Age-related degeneration of the bone marrow contributes to delayed fracture-healing and osteoporosis-related fractures in the elderly. The mechanisms underlying this degeneration are unknown, but they may relate to the level of Wnt signaling, a type of hormone, within the aged bone marrow. Engineered mice were used in conjunction with bone-grafts to follow the fates of cells involved in the engraftment. Cells in the bone graft demonstrated seemed expressed fewer bone-forming genes and more fat-forming genes. This age-related fat-forming shift was accompanied by reduced Wnt signaling and a loss in bone-forming potential. In both large and small animal models, bone-forming potential was restored to aged bone grafts by addition of the hormone Wnt3a. We developed an effective, clinically applicable, regenerative medicine-based strategy that has the potential to revitalize bone grafts in aged patients.