Abstract
Purpose: To study the influence of bone morphogenetic protein 2/7 (BMP2/7) on repair of bone defect, and the mechanism involved.Methods: Bone marrow stromal cells (BMSCs) were randomly assigned to 2 groups: control and transfection groups. The cells were transfected with rBMP2/7 recombinant adenovirus. Cell growth and alkaline phosphatase (ALP) activity were determined in both groups. Rabbit model of femoral bone defect was prepared using standard methods. Male New Zealand white rabbits were randomly assigned to 3 groups, each of which had 10 rabbits: control, gelatin and BMP2/7 groups. Histopathological and xray examinations, and three-point bending flexural test were used to compare the potential of gelatin and BMP2/7 to repair bone defects.Results: Transfection of BMSCs with rBMP2/7 recombinant adenovirus significantly enhanced their growth (p < 0.05). Alkaline phosphatase (ALP) level was also markedly and time-dependently higher in transfection group than in control group (p < 0.05). Rabbits with grade 4 bone healing or above were more in BMP2/7-treated category than in control and gelatin groups. New bone hyperplasia with typical lamellar bone structure, irregular medullary cavity, as well as transition from osteoblast to osteocyte were observed in BMP2/7 group. Moreover, maximum flexural strength and repair were significantly higher in BMP2/7-transfected group than in control.Conclusion: These findings indicate that BMP2/7 promotes the repair of bone defect via induction of endochondral ossification in rabbits. Thus, this protein may be useful for the repair of bone defects in humans.
 Keywords: Alkaline phosphatase, Bone lesions, BMP2/7, Endochondral ossification
Highlights
Bone defects are caused by trauma, bone disease or tumor, congenital abnormalities, infection and failed arthroplasty
The present investigation focused on the influence of bone morphogenetic protein 2/7 (BMP2/7) on repair of bone defect, and the mechanism involved
The cells were transfected with rBMP2/7 recombinant adenovirus
Summary
Bone defects are caused by trauma, bone disease or tumor, congenital abnormalities, infection (osteomyelitis) and failed arthroplasty. A member of the transforming growth factor (TGF) β superfamily, BMG stimulates BMSCs to differentiate into osteoblasts and chondrocytes It induces ectopic bone formation during healing and repair of bone defects [5]. The present investigation focused on the influence of BMP2/7 on repair of bone defect, and the mechanism involved. Bone marrow extracted from New Zealand white male rabbits was dispersed into individual cells by subjecting it to density gradient centrifugation at 1500 rpm for 15 min at 4 °C using lymphocyte separation solution (a mixture of Ficoll and sodium diatrizoate) as the density gradient solution. Sodium pentobarbital injection was bought from Shanghai New Asia Pharmaceutical Co. Ltd. The bone defect area was filled with collagen sponge containing BMP. Values of p < 0.05 were taken as indicative of statistically significant differences
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