Abstract
In a recent paper Kay 1 states that he observed an increase in plasma phosphatase following fracture, and indirectly he suggests a similar rise in bone phosphatase. In view of our findings on the breaking strength of fractured fibulae of rats, 2 we were of the opinion that a positive correlation existed between the breaking strength and bone phosphatase. This we sought to demonstrate. It was also believed that if the activity of phosphatase in the healing process of fractures is antagonized, after the primary callus has formed on the fifteenth day, by the hormone of the parathyroid gland, as we suggested else where, 2 that subsequent to the fifteenth day the bone phosphatase should be reduced.
The method of selecting, feeding and fracturing the right fibulae of the albino rats has been described. 2 The bone phosphatase of the combined unfractured left fibula and tibia, as well as the bone phosphatase of the combined fractured right fibula and its tibia, were estimated by a method personally suggested by Kay, 1 the details of which will be published later. The results are tabulated in Table I.
Our findings, incomplete as they are, strongly indicate that the level of bone phosphatase in the fractured fibula rises with the formation of the primary callus and falls as the medullary space is developed. The rapid loss of callus strength during the formation of the medullary space, between the fifteenth and twenty-first days, has been suggested elsewhere as being due to a powerful circulatory decalcifying substance which may possibly be the parathyroid hormone. 2 The sharp reduction in the phosphatase content of the fractured right fibula and its normal tibia, subsequent to the formation of the primary callus on the fifteenth clay, and during the formation of the medullary cavity, suggests that an actual antagonism does exist between phosphatase, and this at present unknown decalcifying substance.
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