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Research Article Free access | 10.1172/JCI106328

Formation, mineralization, and resorption of bone in vitamin D—deficient rats

D. Baylink, M. Stauffer, J. Wergedal, and C. Rich

1University of Washington School of Medicine and Veterans Administration Hospital, Seattle, Washington 98108

Find articles by Baylink, D. in: PubMed | Google Scholar

1University of Washington School of Medicine and Veterans Administration Hospital, Seattle, Washington 98108

Find articles by Stauffer, M. in: PubMed | Google Scholar

1University of Washington School of Medicine and Veterans Administration Hospital, Seattle, Washington 98108

Find articles by Wergedal, J. in: PubMed | Google Scholar

1University of Washington School of Medicine and Veterans Administration Hospital, Seattle, Washington 98108

Find articles by Rich, C. in: PubMed | Google Scholar

Published June 1, 1970 - More info

Published in Volume 49, Issue 6 on June 1, 1970
J Clin Invest. 1970;49(6):1122–1134. https://doi.org/10.1172/JCI106328.
© 1970 The American Society for Clinical Investigation
Published June 1, 1970 - Version history
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Abstract

Quantitative histologic methods have been devised to measure several processes dealing with formation and mineralization of matrix and bone resorption. In vitamin D-deficient rats, the total osteoblastic matrix formation rate was 20% less and the total osteoclastic bone resorption rate was 80% more than in pair-fed control rats. These changes were found to be primarily because of changes in the rates of matrix formation and of bone resorption per unit area of forming or resorbing surfaces rather than to changes in the areas of these surfaces. The rate of maturation of osteoid and the rate of initial mineralization both were reduced to half of normal in the vitamin D-deficient rats. These variables related to matrix formation and mineralization were significantly correlated with the concentration of calcium but not with the concentration of phosphate in serum. The occurrence of hypocalcemia is interpreted as the consequence, both of reduced calcium absorption and of inadequate resorptive response of bone cells to homeostatic stimuli, such that, although bone resorption was greater than normal, it did not adequately compensate for the reduced intestinal absorption.

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