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THE purpose of this paper is to set forth the evidence upon which is based the view that generalized osteitis fibrosa (von Recklinghausen) is a disease of endocrine origin. According to this view the changes in the bones are due to hyperparathyroidism, a condition associated with hyperfunction of a parathyroid tumour. Four such cases are described, and in three the effects of removal of a parathyroid tumour are recorded. Four cases of focal osteitis fibrosa are described in order to place on record the absence of any evidence of hyperparathyroidism in this disease. Finally, a case of osteomalacia is recorded. Here the blood chemistry, metabolism, and histology suffice to show that osteomalacia and generalized osteitis fibrosa are unrelated diseases. EFFECTS OF TEE PARATHYROID HORMONE.The parathyroid glands exert a specific effect upon calcium metabolism. Thc pioneer work of MacCallum and Voegtlin (1909) demonstrating a reduction of serum calcium in dogs after parathproidectomy has been abundantly confirmed. It is well established that this condition is relieved by the administration of calcium salts. The idea that it is due to guanidine intoxication remains unsupported by adequate evidence.Since the isolation by Hanson (1924) and Collip (1925) of the active principle of the parathyroid gland (parathormone) it has been repeatedly demonstrated that the injection of the extract causes an elevation of the serum calcium. Brehme and Gyorgy (1927) found that parathormone lowers the blood phosphorus and shifts the pH of the blood towards the acid side without affecting the CO, combining power of the blood. Reiss (1928) and Aub (1928) found independently that parathormone lowers the level of the blood phosphorus. This appears to be the first action, the elevation of serum calcium following only after a long latent period. Whether the effect on phosphorus is the primary effect of parathormone remains for further work

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