Nitric oxide-associated chondrocyte apoptosis in trauma patients after high-energy lower extremity intra-articular fractures

The primary goal of this study was to identify nitric oxide (NO)-induced apoptosis in traumatized chondrocytes in intra-articular lower extremity fractures and the secondary goal was to identify the timeline of NO-induced apoptosis after injury. Materials and

The data showed the involvement of NO-induced apoptosis of chondrocytes after high-energy trauma, which decreased with time from injury.

This is a prospective collection of samples of human cartilage harvested at the time of surgery to measure apoptotic cell death and the presence of NO by immunohistochemistry. Three patients met the criteria for control subjects and eight patients sustained high-energy intra-articular fractures and were included in the study. Subjects who sustained intra-articular acetabular, tibial, calcaneal and talus fracture had articular cartilage harvested at the time of surgical intervention. All 8 patients underwent open reduction and internal fixation of the displaced intra-articular fractures. The main outcome measures were rate of apoptosis, degree of NO-induced apoptosis in chondrocytes, and the timeline of NO-induced apoptosis after high-energy trauma.

The percentage of apoptotic chondrocytes was higher in impacted samples than in normal cartilage (56 vs 4 %), confirming the presence of apoptosis after intra-articular fracture. The percentage of cells with NO was greater in apoptotic cells than in normal cells (59 vs 20 %), implicating NO-induction of apoptosis. The correlation between chondrocyte apoptosis and increasing time from injury was found to be -0.615, indicating a decreasing rate of apoptosis post injury. Conclusions: The data showed the involvement of NO-induced apoptosis of chondrocytes after high-energy trauma, which decreased with time from injury.