骨形态发生蛋白复合带血供肌瓣修复骨缺损成骨过程中骨骼肌的转归

背景局部软组织条件不好的难治性骨缺损修复是临床的重大难题和亟待解决的问题.目的探讨带血供肌瓣作为骨形态发生蛋白载体修复骨缺损成骨过程中骨骼肌的变化.设计观察对比实验.单位南方医科大学南方医院实验动物中心.对象重组人骨形态发生蛋白2;清洁级健康新西兰大白兔20只,1.5～2.5 kg,雌雄不拘.方法实验于2000-01/2002-08在南方医科大学南方医院实验动物中心完成.取10只兔,制作兔桡骨下段15 mm骨缺损,将指深屈肌肌瓣去神经后,转位至缺损区,将纤维蛋白与重组人骨形态发生蛋白2复合物植入肌瓣中.分别于1,2,4,6,8周麻醉状态下各处死4只兔,进行骨缺损区肌瓣大体观察、组织学、原位末端标记及超微结构观察.主要观察指标兔桡骨缺损区肌瓣大体观察、组织学检查、原位末端标记法染色结果及超微结构.结果20只兔均进入结果分析.①兔桡骨缺损区肌瓣大体观察结果骨骼肌逐渐发生萎缩,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.②兔桡骨缺损区肌瓣组织学检查结果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.③兔桡骨缺损区肌瓣细胞凋亡情况原位末端标记法染色萎缩的骨骼肌纤维内大量显色阳性的细胞核或核碎片.④兔桡骨缺损区肌瓣超微结构骨骼肌肌丝随时间延长逐渐消失,细胞核出现染色质边集、固缩、碎裂,呈典型的凋亡改变.结论带血供肌瓣复合骨形态发生蛋白修复骨缺损成骨过程中,肌纤维逐渐发生萎缩、凋亡,最终被骨组织所替代.

Skeletal muscular transformation in osteogenetic process of bone defect repaired with compound vascularized muscle flap with bone morphogenetic protein

BACKGROUND: Intractable repair of bone defect with bad local soft tissues is the essential question in clinic and is expected to deal with.OBJECTIVE: To probe into skeletal muscular changes during osteogenetic process in bone defect repair with vascularized muscle flap that was taken as the carrier of bone morphogenetic protein (BMP).DESIGN: Observation and comparison were designed in the experiment.SETTING: Experimental Animal Center of Nanfang Hospital affiliated to Southern Medical University.MATERIALS: rhBMP-2, 20 New Zealand healthy white rabbits of clean grade, weighted varied from 1.5 to 2.5 kg, of either gender.METHODS: The experiment was performed in Experimental Animal Center of Nanfang Hospital affiliated to Southern Medical University from January 2000 to August 2002. Ten rabbits were employed and bone defect was modeled 15 mm long on the lower section of radium. After nerve removed,the muscular flap of deep flexor muscle of fingers was implanted into the defect. In addition, the compound of fibrin and rhBMP-2 was grafted into the muscular flap. Four rabbits were sacrificed in 1, 2, 4, 6 and 8 weeks successively under anesthetization for gross observation, histological, TUNEL and ultrastructure examinations of muscular flap on bone defect.MAIN OUTCOME MEASURES: Gross observation, histological, TUNEL and ultrastrncture examinations of muscular flap on bone defect in rabbits tion of muscular flap on radial defect in rabbits: Skeletal muscle was atrophic gradually and muscle fiber almost disappeared in 8 weeks and reamination of muscular flap on radial defect in rabbits: It was displayed in histology that while skeletal muscle was atrophic, a part of cell karyon apmuscular flap of radial defect in rabbits: It was indicated with TUNEL staining that there were large amounts of colored positive karyons or karyon flap in radial defect of rabbits: Skeletal muscular filaments disappeared gradually by time lasting, karyon presented chromatin bordering, pyknosis and fragmentation, indicating typical apoptotic alternations.CONCLUSION: During osteogenetic process of bone defect repaired with compound BMP vascularized muscular flap, muscle fibers were atrophic gradually and apoptotic, terminally, substituted by bone tissues.