Pathogenesis and Treatment of Glucocorticoid-Induced Osteoporosis

ISSN： 1170-229X

Source： Drugs & Aging, Vol.12, Iss.6, 1998-06, pp. : 477-484

Disclaimer: Any content in publications that violate the sovereignty, the constitution or regulations of the PRC is not accepted or approved by CNPIEC.

Previous Menu Next

Abstract

Aging is associated with a marked decline in bone mineral density (BMD), an increased likelihood of falling and a much greater propensity for fracture. Several factors contribute to aging-related bone loss, including reduced bone formation, increased bone resorption, recent bodyweight loss, poor nutritional status and the coexistence of other, often rheumatological, conditions. Any of these factors can lead to an uncoupling of the bone remodelling unit. In addition, the frequent use of glucocorticoids to treat a vast array of conditions has contributed to an ever-expanding group of elderly individuals who are at extremely high risk for spine and hip fractures. Owing to the surprisingly high morbidity and mortality associated with these fractures in the elderly, an understanding of the pathogenesis and epidemiology of glucocorticoid-induced osteoporosis is paramount. The factors that contribute to bone loss in older individuals treated with glucocorticoids include reduced muscle mass, poor nutrition, hypogonadism, vitamin D deficiency and secondary hyperparathyroidism. Recent studies suggest that a prophylactic approach to this problem could have a huge impact on the medical, social and economic costs of osteoporosis.