The skeleton of young animals is profoundly affected by an abnormal amount of vitamin A in the body. In vitamin A deficiency changes in the functional activity of the osteoblasts and osteoclasts allow bone to be deposited in places where it would normally be removed, so producing excessive thickening of certain parts of the skeleton (Mellanby, 1938, 1939). Conversely, excessive vitamin A causes osteoporosis and spontaneous fractures, although the formation of new bone is not inhibited (Strauss, 1934; Wolbach & Bessey, 1942; Irving, 1949). Recent experiments have shown that the vitamin has a direct effect on skeletal tissues grown in vitro. Fell & Mellanby (1952) cultivated the long-bone rudiments of embryonic chicks and mice in medium containing vitamin A in concentrations similar to those found in the blood of animals suffering from hypervitaminosis A; in such explants the cartilage matrix lost its metachromasia and gradually disappeared (chicks, mice) while bone (mice) was rapidly resorbed.
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