Tob-deficiency Prevents Ovariectomy-induced Bone Loss through the Super-enhancement of Osteoblastic Activities

Osteoporosis is a bone disease in which a loss of bone volume and bone strength leads to fragility factures, which is also suggested to be one of the risk factors of periodontitis. This disease is caused by both an increase in bone resorption and relative negative balance between such bone resorption and accelerated bone formation. Tob (transducer of erbB2) is a member of the antiproliferative family of proteins and acts as a negative regulator of bone morphogenic protein (BMP) signaling. Recently, we found that bone volume in ovariectomised Tob-deficient mice was comparable to sham-operated wild-type mice, and that Tob could be a target in the development of new therapeutic measures for osteoporosis. This review addresses (a) the concept and therapy of osteoporosis, (b) the prospect of Tob, and (c) the mechanism whereby Tob-deficiency protects against ovariectomy-induced bone loss.