BACKGROUND: Impact injury to articular cartilage can lead to posttraumatic osteoarthritis. HYPOTHESES: This study tests the hypotheses that (1) chondrocyte injury occurs after impact at energies insufficient to fracture the cartilage surface, and that (2) cartilage injury patterns vary with impact energy, time after injury, and cartilage thickness. STUDY DESIGN: Controlled laboratory study. METHODS: Fresh bovine osteochondral cores were randomly divided into 5 groups: (1) control, (2) 0.35 J, (3) 0.71 J, (4) 1.07 J, and (5) 1.43 J impact energies. Cores were subjected to computer-controlled impact loading and full-thickness sections were then prepared and incubated in Dulbecco's Modified Eagle's Medium/F12 at 37 degrees C. Adjacent sections were harvested 1 and 4 days after impact for viability staining and fluorescent imaging. The area of dead and living chondrocytes was quantified using custom image analysis software and reported as a percentage of total cartilage area. RESULTS: The highest impact energy fractured the cartilage in all cores (1.43 J, n = 17). Seventy-three percent and 64% of the osteochondral cores remained intact after lower energy impacts of 0.71 J and 1.07 J, respectively. At lower energy levels, fractured cores were thinner (P <.01) than those remaining intact. In cores remaining intact after impact injury, chondrocyte death increased with increasing impact energy (P <.05) and with greater time after impact (P <.05). A progressive increase in dead cells near the bone/cartilage interface and at the articular surface was observed. CONCLUSION: These data showing progressive chondrocyte death after impact injury at energies insufficient to fracture the cartilage surface demonstrate a potential need for early chondroprotective therapy. CLINICAL RELEVANCE: These data show that efforts to reduce chondrocyte morbidity after joint injury may be a useful strategy to delay or prevent the onset of posttraumatic osteoarthritis.
BACKGROUND:Impact injury to articular cartilage can lead to posttraumatic osteoarthritis. HYPOTHESES: This study tests the hypotheses that (1) chondrocyte injury occurs after impact at energies insufficient to fracture the cartilage surface, and that (2) cartilage injury patterns vary with impact energy, time after injury, and cartilage thickness. STUDY DESIGN: Controlled laboratory study. METHODS: Fresh bovine osteochondral cores were randomly divided into 5 groups: (1) control, (2) 0.35 J, (3) 0.71 J, (4) 1.07 J, and (5) 1.43 J impact energies. Cores were subjected to computer-controlled impact loading and full-thickness sections were then prepared and incubated in Dulbecco's Modified Eagle's Medium/F12 at 37 degrees C. Adjacent sections were harvested 1 and 4 days after impact for viability staining and fluorescent imaging. The area of dead and living chondrocytes was quantified using custom image analysis software and reported as a percentage of total cartilage area. RESULTS: The highest impact energy fractured the cartilage in all cores (1.43 J, n = 17). Seventy-three percent and 64% of the osteochondral cores remained intact after lower energy impacts of 0.71 J and 1.07 J, respectively. At lower energy levels, fractured cores were thinner (P <.01) than those remaining intact. In cores remaining intact after impact injury, chondrocyte death increased with increasing impact energy (P <.05) and with greater time after impact (P <.05). A progressive increase in dead cells near the bone/cartilage interface and at the articular surface was observed. CONCLUSION: These data showing progressive chondrocyte death after impact injury at energies insufficient to fracture the cartilage surface demonstrate a potential need for early chondroprotective therapy. CLINICAL RELEVANCE: These data show that efforts to reduce chondrocyte morbidity after joint injury may be a useful strategy to delay or prevent the onset of posttraumatic osteoarthritis.
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