Glucocorticoid-related bone changes from endogenous or exogenous glucocorticoids.

Academic Article


  • PURPOSE OF REVIEW: Glucocorticoids have a negative impact on bone through direct effects on bone cells and indirect effects on calcium absorption. Here, recent findings regarding glucocorticoid-induced osteoporosis, bone changes in patients with endogenous glucocorticoid derangements, and treatment of steroid-induced bone disease are reviewed. RECENT FINDINGS: Although the majority of our understanding arises from the outcomes of patients treated with exogenous steroids, endogenous overproduction appears to be similarly destructive to bone, but these effects are reversible with cure of the underlying disease process. Additionally, there are bone changes that occur in diseases that interrupt adrenal glucocorticoid production, both in response to our inability to perfectly match glucocorticoid replacement and also related to the underlying disease process. More investigation is required to understand which patients with endogenous overproduction or underproduction of glucocorticoid would benefit from osteoporosis treatment. Better understood is the benefit that can be achieved with currently approved treatments for glucocorticoid-induced osteoporosis from exogenous steroids. With growing concern of long-term use of bisphosphonates, however, further investigation into the duration of use and use in certain populations, such as children and premenopausal women, is essential. SUMMARY: Glucocorticoid-induced osteoporosis is a complex disease that is becoming better understood through advances in the study of exogenous and endogenous glucocorticoid exposure. Further advancement of proper treatment and prevention is on the horizon.
  • Keywords

  • Adrenocortical Hyperfunction, Bone Density, Bone and Bones, Calcium, Cushing Syndrome, Diphosphonates, Female, Glucocorticoids, Hormone Replacement Therapy, Humans, Osteoporosis
  • Digital Object Identifier (doi)

    Author List

  • Warriner AH; Saag KG
  • Start Page

  • 510
  • End Page

  • 516
  • Volume

  • 20
  • Issue

  • 6