PMID: 18180599Jan 9, 2008Paper

Glucocorticoid-induced osteoporosis: an osteoblastic disease

Aging Clinical and Experimental Research
Silvia MigliaccioNazzarena Malavolta

Abstract

It is well-known that glucocorticoid-induced osteoporosis (GIO) is the most common form of secondary osteoporosis. It is estimated that 30% to 50% of patients receiving chronic glucocorticoid therapy suffer vertebral or hip fractures, which are often asymptomatic. Vertebral fractures occur early after exposure to glucocorticoids, at a time when bone mineral density (BMD) declines rapidly. Glucocorticoids impair osteoblast homeostasis and induce apoptosis of both osteoblasts and osteocytes, leading to suppression of bone formation. Glucocorticoids also favor osteoclastogenesis and, as a consequence, increase bone resorption. The end-point of these alterations is a net decrease in BMD and alterations in bone quality. Bisphosphonates have been approved for both prevention and treatment of GIO. At the present time, anabolic therapeutic agents are still under investigation.

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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