Osteocyte Igf1 cKO mice formed smaller calluses with less cartilage but more bony tissue than wild-type littermates.
Conditional deletion of Igf1 in osteocytes promoted remodeling of endochondral bone during fracture repair.
Conditional deletion of Igf1 in osteocytes accelerated bony union of the fracture gap.
The accelerated bony union was associated with suppression of Sost expression and increased Bmp2 expression at the fracture site.
Accelerated bony union in osteocyte Igf1 cKO mice was due to upregulation of Wnt signaling, which favors intramembranous bone repair.