A histopathological study of the condylar cartilage in experimental osteolathyrism
Several changes of the chondrocyte
1984 Volume 30 Issue 4 Pages 392-398
Details
1984 Volume 30 Issue 4 Pages 392-398
Recently, peculiar changes in the epiphyseal cartilage of growing rats with osteolathyrism have drawn much attention.
In this study, the proliferation and differentiation of mandibular cartilage as well as the disturbance of endochondral bone formation in this pathology were examined.
This study was thus performed in experimentally induced osteolathyrismic rats using aminoacetonitrile (ANN).
Experimental methods:
Growing Wister male rats of 4 weeks post partum were used as experimental animals, 2% ANN in physiological saline solution was given to all rats at a dose level of 20mg per 100g body weight per day for 7 days in succession by intraperitoneal route in order to produce osteolathyrism.
Some experimental aminlas were sacrified by decapitation on 1, 3 and 6 days after ANN dosing respectively, and each sample was examined soft-radiographically, light-microscopically and electro-microscopically.
Experimental results:
The growth of rats was predominantly suppressed around 3 days after ANN administration, showing an intensive systemic distrubance.
In the craniofacial bone specimens from rats continuously received ANN for 7 days, retarded growing was seen.
Histopathologically, almost no change occurred in rats given ANN for 1 day but a suppressed proliferation of fibroblasts which normally differentiate to chondrocytes was observed in the mandibular cartilage of rats sacrified 3 days after ANN administration. In rats sacrified 7 days after ANN, decreased numberof chondroblasts and chondrocytes with thinned chondocyte zone appeared. Among these chondrocytes, deformed nuclei and invaginated nuclear membrane were observed. On the other hand, poorly developed mitochondria, rough endoplasmic reticulum and Golgi's apparatus were found is some cytoplasmic organellae, suggesting abnormal cell metabolism. In addition, the boundary between hypertrophic chondrocyte zone and bone marrow epiphysis was irregular, and decrased fine bone trabecular formation was observed.
These findings suggest that abnormal endochondral bone formation was caused by ANN.
