Glucocorticoid induced osteoporosis

Abstract

Introduction: Glucocorticoid-induced osteoporosis is the most common secondary cause of osteoporosis. Despite this, many patients receiving glucocorticoids are not evaluated for their skeletal health.

Areas covered: Glucocorticoids have profound effects on bone cells, resulting in increases in bone resorption and impairments in bone formation. Bone loss and subsequent increases in fracture risk occur early after the administration of glucocorticoids. Incidence of fractures is highest within the first 6 months of glucocorticoid treatment, and declines with longer exposure. Decreases in bone mass follow a dose-dependent relationship with glucocorticoid dosage. Pharmacologic prevention and treatment for osteoporosis are recommended for all patients receiving glucocorticoids. Oral bisphosphonates, with concomitant vitamin D and calcium supplementation, are considered as the first-line treatment option. However, a number of alternative treatment options, including intravenous bisphosphonates, anabolic agents, and denosumab have all proven efficacy in increasing lumbar spine or hip bone mineral density. The mechanism of action and recent controlled trials for these therapies are reviewed. The literature search was conducted within PubMed in November 2018. 492 articles were found and 45 were included.

Expert opinion: Future studies will likely evaluate the safety profiles of alternative treatments, while focusing on its ability to reduce fracture risk.

Keywords: Glucocorticoid; bisphosphonate; denosumab; osteoporosis; teriparatide.