Histological disorders related to the focal disappearance of the epiphyseal growth plate in rats induced by high dose of vitamin A

Citation
S. Soeta et al., Histological disorders related to the focal disappearance of the epiphyseal growth plate in rats induced by high dose of vitamin A, J VET MED S, 62(3), 2000, pp. 293-299
Citations number
20
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
JOURNAL OF VETERINARY MEDICAL SCIENCE
ISSN journal
09167250 → ACNP
Volume
62
Issue
3
Year of publication
2000
Pages
293 - 299
Database
ISI
SICI code
0916-7250(200003)62:3<293:HDRTTF>2.0.ZU;2-4
Abstract
The histological disorders related to the focal disappearance of the epiphy seal growth plate were examined histochemically in the proximal tibia of ra ts administered a high dose of vitamin A. Animals were given 100,000 IU/100 g body weight/day of vitamin A for 5 days from 4 weeks after birth (VA rat s) or given deionized water as control and sacrificed on Day 12 and 19 of t he experiment. Tibiae were examined by immunohistochemistry for type I, II and X collagens, lectin-histochemistry for Helix pomatia and backscattered electron imaging. On Day 12, the abnormally developed calcified cartilage m atrix was detected within the epiphyseal growth plate in VA rats. The uncal cified cartilage matrix contained type I collagen but lacked type II collag en. In addition, the eroded regions accompanied with numerous osteoclasts a nd osteoblasts were detected in the epiphyseal growth plate. On day 19, ero ded regions penetrated the epiphyseal growth plate to result in its focal d isappearances with the eroded surfaces entirely covered with bone tissue in VA rats. These findings suggested that the cartilage matrix of the epiphys eal growth plate was abnormally calcified and showed the phenotypes like bo ne matrix. The eroded regions of the epiphyseal growth plate seemed to be c aused by the invasion of osteoclasts into the altered cartilage matrix and might develop to the focal disappearances by the modeling or remodeling due to action of osteoclasts and osteoblasts.