Skeletal integrity requires continuous bone remodelling by osteoblasts and osteoclasts, and thyroid hormone (TH) is a key regulator of bone remodelling. Excess TH (hyperthyroidism) causes net bone loss, resulting in osteoporosis and increased fracture risk; lack of TH (hypothyroidism) also increases fracture risk because bones become brittle from decreased bone turnover . TH stimulates bone formation and resorption through processes that are only partly defined; it enhances osteoblast proliferation and differentiation, and induces osteoblast production of the osteoclast differentiation factor RANKL (receptor activator of nuclear factor-κB ligand). Nuclear TH receptors (THR-α and THR-β) act as transcriptional regulators and generate the hormone’s classic “genomic” effects . In different cell types, TH also has transcription-independent (“non-genomic”) effects, including stimulation of the MEK/Erk and PI3K/Akt/mTOR kinase cascades, but the molecular mechanisms mediating these non-genomic effects are largely unknown.