Fig. 6

APEX1 function is needed in mesenchymal progenitor cells during the inflammatory phase of fracture healing. a Genetic strategy for Apex1 silencing in chondrocytes during endochondral ossification using Acan Cre deleter. b Representative radiographic planes, 3D reconstruction, and segmentation at 14-dpf for WT (n = 15) and A^ER-Apex1^KO (n = 10). c Quantification of the total, soft (nonmineralized) and stiff (mineralized) callus volume at 14-dpf. Results are expressed as median and interquartile range; whiskers represent maximum and minimum values. P values determined by two-tailed Student’s t test. d Genetic strategy for Apex1 silencing during intramembranous ossification. e Representative radiographic planes and 3D reconstruction of femoral diaphysis at 11-, 14- and 25-days post-surgery (-dps) of WT (11-dps, n = 5; 14-dps, n = 5; 25-dps, n = 2), and P-Apex1^KO (11-dps, n = 5; 14-dps, n = 7; 25-dps, n = 4) mice that received a subcritical (0.8 mm) monocortical bone defect. Yellow arrow indicates the position of the monocortical defect. f Upper panel, rescue strategy for the phenotype of Apex1 silencing during intramembranous ossification. Lower panels, representative radiographical planes of the femoral diaphysis at 9-, 11-, and 14-dps of WT (n = 3 each time point) and P-Apex1^KO (n = 3 each time point) that received a subcritical unicortical bone defect and an implant of absorbable collagen sponge containing 100 ng of rhBMP-2. Yellow arrowheads indicate the position of the monocortical defects