Article Sidebar
Published:
Mar 17, 2021DOI:
10.4314/tjpr.v20i1.6Keywords:
Article Details
Submission of a manuscript to this journal is a representation that the manuscript has not been published previously and is not under consideration for publication elsewhere.
All authors named in each manuscript would be required to sign a form (to be supplied by the Editor) so that they may retain their copyright in the article but to assign to us (the Publishers) and its licensees in perpetuity, in all forms, formats and media (whether known or created in the future) to (i) publish, reproduce, distribute, display and store the contribution, (ii) translate the contribution into other languages, create adaptations, reprints, include within collections and create summaries, extracts and/or abstracts of the contribution, (iii) create any other derivative works(s) based on the contribution, (iv) to exploit all subsidiary rights in the contribution, (v) the inclusion of electronic links from the contribution to third party material where-ever it may be located, and (vi) license any thrid party to do any or all of the above.
Main Article Content
Bone morphogenetic protein 2/7 promotes repair of bone defect via induction of endochondral ossification
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
