Abnormal hyperplasia of chondrocytes in a rat model of glucocorticoid-induced osteonecrosis of the femoral head

OBJECTIVE: The aim of our study was to determine whether abnormal hy-perplasia of chondrocytes occurs in glucocorti-coid-induced osteonecrosis of the femoral head (GC-ONFH) using a well-established rat model.MATERIALS AND METHODS: Rats were in-jected with lipopolysaccharide and methylpred-nisolone to induce GC-ONFH, while control an-imals were injected with saline (12 animals per group). Establishment of the disease model was confirmed using micro-computed tomography and hematoxylin-eosin (HE) staining of femoral head tissue sections. Chondrocyte hyperplasia was detected using HE staining and semi -quan-titated using toluidine blue and saffron O stain-ing. Expression of the autophagy marker LC3B was assessed in cartilage tissues of femoral head using immunohistochemistry.RESULTS: GC-ONFH animals showed signifi-cantly greater area of abnormal chondrocyte hy-perplasia in femoral head tissue sections than control animals. They also showed significantly higher expression of LC3B in articular cartilage of the femoral head.CONCLUSIONS: GC-ONFH may be associat-ed with abnormal chondrocyte hyperplasia in articular surface cartilage, which may be relat-ed to glucocorticoid-induced overactivation of autophagy.

Automated summary

This study used a rat model to investigate the association between glucocorticoid-induced osteonecrosis of the femoral head (GC-ONFH) and abnormal chondrocyte hyperplasia in articular surface cartilage. The results suggest that the abnormal chondrocyte hyperplasia may be related to glucocorticoid-induced overactivation of autophagy.