Histological changes in the epiphyseal plate of growing young adult male rats after long-term hydrocortisone and salmon calcitonin administration

Abstract

Introduction: Glucocorticosteroids decrease the longitudinal growth of bones. It has been reported that skeletally immature rats on calcitonin treatment grow longer and slimmer. The aim of this study was to assess whether concomitant treatment with calcitonin would influence longitudinal growth and histology of epiphyseal plate in hydrocortisone-treated rats.
Material and methods: Fifty six growing male Wistar rats were randomly divided into two control and four experimental groups. Rats in the first two experimental groups were treated i.p. b.i.d. with hydrocortisone, while to the other experimental animals salmon calcitonin s.c. was administered concomitantly. The controls received appropriate vehicula. The rats were kept under standardised conditions. The first phase of the experiment was completed after 28 days and right femora and tibiae were harvested from groups and preserved in 4% buffered formalin. Lengths of the fresh femora were measured with an electronic caliper. After preservation, tibial bones were decalcified in 5% EDTA at room temperature. Paraffin-embedded coronal slices 10 μm thick from proximal tibia were taken and stained with hematoxylin/ eosin and alcian blue for histological assessment of the epiphyseal plate. A similar procedure was repeated after 56 days in the second phase of the experiment.
Results: The femora of hydrocortisone-treated rats were significantly shorter than those of controls, but after concomitant administration of salmon calcitonin the difference was insignificant. The histological assessment showed that depressed function of growth plate in hydrocortisone-treated animals after both phases of the experiment was partially reversed by salmon calcitonin treatment.
Conclusions: Prolonged concomitant treatment with high-doses of salmon calcitonin partially reverses glucocorticoid-induced depression of rat growth plate. (Pol J Endocrinol 2011; 62 (1): 18-23)