While osteoblast-specific Bmpr1a deletion led to a osteosclerotic bone phenotype as described before32, thyroid hormone treatment did not promote bone resorption or bone loss in male and female Bmpr1afl/fl;Osx-Cre-positive mice revealing an important role of osteoblastic BMPR1A in the pathogenesis of hyperthyroidism-induced bone loss and fragility. Here, BMPR1A is linked to hyperthyroidism.