TSH (Thyroid stimulating hormone) is well established as a regulator of thyroid hormone (thyroxine). We found that TSH receptor knockout mice show high turnover osteoporosis and TSH inhibits osteoclast and osteoblast formation by acting directly in bone. TSH receptors are expressed in both cell types where the expression levels were upregulated in osteoclast formation. We also have found that the pro-inflammatory cytokine TNFa plays major role in TSH function with regards to modulation of osteoclastogenesis. We have thus focused on study how TSHR overexpression in osteoclast progenitors affect osteoclast formation and bone remodeling, and how TNFa expression is regulated in osteoclast and osteoblast progenitors.