Update on Glucocorticoid-Induced Osteoporosis: Emerging Therapeutic Strategies

Glucocorticoids are widely prescribed for inflammatory diseases, but their adverse skeletal effects, particularly osteoporosis and fracture, remain clinically important. Glucocorticoid-induced osteoporosis (GIOP) is characterized by rapid disruption of bone remodeling, with an early increase in bone resorption followed by suppression of bone formation. These changes substantially increase the risk of vertebral fracture. Fracture risk in GIOP cannot be explained by reductions in bone mineral density alone; it is also thought to reflect glucocorticoid-related deterioration in bone quality and microarchitecture. Current international guidelines recommend fracture risk assessment when glucocorticoid therapy is initiated and support a risk-stratified therapeutic approach. Oral bisphosphonates remain first-line therapy for individuals at low to moderate fracture risk. For patients at higher risk, more potent antiresorptive agents, including zoledronic acid and denosumab, have been shown to improve bone mineral density. In individuals at very high fracture risk, anabolic therapy followed by antiresorptive treatment is increasingly recommended. Careful attention to treatment sequencing is essential, particularly after denosumab discontinuation, for preventing rebound-associated vertebral fractures. Recent guideline updates and comparative clinical studies have placed greater emphasis on anabolic therapy and structured treatment sequencing in order to improve skeletal outcomes. This review summarizes evolving risk-based management strategies for GIOP, focusing on treatment selection by fracture risk category and planned transitions between osteoporosis therapies.