Estrogen deficiency leads to decrease in chondrocyte numbers in the rabbit growth plate

In the pubertal growth plate, sex hormones play important roles in regulating the proliferation, differentiation, maturation, and programmed death of chondrocytes. Although many studies have been reported on the regulation of estrogen in long-bone growth, some of the mechanisms have remained unclear, including its role in cell kinetics in growth plate chondrocytes. The aim of this study was to clarify the effect of a deficiency of estrogen on growth plate chondrocytes.

We obtained growth plates of the femoral head from normal and ovariectomized Japanese white rabbits at 10, 15, 20, and 25 weeks of age. The effects of estrogen deficiency on the cell kinetics of growth plate chondrocytes were investigated immunohistochemically using antibodies for an apoptotic marker, caspase-3, and for proliferating cell nuclear antigen (PCNA).

Both the length of the femur and the height of the growth plate in the ovariectomized rabbits tended to be larger than those in the normal rabbits. There were fewer chondrocytes in the ovariectomized rabbits than in the normal ones. Caspase-3-positive cells were detected mainly in the hypertrophic zone, whereas PCNA-positive cells were found in the proliferating to upper hypertrophic zones. The ovariectomized rabbits showed a higher caspase-3-positive rate at 20 weeks of age and a lower PCNA-positive ratio in all age groups than the normal rabbits.

This study indicated that ovariectomy led to a decreased number of growth plate chondrocytes, which resulted from decreased cell-proliferating ability and probably acceleration of the number of chondrocytes undergoing apoptosis.