becomes filled by callus consisting of fibrocartilage, cartilage and woven bone within four weeks. The cartilage is resorbed and replaced by new bone in four to eight weeks. Woven bone is then resorbed, colonised by bone marrow cells and remodelled into lamellar bone. Union of the defect is produced by 12 weeks. Control defects filled with autogeneic cortical bone chips unite after the same period. In regeneration induced by bone morphogenetic protein (BMP) and in repair enhanced by bone graft, union depends upon the proliferation of cells within and around the bone ends. Our working hypothesis is that BMP induces the differentiation of perivascular connective tissue cells into chondroblasts and osteoprogenitor cells and thereby augments the process of bone regeneration from the cells already present in the endosteum and periosteum.
在犬类中，切除一段长度等于尺骨中轴直径两倍的尺骨会留下一个始终无法愈合的缺损。在植入100毫克牛骨形态发生蛋白（BMP）后，缺损在四周内被由纤维软骨、软骨和编织骨组成的骨痂填充。软骨在四至八周内被吸收并被新骨替代。然后编织骨被吸收，骨髓细胞侵入并重塑为板层骨。缺损在12周时实现愈合。填充自体皮质骨碎片的对照缺损在同一时期后愈合。在骨形态发生蛋白（BMP）诱导的再生以及骨移植增强的修复过程中，愈合取决于骨端内部及周围细胞的增殖。我们的工作假设是，BMP诱导血管周围结缔组织细胞分化为成软骨细胞和骨祖细胞，从而增强由骨内膜和骨膜中已存在的细胞进行的骨再生过程。
