rhVEGF 165 delivered in a porous beta-tricalcium phosphate scaffold accelerates bridging of critical-sized defects in rabbit radii.

Abstract

Segmental bone defects are a common obstacle in major orthopedic procedures, and the treatment of these defects remains a challenging clinical problem. Bone tissue engineering has been attracting much attention in recent years. We evaluated the ability of the specific combination of 3 microg rhVEGF(165) with a novel porous beta-tricalcium phosphate (beta-TCP) scaffold coated with fibrin sealant (FS) to facilitate bone regeneration. Unilateral 15-mm long critical-sized defects were prepared in the radial diaphysis of rabbits and treated with rhVEGF(165)/FS/scaffold or FS/scaffold. Healing of the defects was assessed at 4, 8, and 12 weeks, radiologically, histologically, and biomechanically. The results of the study demonstrated that the critical-sized defects in the midshaft of the rabbit radius, treated with rhVEGF(165) incorporated in porous beta-TCP scaffold by FS, can be completely bridged by cortical bone in 12 weeks. The bone marrow space was also reformed histologically and radiologically at 12 weeks postsurgery in the rhVEGF(165)-treated group. Furthermore, biomechanical examination demonstrated that the segmental bone defects were not only radiologically and histologically repaired but were also mechanically repaired. Interestingly, none of the defects was completely repaired at 12 weeks following treatment with FS/scaffold without rhVEGF(165). A solution-driven process is likely the predominant mechanism of accelerating biodegradation of the beta-TCP scaffold in the presence of rhVEGF(165); furthermore, cell-mediated phagocytosis also contributes to biodegradation of the biomaterials.