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Glucocorticoid-induced osteoporosis: pathophysiology and therapy
E Canalis1, G Mazziotti, A Giustina
1Saint Francis Hospital and Medical Center, Hartford, CT 060105, USA.
Summary
Glucocorticoid-induced osteoporosis (GIO) is common, causing fractures early in therapy. Glucocorticoids harm bone cells, reducing formation and increasing resorption, but bisphosphonates are effective treatments.
Area of Science:
- Endocrinology
- Bone Biology
- Pharmacology
Background:
- Glucocorticoid-induced osteoporosis (GIO) is the most frequent secondary osteoporosis.
- Fractures affect 30-50% of patients on chronic glucocorticoid therapy, often asymptomatically.
- Vertebral fractures occur early, coinciding with rapid bone mineral density (BMD) loss.
Purpose of the Study:
- To review the pathogenesis of GIO.
- To discuss the effects of glucocorticoids on bone cells.
- To outline current and emerging therapeutic strategies for GIO.
Main Methods:
- Review of existing literature on glucocorticoid effects on bone.
- Analysis of cellular mechanisms underlying GIO.
- Evaluation of clinical data on fracture incidence and BMD changes.
Main Results:
- Glucocorticoids directly impair osteoblast function and induce osteocyte apoptosis, suppressing bone formation.
- Glucocorticoids promote osteoclastogenesis, increasing bone resorption.
- Fractures in GIO occur at higher BMD levels compared to postmenopausal osteoporosis.
Conclusions:
- GIO is characterized by suppressed bone formation and increased bone resorption due to glucocorticoid action on bone cells.
- Bisphosphonates are established treatments for preventing and managing GIO.
- Anabolic therapies are being investigated for GIO treatment.
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