Abstract

Investigation of 20 patients with skeletal fluorosis showed that five had clear evidence of secondary hyperparathyroidism. The hyperactivity of the parathyroid glands in skeletal fluorosis in the presence of decreased solubility of the bone mineral (fluoroapatite) strongly suggests that it is a compensatory attempt to maintain a normal extracellular ionized calcium equilibrium. Further study of the parathyroid glands and of bone lesions in skeletal fluorosis is in progress.