Jessica E. Goetz, Marc J. Brouillette, Maxwell Y. Sakyi, Danielle P. Paulsen, Emily B. Petersen, Douglas C. Fredericks

A New Method for Creating Impact-Induced Intra-Articular Fractures in a Rabbit Model Induces Severe Post-traumatic Osteoarthritis

  • Orthopedics and Sports Medicine
  • General Medicine
  • Surgery

Objectives: The objective of this work was to develop a model of intra-articular fracture in a rabbit and document the speed and severity of degenerative joint changes after fracture fixation. Methods: With IACUC approval, impact-induced intra-articular fractures were created in the distal tibia of 16 New Zealand White rabbits. Fractures were fixed with a plate and screws. Pain and function were monitored at regular postoperative intervals with limb loading analysis. 12 or 26 weeks after fracture, animals were euthanized for histological assessment of cartilage degeneration and micro-CT analysis of bone histomorphometry. Results: Eleven animals successfully completed the study. Maximum foot force in the fractured limb was 41±21% lower than preoperative values (p=0.006) 12 weeks after fracture and remained 25±13% lower (p=0.081) after 26 weeks. Cortical bone mineral density in micro-CT images was 34±13% lower 12 weeks after fracture (p<0.001) and remained (42±8%) lower 26 weeks after fracture (p<0.001). Twelve weeks after fracture, Mankin scores of cartilage degeneration were significantly higher in the medial talus (p=0.007), lateral talus (p<0.001), medial tibia (p=0.017), and lateral tibia (p=0.002) of the fractured limb compared to the uninjured contralateral limb. Average Mankin scores in the talus increased from 12 to 26 weeks (5.9±0.9 to 9.4±0.4; p<0.001 lateral; 5.4±1.8 to 7.8±2.0; p=0.043 medial), indicating substantial and progressive joint degeneration. Conclusions: The ankle joint of the New Zealand White rabbit provides the smallest available model of impact-induced intra-articular fracture that can be treated with clinically relevant techniques and replicates key features of healing and degeneration found in human patients.

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