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PREVENTION OF BONE BRIDGE FORMATION USING TRANSPLANTATION OF THE AUTOGENOUS MESENCHYMAL STEM CELLS TO PHYSEAL DEFECTS: AN EXPERIMENTAL STUDY IN RABBITS



Abstract

Physeal cartilage is known to have poor self-repair capacity after injury. Evaluation of the ability of cultured mesenchymal stem cells to repair damaged physis is the actual research topics. In 10 immature New Zealand white rabbits autogenous mesenchymal stem cells were transplanted into iatrogenic physeal defect in lateral portion of distal growth plate of the right femur. The same defect without stem cells transplantation in the left femoral distal physis served as a control. In our study, we used our own technique of implantation of MSCs with a newly modified gel scaffold (New Composite Hyaluronate/Collagen Type I/Fibrin Scaffold). The rabbits were euthanized 4 months after transplantation. Bone length discrepancy and valgus deformity were measured from femoral radiographs. Healing of the defect was investigated histologically. The ability of mesenchymal stem cells to survive and promote cartilage healing in the physeal defect was assessed by immunofluorescence. Average difference in femur length measured from surgery to euthanasia (4 months) was 0.61? 0.19 cm after preventive transplantation of MSCs in right femur, but only 0.11 ? 0.07 cm in left femur. Average angular (valgus) deformity of right femur with MSCs preventively transplanted to iatrogenically damaged distal femoral physis was 1.2? 0.72°. Valgus deformity in left femur was 5.4? 2.5°. Prophylactic transplantation of autogenous mesenchymal stem cells to iatrogenically damaged distal growth plate of rabbit femur prevented bone bridge formation and resulted in healing of the physeal defect with hyaline cartilage. Immunofluorescence examination showed that the chondrocytes newly formed in growth zone are the result of implanted MSCs differentiation. Femur growth in traumatized physis was maintained even after transplantation of autogenous MSCs. As compared with the opposite femur (with physeal defect but without transplanted MSCs), the bone showed no significant shortening or valgus deformity (p=0.018).

Correspondence should be addressed to: EFORT Central Office, Technoparkstrasse 1, CH – 8005 Zürich, Switzerland. Email: office@efort.org