Abstract

THE changes in bone in avitaminosis A have been reported by Mellanby1, Wolbach and Bessey2, and Wolbach3, who consider that the vitamin is concerned with the control of bone modelling. Mellanby found excessive formation of bone in certain areas during avitaminosis and that the osteoblasts and osteoclasts could reverse their positions at the effective bony surfaces. Wolbach3 considered that appositional bone formation continued in the normal site, but that concurrent resorption of bone ceased. Excessive doses of vitamin A have been found by many writers to cause spontaneous fractures of bones and internal haemorrhages (see Moore and Wang4 for a review of the literature). Wolbach3 considered that bone remodelling was greatly accelerated and that a defective tissue was laid down.

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