Abstract
The repair of segmental bone defects remains a significant challenge for orthopaedic surgeons. Endothelial progenitor cells (EPCs) have successfully promoted the repair of acute defects in animal models; however, the ability of EPCs to induce the repair of chronic nonhealing defects, such as those often encountered clinically, has not been investigated. Therefore, the purpose of this study was to investigate the ability of EPCs delivered in delayed fashion to induce the repair of nonhealing defects in a clinically relevant model. In order to simulate delayed treatment, 5 mm segmental defects in Fischer 344 rat femora were treated with bone marrow-derived EPCs on a Gelfoam scaffold at 3 weeks post creation of the defect. At ten weeks posttreatment, 100% of EPC-treated defects achieved union, whereas complete union was only achieved in 37.5% of defects treated with Gelfoam alone. Furthermore, significant increases in ultimate torque (p = 0.022) and torsional stiffness (p = 0.003) were found in EPC-treated defects compared to controls. Critically, no differences in outcomes were observed between acute and delayed EPC treatments. These results suggest that EPCs can enhance bone healing when applied in an acute or delayed fashion and that their use may represent a clinically translatable therapy for bone healing in humans.
Highlights
Despite recent advances in surgical techniques and implants, the repair of bone defects and nonunion secondary to trauma or infection remains a significant challenge
The present study aimed to address this discrepancy, and our findings indicate that Endothelial progenitor cells (EPCs) delivered via open surgery to a previously established bone defect are capable of inducing bone repair
EPCs administered to nonhealing bone defects enhanced bone healing when compared to control treatment, and EPCs could be a clinically translatable therapy aimed at the reconstruction of osseous defects in a delayed fashion
Summary
Despite recent advances in surgical techniques and implants, the repair of bone defects and nonunion secondary to trauma or infection remains a significant challenge. Similar to AICBG, each of these techniques have demonstrated high complication rates and substantial limitations in efficacy. A variety of tissue engineering substitutes, including osteoinductive molecules such as bone morphogenetic proteins (BMPs), osteoconductive scaffolds such as calcium phosphates, and osteoprogenitor cells such as mesenchymal stem cells (MSCs), have been investigated as potentially superior treatments for bone defects [10, 11]. To date these therapies have failed to translate into clinical practice. One potentially significant limitation of each of these therapies is their lack of angiogenic capacity
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