Defects in the growth plate of brachypodism in mice--light and electron microscopic findings and cell proliferation by the method of tritiated thymidine autoradiography.

The basic defect of the human chondrodystrophies with normal chondro-osseous histopathology is speculated to be quantitative decrease in the rate of ossification. Homozygous brachypodism (brp/brp), chondrodystrophic mutant in mice, is characterized by shortening long bones. The light and electron microscopic observations of the growth plate were essentially normal. The method of tritiated thymidine autoradiography showed that the rate of chondrocyte division in the mutant growth plate was decreased. These findings show that the failure of chondrocytes to divide at a normal rate can produce the growth disturbance of bone without abnormal chondro-osseous histopathology.