With hyperthyroidism, Bmpr1afl/fl;LysM-Cre mice presented osteoporotic bones with impaired bone strength independent of osteoclast progenitor-specific Bmpr1a deletion, indicating that either BMPR1A plays only a minor role mediating effects of thyroid hormones on osteoclastogenesis and osteoclast-osteoblast coupling or that osteoclasts per se are not directly responsive to thyroid hormone treatment. This evidence concerns the gene BMPR1A and hyperthyroidism.