Glucocorticoid-induced osteoporosis is the most common cause of secondary osteoporosis and constitutes an important health problem, associated with an increased risk of fractures, significant morbidity and mortality, and long-term decreased quality of life. Aging is linked to extensive multimorbidity, polypharmacy, physical and mental disability, and an increased risk of falls, rendering management of glucocorticoid-induced osteoporosis in the older population particularly challenging. On a pathophysiological level, aging is associated with declining osteoblast activity, increased osteoclast activity, and increased bone marrow adiposity; effects that are all accentuated by glucocorticoids. In this narrative review, we discuss the pathophysiology of glucocorticoid-induced osteoporosis, and focus on the mechanism of action, pharmacokinetics, and pharmacodynamics of the various pharmaceutical agents used in the treatment of glucocorticoid-induced osteoporosis, as well as their efficacy, tolerability and safety, especially in older individuals.