An
aging population, decreased activity levels and increased combat
injuries, have led to an increase in critical sized bone defects.
As more defects are treated using allografts, which is the current
standard of care, the deficiencies of allografts are becoming more
evident. Allografts lack the angiogenic potential to induce sufficient
vasculogenesis to counteract the hypoxic environment associated with
critical sized bone defects. In this study, aptamer-functionalized
fibrin hydrogels (AFH), engineered to release vascular endothelial
growth factor (VEGF), were evaluated for their material properties,
growth factor release kinetics, and angiogenic and osteogenic potential in vivo. Aptamer functionalization to native fibrin did
not result in significant changes in biocompatibility or hydrogel
gelation. However, aptamer functionalization of fibrin did improve
the release kinetics of VEGF from AFH and, when compared to FH, reduced
the diffusivity and extended the release of VEGF several days longer.
VEGF released from AFH, in vivo, increased vascularization
to a greater degree, relative to VEGF released from FH, in a murine
critical-sized cranial defect. Defects treated with AFH loaded with
VEGF, relative to nonhydrogel loaded controls, showed a nominal increase
in osteogenesis. Together, these data suggest that AFH more efficiently
incorporates and retains VEGF in vitro and in
vivo, which then enhances angiogenesis
and osteogenesis to a greater extent in vivo than
FH.
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