Glucocorticoid-associated osteoporosis in chronic inflammatory diseases: epidemiology, mechanisms, diagnosis, and treatment.

Children with chronic illnesses such as Juvenile Idiopathic Arthritis and Crohn's disease, particularly when taking glucocorticoids, are at significant risk for bone fragility. Furthermore, when childhood illness interferes with achieving normal peak bone mass, life-long fracture risk is increased. Osteopenia and osteoporosis, which is increasingly recognized in pediatric chronic disease, likely results from numerous disease- and treatment-related factors, including glucocorticoid exposure. Diagnosing osteoporosis in childhood is complicated by the limitations of current noninvasive techniques such as DXA, which despite its limitations remains the gold standard. The risk:benefit ratio of treatment is confounded by the potential for spontaneous restitution of bone mass deficits and reshaping of previously fractured vertebral bodies. Bisphosphonates have been used to treat secondary osteoporosis in children, but limited experience and potential long-term toxicity warrant caution in routine use. This article reviews the factors that influence loss of normal bone strength and evidence for effective treatments, in particular in patients with gastrointestinal and rheumatologic disorders who are receiving chronic glucocorticoid therapy.