Long-term glucocorticoid (GC) therapy induces glucocorticoid-induced osteoporosis (GIOP) and its associated fractures. Most specialty organizations recommend bisphosphonates as first-line therapies based only on bone mineral density efficacy data. Effective treatment of GIOP based on head-to-head trials with fracture endpoint has not yet been established. The pathophysiologic mechanisms of GIOP that lead to the detrimental effects on bone are not yet fully elucidated. Although GCs in an early and transitory period promote osteoclastic activity, in the current paper, we outline why GIOP is in fact a disease of the bone formation and then provide the rationale for the use of bone-forming agents as first-line therapy for patients with high fracture risk in GIOP.