Vitamin A and bone growth : the reversibility of vitamin A-deficiency changes / by E. Mellanby.

  • Mellanby, Edward, Sir, 1884-1955.
Date:
[1947?]
Catalogue details

Licence: In copyright

Credit: Vitamin A and bone growth : the reversibility of vitamin A-deficiency changes / by E. Mellanby. Source: Wellcome Collection.

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    In the Croonian Lecture of 1943 it was shown that a -A diet produced a thick cancellous basi-occipital bone, the abnormal thickness of which was caused largely by lack of absorption of surface 1; indeed, actual deposition of additional bone on this surface (Text-fig. 1) could be seen at certain early stages of growth on these deficient diets. It appeared that absorption was greatly reduced or had even ceased because the osteoclasts, normally active and abundant in this position during growth, gave way to active osteoblasts. Conversely, on surface 2 osteoblastic activity had ceased and been succeeded by osteoclastic activity. This is shown in PI. 2 a, 6, photomicrographs of mesial sagittal sections of the basi-occipital bone. Vitamin A deficiency caused but little change on surfaces 3 and 4, so that the outer table of bone continued to grow normally and therefore to withdraw from the inner table, with the consequent enlargement of the marrow cavity and thickening of the bone. The above facts apply to dogs killed when 20-30 weeks old, which, judged by their behaviour during life, had been depleted of vitamin A stores for 8 or more weeks. In older animals the rate of growth of the basi-occipital bone diminishes and the differences between the number and activity of osteoclasts and osteo¬ blasts on surfaces 1 and 2 in -1- A and - A dogs, although still evident, are not as obvious as in the younger animals (see PI. 3a, 6, compared with PL 2a, b). Drawings of coronal sections of the central portion of the basi-occipital bone of older -f A and - A litter-mates, animals which were 33 weeks old at death, can be seen in PL 4. In the -I-A dog (PL 4a), which had 6000 i.u. vitamin A daily, the inner and outer tables of bone have fused to form a compact structure and the marrow cavity has been eliminated. In the - A dog (PL 46) the bone is cancellous, with a large marrow space, and surface 1 is almost flat as compared with that of the -1- A animal, which is modelled to the natural shape of the brain stem. It will be seen that on this surface in the -b A dog there are still abundant osteoclasts which are more numerous in the centre than at the sides, a fact which may account for the hollowing near the midline. In the - A dog, on the other hand, there are osteoblasts at work, but no active osteoclasts. Thus, so far as surface 1 is concerned, the absence of vitamin A, as in the younger animLl previously described, has reversed the type of bone cell at work. Surface 2, however, of the older - A dog (PL 46) is different from that of the younger animal (PL 26) in that there are no active osteoclasts. It is indeed interesting that the fusion of the inner and outer tables of bone in the -b A dog appears to be accompanied in the corresponding - A animal with the disap¬ pearance of all active bone cells, both osteoclasts and osteoblasts, from surfaces 2 and 3 (PL 46). In the case of surface 4, there are only a few scattered active osteoclasts left in the -bA animal (PL 4a), whereas in the -A there are no osteoclasts and only a few active osteoblasts laterally (PL 46). The basi-occipital bone of a litter-mate which was killed at about the same age, having received an A-deficient diet for 24 weeks of the experiment and.