Rate of Decalcification and the Sites of Bone Lesions in Experimental Hyperparathyroidism. ∗

Abstract

A relatively rapid rate of mineral metabolism is associated with rapid bone growth in young animals. Our studies in acute and chronic experimental hyperthyroidism have shown a greater susceptibility to parathormone and a more rapid excretion of calcium in the young than in the adult. 1 , 2

Bauer, Aub and Albright 3 stated that in bone resorption the calcium of the trabeculae is “labile” and is drawn upon in the first instance, while the calcium of the compact bone (“the structural part of the bone”) becomes available only “in the case of unusual body demands.” Our studies suggest another conception: If we are to speak of labile calcium, it is the calcium in the regions of most active growth; if we are to speak of less readily available calcium, it is the calcium in the regions of less active growth.

We have examined the skeletons of about 150 young guinea pigs, 50 old guinea pigs, 25 young dogs, and 10 rats. The so-called characteristic lesions were severest and most easily produced in young animals suffering from acute and chronic hyperparathyroidism. The bones and portions of bones most affected were the metaphyses of the long tubular bones, and the cortex of the shaft, particularly near the epiphyseal cartilage plates; the costochondral junctions, and the cortex of the ribs used most in the respiratory act; the bones of the skull and of the lower jaw. The metaphyses of the slower growing short tubular bones showed relatively few lesions; the cortex of the shafts of these bones showed practically none. In the guinea pig, most epiphyses are already formed and the centers of ossification for the tarsal and carpal bones are present at birth. No specific lesions were found in these bones, at most a simple atrophy of their trabeculae was observed.