Experimentally Induced Femoroacetabular Impingement Results in Hip Osteoarthritis A Novel Platform to Study Mechanisms of Hip Disease

Background: We previously established a small animal model of femoral head-neck cam-type hip deformity by inducing physeal injury in immature rabbits. We investigated whether this induced deformity led to hip osteoarthritis (OA) within 4 months. Methods: Six-week-old immature New Zealand White rabbits underwent surgery to induce physeal injury in the right femoral head, causing growth arrest and secondary head-neck deformity. Animals were divided into early-pre-OA (4 weeks) and late-OA (16 weeks) groups. Left hips served as (nonsurgical) controls. Radiographs were made to visualize deformities and OA progression. The Beck classification was used to assess macroscopic cartilage damage and OA on the acetabulum and femoral head. Micro-computed tomography (CT), histological scoring, and gene expression were used to evaluate OA progression. The Wilcoxon signed-rank test was used for group comparisons. Significance was set at p < 0.05. Results: At 16 weeks, the injured hips showed radiographic evidence of joint space narrowing and a higher OA grade than the control hips (p = 0.0002). Micro-CT confirmed degenerative OA changes and a higher femoral head bone volume fraction (BV/TV) and trabecular thickness (Tb.Th) in the injured hips than in the control hips (BV/TV: p = 0.0001, Tb.Th: p = 0.0007). Macroscopically, the injured hips exhibited a greater prevalence and severity of chondral lesions at 4 weeks (83.3%, p = 0.015) and 16 weeks (100.0%, p = 0.002) post-injury compared with the control hips (0%), with worsening over time (4 versus 16 weeks: p = 0.016). The Osteoarthritis Research Society International (OARSI) score and synovitis score increased from 4 to 16 weeks post-injury. Compared with the control hips, the injured hips showed decreased Col2 expression and increased Col10 and MMP13 expression at 16 weeks post-injury (p = 0.062, p = 0.016, p = 0.041, respectively), confirming catabolism and OA progression. Conclusions: To our knowledge, we have created the first small animal model of hip OA secondary to experimentally induced head-neck deformity. In this model, the deformity resulted in hip OA at 16 weeks post-injury.