title: Glucocorticoids and the osteoclast.
abstract: 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.
authors.affiliation: Washington University School of Medicine, St. Louis Missouri, USA. teitelbs@wustl.edu.
authors.forename: Steven L
authors.initials: SL
authors.lastname: Teitelbaum
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D050071:Bone Density Conservation Agents / Q000627:therapeutic use; D001862:Bone Resorption / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D010010:Osteoclasts / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D010024:Osteoporosis / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D012307:Risk Factors
chemical_list: D000893:Anti-Inflammatory Agents; D050071:Bone Density Conservation Agents; D005938:Glucocorticoids