Session II - Basic Science

The Death of Articular Chondrocytes after Intraarticular Fracture

Martha M. Murray, MD; Carol Trahan; Mark S. Vrahas, MD, Brigham and Women's Hospital, Boston, MA

Purpose: Posttraumatic arthritis (PTA) is a rapidly developing form of secondary osteoarthritis that often follows injury to a joint. It has long been presumed that impact injury causes PTA, but the mechanism is unknown. Recent work suggests that the triggering of programmed death of chondrocytes (apoptosis) plays a large part in the development of degenerative arthritis. We evaluated the rate of chondrocyte death after a joint impact severe enough to cause an articular fracture.

Methods: Twenty-one articular fracture fragments too small to be used in the surgical reconstruction were obtained from patients undergoing ORIF of intraarticular fractures of the lower extremity during the first two weeks after injury. There were 14 acetabular fractures, 1 femoral condyle fracture, 2 patella fractures, 1 tibial plateau fracture, 2 pilon fractures, and 1 talus fracture. The tissue was fixed, decalcified, embedded, and sectioned perpendicular to the joint surface. Sections were labeled using the TUNEL assay to identify dead or dying cells. Cell counts were performed in three zones of cartilage: deep (within 250 mm of the tidemark), middle (between deep and superficial), and superficial (within 250 mm of the surface).

Results: Dead or dying cells were identified in 19 of 21 fracture fragments, with an average rate of cell death of 37%. A higher percentage of dying cells was seen in the superficial (44 ± 8%) and middle zones (45 ± 8%) of cartilage than in the deep zone (24± 8%, P < 0.02 for both). Rates of cell death higher than 90% were seen in 4 of the 21 specimens studied.

Conclusions: Cell death, or apoptosis, has been implicated as a possible cause for osteoarthritis. This study demonstrates that this process also occurs in articular cartilage after intraarticular fracture. Although rates of apoptosis in osteoarthritis have been reported to average 15%, in the fracture patients we studied, the average rate was more than twice this value (37%). Apoptosis rates in normal cartilage are less than 1%. Thus, in the first 48 hours after trauma to the joint, articular chondrocytes die at an increased rate, one that is more than double that seen in end-stage osteoarthritis. It is believed that apoptosis leads to the release of degradative enzymes, which ultimately destroys the cartilage and leads to arthritis. The high rate of cell death noted in this study may explain the connection between impact injury and posttraumatic arthritis.