Abstract
Canal 1 showed that calcium fails to be deposited in the callus following fracture in parathyroidectomized rats, and Morel 2 noticed a similar defect in cats. Erdheim 3 concluded that the deficient calcification in the callus throughout the skeleton of parathyroidectomized rats resembles that of rickets and osteomalacia. The above experiments were conducted when exact knowledge of dietary requirements were wanting and hence, there is a possibility that the diet may have contributed to the failure of calcification in the callus in the presence of a parathyroid deficiency. The following experiments were conducted to ascertain the effect of alterations in the calcium and phosphorus diet and of viosterol on callus calcification.
The procedure and diets have been briefly described. 4 The radii and ulnae of rats were fractured while under amytal anaesthesia. The rats were placed on a low calcium diet until tetany developed and then they were divided into groups according to the diet they were to receive. X-rays of the fractured bones were taken weekly until the rats were killed.
The results may be summarized as follows:
1. (a) Low calcium diet. In spite of the low calcium diet the calcification of the callus progressed moderately within 30 days as evidenced by X-ray. The serum calcium in this group remained low and the animals continued to have tetany.
(b) When 1% CaCO3 was added to the diet, the calcification in the callus seemed somewhat denser.
(c) Stock diet. Very good calcification of the callus was observed within 20 days.
(d) Steenbock rachitogenic diet. In spite of its being a ricketsproducing diet, the calcium deposition in the callus was marked.
(e) High phosphorus and low calcium diet. The deposition of calcium salts was very poor, even after a month.
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