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La osteoporosis esteroidea es la causa más frecuente de osteoporosis secundaria. La exposición a altas dosis de glucocorticoides produce una disminución en la densidad mineral ósea que conlleva un mayor riesgo de fracturas vertebrales y de cadera. Sin embargo, los mecanismos de acción de los glucocorticoides sobre el tejido óseo no se conocen con detalle. Los glucocorticoides en dosis suprafisiológicas actúan fundamentalmente sobre el hueso, disminuyendo el número de osteoblastos, y por ende, la formación ósea. Estudios recientes han demostrado que los glucocorticoides también afectan directamente al osteocito y al osteoclasto. Glucocorticoid-induced osteoporosis is the leading cause of secondary osteoporosis. Patients exposed to high doses of glucocorticoids have decreased bone mineral density, this entailing greater risk of vertebral and hip fractures. Nevertheless, the molecular mechanisms of glucocorticoid-induced osteoporosis on bone tissue are not well known. Supra-physiological doses of glucocorticoids mainly act on the bone, decreasing osteoblast number and therefore bone formation. Recent studies have also shown that glucocorticoids also have direct effects on osteocytes and osteoclasts.
Glucocorticoid-induced osteoporosis is the leading cause of secondary osteoporosis. Patients exposed to high doses of glucocorticoids have decreased bone mineral density, this entailing greater risk of vertebral and hip fractures. Nevertheless, the molecular mechanisms of glucocorticoid-induced osteoporosis on bone tissue are not well known. Supra-physiological doses of glucocorticoids mainly act on the bone, decreasing osteoblast number and therefore bone formation. Recent studies have also shown that glucocorticoids also have direct effects on osteocytes and osteoclasts.
