Clinically, these results are important to understand the interaction of the cortical and trabecular (cancellous) bone compartments during implant integration and strategies to temporally regulate Wnt16 after implant placement could increase the net pool of progenitor cells able to differentiate into bone-forming osteoblasts leading to improved osseointegration, especially in patients with decreased implant-stabilizing bone volume such as in aging-associated osteoporosis. The gene discussed is WNT16; the disease is osteoporosis.