Glucocorticoid-Induced Bone Loss in Children

ISSN： 1534-8644

Source： Clinical Review in Bone and Mineral Metabolism, Vol.2, Iss.1, 2004-03, pp. : 37-52

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Abstract

This article defines what is meant by glucocorticoid-induced bone loss (GIBL) in children, as opposed to glucocorticoid-induced osteoporosis. GIBL is found in various conditions, including therapy of chronic inflammatory states, antenatal and postnatal glucocorticoid administration to reduce respiratory distress syndrome risk, pre- and postorgan transplantation, and in certain malignancies. The prevalence of GIBL has not been determined for all conditions, but the published literature indicates a general occurrence rate between 25 and 33%.The effects of glucocorticoids on bone cells are discussed, including dimerization of the receptor, nuclear transport, and stimulation of nuclear transcription factors. Nongenomic actions are also mentioned. The glucocorticoid-induced apoptosis of osteoblasts and osteocytes and the reduction of marrow stromal cell differentiation into osteoblasts are mentioned, and it is postulated that osteocyte apoptosis may alter mechanical transduction and contribute to the creation of microdamage in the bone and an increase in fracture risk. Cushing's disease is employed as a model of pure GIBL, whereas other conditions are more complex because additional factors may contribute to bone loss, such as the excessive monocytic production of pro-inflammatory cytokines in inflammatory conditions, and the use of cyclosporin A posttransplantation. Algorithms for the diagnosis and management of GIBL are provided, and consideration of the relative risk of inhaled steroids is also mentioned.