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Am J Physiol Endocrinol Metab 264: E938-E942, 1993;
0193-1849/93 $5.00
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AJP - Endocrinology and Metabolism, Vol 264, Issue 6 E938-E942, Copyright © 1993 by American Physiological Society

ARTICLES

Salmon calcitonin reduces vertebral bone loss in glucocorticoid-treated beagles

K. W. Lyles, T. W. Jackson, T. Nesbitt and L. D. Quarles
Geriatric Research Education and Clinical Center, Veterans Affairs Medical Center, Durham 27705.

Glucocorticoids induce bone loss by increasing bone resorption and decreasing bone formation. In this study we have investigated the potential of salmon calcitonin to attenuate glucocorticoid-induced bone loss in a dog model. Male beagles were divided into three groups: 1) untreated controls, 2) prednisone-treated dogs (1 mg.kg-1.day-1 orally), and 3) prednisone-calcitonin-treated dogs (1.5 U.kg-1.day-1 calcitonin subcutaneously and 1 mg.kg-1.day-1 prednisone orally). Assessment of bone mass by dual energy X-ray absorptiometry demonstrated that bone density remained stable in controls throughout 48 wk. Prednisone-treated dogs lost 13.2% of their initial bone mass by 48 wk. Concomitant calcitonin treatment attenuated prednisone-induced bone loss to only 3.2% at 48 wk. Bone histomorphometry of the spine showed reduced trabecular bone volume in prednisone-treated dogs, whereas control and prednisone-calcitonin-treated animals maintained normal trabecular bone volume. Both prednisone- and prednisone-calcitonin-treated dogs acquired a defect in osteoblastic function as evidenced by a reduction in mean wall thickness and trabecular thickness. Thus calcitonin attenuates the early bone loss induced by glucocorticoids. However, calcitonin failed to prevent glucocorticoid-induced osteoblast dysfunction.


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