EXPERIMENTAL RICKETS IN RATS : IV. THE EFFECT OF VARYING THE INORGANIC CONSTITUENTS OF A RICKETS-PRODUCING DIET

1. Rachitic bone lesions may be produced in rats by a diet containing an excess of calcium, but deficient in phosphates. 2. Similar lesions follow a diet deficient in calcium, but containing an excess of phosphates. The endochondral lesions, however, are less pronounced. 3. A diet deficient in both calcium and phosphate induces atypical rickets. 4. Inorganic salts other than calcium or phosphate seem to be without influence upon the development or prevention of rachitic lesions. 5. The minimal amount of phosphate (calculated as P) required for normal calcification in young growing rats (30 to 50 gm.) on the diets used in these experiments is approximately 160 mg. per 100 gm. of diet. At 135 mg. individual variations come into play; at 110 mg., or less, rickets invariably follows. 6. An excess of calcium is not necessary to the production of the rachitic lesions. A reduction of the calcium lactate of Diet 84 to 0.6 per cent (111 mg. of Ca per 100 gm. of diet) still results in the development of typical rickets. 7. Adult rats react to a deficiency of phosphate in the diet by the production of calcium-free osteoid in abnormal amount about the spongiosa and cortex. There is not produced any alteration of the epiphyseal cartilage, as in growing animals.