Growth rates of epiphyseal plates in normal kittens and in kittens fed excess vitamin A: A fluorescent labelling and histological study

Abstract

The growth and structure of epiphyseal plates was studied in normal kittens, and in kittens given an excess of vitamin A for 7 days prior to necropsy. Growth measurements were made on 10 different epiphyseal plates from each animal by means of in vivo labelling with a fluorescentdye. It was found that the growth of all plates was retarded in kittens which had received an excess of vitamin A. The absolute retardation of growth of each plate was directly proportional to its normal rate of growth as assessed in the control animals. The opposite limbs of each kitten were used for the study of histopathological changes and the measurement of various cellular parameters. Epiphyseal plates from the test animals were reduced in depth, contained fewer chondrocytes arranged in shorter, irregular columns and the hypertrophic cells were smaller. The cartilaginous matrix exhibited a diffuse loss of basophilia and of metachromasia, and coarse fibrillation. Measurements of growth rate and various cellular parameters were used to calculate the rate of cell formation per column and the average cell life span in epiphyseal plates from the control animals. Owing to the rapid development of pathological changes upsetting the state of dynamic equilibrium in the test plates, similar estimations in these would not have been valid. However, arguments are presented to suggest that an excess of vitamin A retards the growth of epiphyseal plates by affecting the rate of formation of new chondrocytes and, either directly or indirectly, the maximum size reached by the chondrocytes in the hypertrophic cell zone. It was further concluded that, although differential susceptibility of certain epiphyseal plates to an excess of vitamin A has been reported in kittens dosed for longer periods, it is most likely that vitamin A primarily affects epiphyseal plates in proportion to their normal rates of growth. With increasing time secondary factors probably act on the abnormal plates, accounting for differences in the severity of lesions exhibited by them. Reasons are put forward to suggest that the stress of weight bearing may well be the most important factor involved in this process.