Glucocorticoid-induced osteoporosis: who to treat with what agent?

Nat Rev Rheumatol. 2015 Feb;11(2):98-109. doi: 10.1038/nrrheum.2014.188. Epub 2014 Nov 11.


Among the adverse events of glucocorticoid treatment are bone loss and fractures. Despite available, effective preventive measures, many patients receiving or initiating glucocorticoid therapy are not appropriately evaluated and treated for bone health and fracture risk. Populations with, or at risk of, glucocorticoid-induced osteoporosis (GIOP) to target for these measures are defined on the basis of dose and duration of glucocorticoid therapy and bone mineral density. That patients with GIOP should be treated as early as possible is generally agreed upon; however, diversity remains in intervention thresholds and management guidelines. The FRAX(®) algorithm provides a 10-year probability of fracture that can be adjusted according to glucocorticoid dose. There is no evidence that GIOP and postmenopausal osteoporosis respond differently to treatments. Available anti-osteoporotic therapies such as anti-resorptives including bisphosphonates and the bone anabolic agent teriparatide are effective for the management of GIOP. Prevention with calcium and vitamin D supplementation is less effective than specific anti-osteoporotic treatment. Anti-osteoporotic treatment should be stopped at the time of glucocorticoid cessation, unless the patient remains at increased risk of fracture.

Publication types

  • Review

MeSH terms

  • Bone Development / drug effects
  • Bone and Bones / drug effects
  • Calcium / administration & dosage
  • Diphosphonates / administration & dosage
  • Glucocorticoids / adverse effects*
  • Humans
  • Intestinal Absorption / physiology
  • Osteoporosis / chemically induced*
  • Osteoporosis / physiopathology
  • Osteoporotic Fractures / chemically induced
  • Osteoporotic Fractures / physiopathology
  • Patient Selection
  • Vitamins / administration & dosage


  • Diphosphonates
  • Glucocorticoids
  • Vitamins
  • Calcium