FIGURE 2.

Anti‐DKK1 treatment enhances ASC‐mediated bone formation in a critical size femoral segmental defect. Defects were treated with ASC seeded scaffolds or acellular control scaffolds. Animals were treated with anti‐DKK1 or IgG control (15 mg/kg, SC, twice weekly). A, High‐resolution roentgenography (XR), immediately postoperatively (0 week, first row), at 4 weeks postoperative (second row), 8 weeks postoperative (third row), as well as high magnification of the defect area (bottom row). Each column shows the representative appearance of a treatment group. B, Residual defect span measured on plain films at 8 weeks after surgery. C, Bone mineral density (BMD) of the defect site, as determined by dual‐energy x‐ray absorptiometry at 0, 4, and 8 weeks postoperative. Graphs represent mean and error bars represent 1 SD. See Table S3 for a further summary of animal allocation, treatment regimens, and total cell numbers. *P < .05; **P < .01. ASCs, adipose‐derived stem cells