Histomorphometric profile, pathophysiology and reversibility of corticosteroid-induced osteoporosis

Abstract

Histomorphometric data were collected on undecalcified iliac crest biopsies taken from 5 patients with Cushing's syndrome and 70 osteoporotic patients who had received long-term corticosteroid (CS) treatment. The reversibility of the bone changes induced by CS in two of the patients with Cushing's syndrome was analyzed using dynamic bone histomorphometric methods employing tetracycline double labelling in biopsies taken 3 months after adrenalectomy. The histomorphometric profile of CS osteoporosis was characterized by a marked reduction of trabecular bone volume in comparison to sex and age-matched controls. Trabecular resorption surfaces were increased moderately, as was the mean size of periosteocytic lacunae. Measurement of osteoid parameters showed an increase of trabecular osteoid surfaces and a decrease in the osteoid seam thickness index, while tetracycline double labelling analysis demonstrated a marked depression of the osteoblastic appositional rate. The concentration of serum parathyroid hormone was increased and the serum 25-OH D 3 was reduced. Postadrenalectomy-biopsies revealed a dramatic renewal of osteoblastic activity with extended osteoid surfaces and normal appositional rate, resulting in a positive bone tissue balance. These results indicate that CS's induce bone rarefaction mainly by decreasing osteoblastic activity at the cell level. However, the bone loss is probably magnified by secondary hyperparathyroidism which increases the birthrate of basic multicellular bone remodelling units. This hyperparathyroidism is very likely caused by an impairment of intestinal calcium absorption.