A rat model of chondrocyte death after closed intra-articular fracture.

OBJECTIVE: The development of osteoarthritis after intra-articular fractures has been described for decades, although the exact mechanical and cellular changes that occur remain poorly understood. There are several animal models to study this phenomenon, but they are mechanistically different from physiologic fractures in several important ways. This article describes a novel model that recreates the kinematics present in high-energy trauma and intra-articular fractures. METHODS: We designed a "drop tower" for the creation of intercondylar femoral fractures in rats and tested it on cadaveric rats to determine the optimal kinetic parameters. Intra-articular fractures were then created in live rats and the animals were killed at 0, 24, and 72 hours after the fracture. Cartilage samples were obtained for live/dead staining, and the relationships among fracture time, cartilage depth, and cell viability were evaluated. RESULTS: The model reproduced intra-articular fractures very similar to those seen in high-energy trauma, although we required significantly higher energies (3600 mJ) than those reported in other fracture models (40-200 mJ). Cartilage viability decreased with time (68% immediately after the fracture and 46% at 72 hours, P = 0.02) and increased with depth from the articular surface (47% at the surface vs. 66% in the deepest layer, P = 0.001). CONCLUSIONS: This model is a physiologically relevant reliable method for creating intra-articular fractures in rats and can produce meaningful data about the biologic changes occurring in cartilage after injury. Cell viability decreases with time postfracture and with proximity to the articular surface.