Observations Suggesting a Local Factor in Pathogenesis and. Healing of Rickets.

Abstract

The pathogenesis of rickets is a moot question. By many it is believed that this disorder is entirely of systemic origin and that the local lesions at the epiphyses are secondary in nature. This point of view has been fortified by the demonstration that a low concentration of inorganic phosphorus in the blood is one of the most constant phenomena of rickets in infants and in animals. There can be no doubt of the participation of the systemic factor. However, as we have pointed out from time to time, rickets may come about occasionally in infants and in animals in spite of the fact that the calcium and the phosphorus in the blood have remained at normal levels. In rats this relationship was noted most often when about 10% dried milk was added to the standard rickets-producing ration. Furthermore, it was observed that the lesions of rickets may fail to become manifest in some infants and animals which are poorly nourished, although the phosphorus in the blood is definitely below the non-rachitic level. This incongruity was noted in some instances among rats which had been fed the Sherman-Pappenheimer diet, which is deficient in several nutritional factors.

Last year this subject was again brought to our attention by the occurrence of a mild degree of rickets in some infants, notwithstanding the fact that they were well nourished and that the calcium and phosphorus content of the blood remained practically unaltered. These infants should have been fully protected as they were fed irradiated dried milk. On further investigation, it was found, however, that this milk had been insufficiently activated, due to a technical error in the course of irradiation.

More recently we found that the subject was open to investigation by means of animal experiment.