肌瓣作为BMP载体构建血管化骨组织修复骨缺损的形态学研究

MORPHOLOGICAL STUDY ON SKELETAL MUSCLE FLAP AS A CARRIER OF BONE MORPHOGENETIC PROTEIN TO FABRICATE VASCULARIZED BONE FOR THE REPAIR OF BONE DEFECT

为探讨肌瓣作为骨形态发生蛋白 (BMP)载体构建血管化骨组织修复骨缺损的可行性及其生物学特征 ,制作兔桡骨下段15mm骨缺损 ,将去神经化的指深屈肌肌瓣转位至缺损区 ,作为BMP载体来修复骨缺损 ,通过大体、X线、组织学、原位末端标记 (TUNEL)等方法观察骨缺损的修复过程及生物学变化。结果发现 ,骨骼肌逐渐发生萎缩 ,2周时肌瓣内可触及串珠状团块 ,有大量软骨细胞生成 ,沿肌间隙分布 ;6周时骨桥与宿主骨紧密结合 ,软骨溶解区有大量编织骨形成 ,出现骨髓腔并与宿主骨髓腔再通 ,肌纤维被增殖的间充质细胞、软骨细胞及结缔组织所分割 ;8周时肌纤维几乎完全消失 ,新生骨组织呈条索状桥接两断端 ;组织学显示骨骼肌萎缩的同时 ,部分细胞核出现崩解 ,并有凋亡小体出现 ;TUNEL染色呈阳性。

To investigate the effect and biological characteristics of skeletal muscle flap as a carrier of bone morphogenetic protein to fabricate vascularized bone for the repair of bone defect, 15mm radius bone defect was made. Denerved flexor digitorum profundus muscle flap with BMP was implanted to repair the bone defect. The osteogenesis and changes of skeletal muscle were investigated by gross, X ray, HE strain and TUNEL strain. The bone defect was filled up with new bone tissue formed in the muscle flap after 2 weeks. The new bone tissue bridged the bone defect after 6 weeks. Histological examination showed that a large amount of cartilage was formed in the gaps of muscles after 2 weeks. The cartilage was absorbed and replaced by normal bone containing bone marrow after 6 weeks with obvious muscle cell atrophy. Histological examination showed a portion of nuclei was collapsed and apoptotic bodies were found with the atrophy of skeletal muscle. Apoptotic nuclei were found by TUNEL. The results indicate that skeletal muscle flap as a effective carrier of bone morphogenetic protein can be used to fabricate vascularized bone for the repair of bone defect.