Harvey Cushing first described the association between excess endogenous glucocorticoids and fractures in 1932. By 1954, a few years after the introduction of prednisone to treat rheumatoid arthritis, the deleterious skeletal effects of exogenous glucocorticoids were reported. Glucocorticoid-induced bone loss is now the most common form of secondary osteoporosis and fractures are glucocorticoids’ most common adverse effect. They are among the most common iatrogenic complications of clinical practice as glucocorticoids are used by 0.5–2.5% of adults. Concomitant factors including the underlying disease for which patients are treated, age, baseline bone mineral density (BMD), the hormonal status of the patient, and individual differences in sensitivity to glucocorticoid also play a role in determining whether or not a patient will develop osteoporosis and fractures. Trabecular bone score and the fracture risk assessment tool have increased physicians’ ability to effectively diagnose glucocorticoid-induced osteoporosis, and randomized clinical controlled trials now guide treatment decisions, allowing for clear recommendations outlined in this chapter.