Fig. 8. A model of the relationship between BMPR1A and canonical Wnt signaling in mouse bone. BMPR1A signaling upregulates sclerostin expression, leading to an inhibition of canonical Wnt signaling and a decrease in bone mass by upregulating osteoclastogenesis through the RANKL-OPG pathway. Sclerostin, the SOST gene product, acts as a downstream effector of BMPR1A signaling, an inhibitor of canonical Wnt signaling and a bone mass-determining factor. Broken line indicates another possibility: that BMP signaling directly upregulates osteoclastogenesis through the RANKL-OPG pathway.