Studies of Bone of Patients with Hyperparathydroidismi by Means of Phosphate Exchange Experiments in Vitro

The history of the interpretation of osteitis fibrosa cystica generalisata as it was described in 1891 by von Recklinghausen (1) explains why the skeletal abnormalities were for so long considered to be the focal point of the clinical concept "hyperparathyroidism." During the 1930's, however, it was observed that many patients with hyperparathyroidism showed no bone abnormalities on either histological or roentgenological examination (2). Recent publications show that only in one-third of the patients with hyperparathyroidism can skeletal deviations be demonstrated roentgenologically (3). This is remarkable, since a direct effect of parathormone on the skeleton has been established. It was demonstrated by treating nephrectomized rats with parathyroid extract (4), and by implanting parathyroid tissue under the skull of the mouse (5). Finally, it was shown that a cell-free parathyroid extract has a direct effect on tissue cultures of the parietal bone of mouse embryos and this by a reinforcement of the osteoclastic bone resorption (6). The discrepancy between the clinical data and the pathophysiology of hyperparathyroidism might be explained by the assumption that the accelerated bone destruction caused by the hormone of the parathyroid gland is compensated for by an increase in bone production. If this hypothesis is correct, on the average, the bone of patients with hyperparathyroidism would be younger than bone of normal individuals of the same age. Evidence which supports this assumption has been found in animal experiments by using qualitative microradiography (7). Using autoradiography, Engfeldt and Hjertquist (8) showed in 1954 that radioactive labeled phosphate is taken up in bone from a surrounding fluid, especially in young structures, and such