Growth hormone and the acquisition of bone mass

Bone remodelling is a continuous, closely coupled process of bone resorption followed by bone formation. This process is regulated by factors and hormones which include GH, IGF-I and gonadal steroids. GH deficiency in childhood results in short stature and delayed bone maturation and a reduced peak bone mass might account for reduced BMC and BMD. Possible pathophysiological mechanisms for reduced bone mass in both childhood-and adult-onset GH deficiency are discussed. GH treatment effects on bone metabolism include increased remodelling, with increases in BMC, BMD and bone area. Increases in BMC and BMD are delayed while these changes are incorporated into the skeleton. BMC increases to a greater extent than BMD. At a cellular level, GH and IGF-I have direct and indirect effects on osteoblast and osteoclast precursors and fully differentiated cells. Osteoblasts possess both oestrogen and androgen receptors and bone loss accelerates with the loss of gonadal function. There are gender differences in GH effects on bone. BMD is related to fracture risk in the hip and lumbar spine in women. CH treatment might decrease fracture risk at a level comparable to oestrogen or bisphosphonate treatment. Patients with the lowest BMD prior to treatment derive the greatest benefit from GH therapy.