Osteoporosis increases chondrocyte proliferation without a change in apoptosis during fracture healing in an ovariectomized rat model.

Abstract

Osteoporotic fractures commonly occur in the elderly. Current studies regarding cell proliferation and apoptosis during osteoporotic fracture healing are limited. In this study, we established an osteoporotic fracture healing model. Bone loss and callus formation were monitored with DXA, cell proliferation was examined using immunohistochemistry with BrdU monoclonal antibody and apoptotic cells were detected using the TUNEL method. Both cell proliferation and apoptosis occurred during the entire period of the study. BrdU immunostaining showed a decreasing tendency in the process of fracture healing. On days 20 and 30 post-fracture, the percentage of BrdU-positive cells in ovariectomized rats was significantly higher compared to sham-operated rats. TUNEL-positive chondrocytes reached a peak on day 20 post-fracture. There was no significant difference between the two groups. Our results indicate that osteoporosis markedly delays the fracture healing process, mostly due to increased chondrocyte proliferation without a change in chondrocyte apoptosis.