Glucocorticoids and the osteoclast

Glucocorticoid-induced osteoporosis uniformly represents suppression of bone formation. The steroid's effects on osteoclasts are, however, controversial. While glucocorticoid administration to patients with inflammatory diseases accelerates bone resorption, osteoclast function falls below normal with prolonged treatment. Thus, administration of anti-resorptive agents, such as bisphosphonates, is justified during early glucocorticoid therapy, but further suppression of osteoclasts, by these drugs, in chronically treated patients will dampen bone remodelling and may compromise skeletal quality, predisposing to fracture.