Loss of BMPR1A in osteoblasts leads to more mature cross-links in collagen.
Loss of BMPR1A leads to a greater mineral–matrix ratio in trabecular compartments.
The hardness and elastic modulus were greater in the cKO trabecular compartments.
Loss of BMPR1A affected cortical and trabecular compartments differently.
Our results uncover novel aspects of BMP signaling on bone quality and bone mass.