In this study, we used male and female conditional knockout mice targeting Bmpr1a expression in either osteoclast precursors (LysM-Cre) or osteoprogenitors (Osx-Cre) and rendered them hyperthyroid to assess whether BMP signaling in osteoblasts or osteoclasts primarily drives the pathogenesis of hyperthyroidism-induced bone loss. This evidence concerns the gene BMPR1A and hyperthyroidism.