Endocrinology and Metabolism

Review Articles

Mineral, bone & muscle
Update on Glucocorticoid-Induced Osteoporosis: Emerging Therapeutic Strategies: Soo-Kyung Cho, Yoon-Kyoung Sung; Endocrinol Metab. 2026;41(3):358-366. Published online June 16, 2026; DOI: https://doi.org/10.3803/EnM.2026.3006

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Abstract PDF PubReader ePub: 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.

Mineral, Bone & Muscle
Update on Glucocorticoid Induced Osteoporosis: Soo-Kyung Cho, Yoon-Kyoung Sung; Endocrinol Metab. 2021;36(3):536-543. Published online June 1, 2021; DOI: https://doi.org/10.3803/EnM.2021.1021

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Glucocorticoids are used to treat many autoimmune and inflammatory diseases. However, an adverse systemic effect is a deleterious effect on bone, which may lead to glucocorticoid-induced osteoporosis, characterized by a rapid and transient increase in bone resorption and fracture risk, which may increase rapidly within 3 months of commencing oral glucocorticoids. Therefore, early risk assessment and intervention are crucial for preventing fractures in patients receiving glucocorticoids. Recent practice guidelines recommend an assessment for fracture risk in patients beginning or receiving glucocorticoids for more than 3 months, and they have suggested fracture risk assessment tool values for identifying patients who need preventive treatment. Bisphosphonates are currently the recommended first-line therapy for the prevention and treatment of glucocorticoid-induced osteoporosis. These have been shown to increase the bone mineral density in the spine and hip and to decrease the incidence of vertebral fractures. Recently, a more potent antiresorptive agent, denosumab, has been shown to increase the bone density in patients receiving glucocorticoids. Teriparatide has been shown to have a preventive effect on vertebral fractures, but not on nonvertebral fractures. In this article we aimed to provide an update on glucocorticoid-induced osteoporosis by focusing on the assessment of its risk and treatment options.

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