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Bone Growth in the Hypovitaminotic a Calf¹

Institute of Nutrition and Food Science, and Storrs (Conn.) Agricultural Experiment Station, University of Connecticut, Storrs, Connecticut 06268

Abnormal bone in growing hypovitaminotic A animals has been attributed to altered endochondral growth, faulty appositional growth, and interference with normal resorption and remodeling. In an attempt to resolve these conflicting findings, bone growth was quantitatively estimated in 16 Holstein male calves fed either 8 or 108 µg vitamin A per kilogram of live weight daily for 16 weeks. The deficient animals (8 µg intake) had low plasma vitamin A concentrations, elevated cerebrospinal fluid (CSF) pressures, impaired absorption of CSF, papilledema and squamous metaplasia of the parotid gland ducts. The volumes of the cranial vaults and the brain weights were less in deficient animals, but when the latter criterion was expressed as weight per unit live weight, the difference was not significant. The dura mater in the hypovitaminotic A calves was thicker over the anterior cerebellum, tentorium cerebelli and in the area of the lumbar vertebrae. While total volumes of the vertebrae of the two groups were similar, the deficient animals had smaller spinal canals and smaller ratios of canal to total volume. Metacarpal diaphyseal sections, labelled with tetracycline and 2,4-bis[N,N'-di(carboxymethyl)aminomethyl]fluorescein, of hypovitaminotic A calves had a significantly increased growth rate in the anterior lateral cortex. The vertebrae of deficient animals tended to have less bone and more osteoid. The results are in accord with the hypothesis that in hypovitaminosis A increased osteoblastic activity results in altered bone growth. Osteoclastic activity appeared to be unaffected.

² Present address: School of Veterinary Science and Medicine, Purdue University, Lafayette, Ind.

Manuscript received 1 August 1969.

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