Experimental osteoporosis in the rat induced by a hypocalcic diet.

The administration of a diet deficient in calcium in the rat quickly produces a reduction in the skeletal mass, with narrowing of the diaphyseal cortex, and less density of the metaphysis. The bone mineral content, determined by a double ray photonic mineralometer, is significantly lower as compared to controls, while histological examination does not reveal defects in calcification. The pathogenetic mechanism is characterised by stimulation of the parathyroid glands in response to a decrease in plasma calcium determined by the insufficient diet. We observed a bone response in two phases: the first, with elevated velocity of remodelling and prevalence of osteoclastic resorption despite the presence of intense osteoblastic activity; the second, with reduced bone remodelling (except for the metaphyseal area). Although these observations do not imply that human osteoporosis involves the same pathogenetic mechanism, it appears possible to use this experimental model to study the effects of endocrine and pharmacological factors on the activity of bone remodelling, which also in human osteoporosis is characterised by the prevalence of osteoclastic resorption.