S21_7

The pathogenesis of glucocorticoid-induced osteoporosis

R.S. Weinstein

Department of Internal Medicine, Division of Endocrinology/Metabolism, The Center for Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA.

ABSTRACT
Decreased bone formation, diminished intestinal calcium absorption and urinary calcium reabsorption, secondary hyperparathyroidism and hypogonadism are some of the proposed mechanisms of the deleterious effects of glucocorticoid excess on bone. Recent evidence suggests that extraskeletal mechanisms may not be essential in steroid-induced osteoporosis and that the major mechanisms of the condition may be a direct result of glucocorticoid administration on the suppression of osteoblastogenesis and osteoclastogenesis and the increased apoptosis of osteoblasts and osteocytes.

Key words
Glucocorticoids, osteoporosis, apoptosis, bone cells, osteonecrosis.

This work was supported by the National Institutes of Health (PO1-AG13918 and RO1-AR46191) and VA Merit Review and Research Enhancement Award Program (REAP) Grants from the Veterans Administration.
Please address correspondence and reprint requests to: Robert S. Weinstein, MD, University of Arkansas for Medical Sciences, 4301 West Markham Street, Slot 587, Little Rock, Arkansas 72205-7199, USA.
E-mail: weinsteinroberts@ exchange.uams.edu