Abstract
Abstract
The natural history of osteoarthritis development in individuals with hip dysplasia diagnosed after skeletal maturity is difficult to predict. While reorienting acetabular osteotomy improves pain and function for those with pre-arthritic hip dysplasia, the impact of dysplastic deformity correction on cartilage health and future cartilage degeneration remains unknown. The rabbit has been used as a preclinical model of hip dysplasia for investigation of joint degeneration and surgical treatment, but there is variability among protocols used to induce and characterize dysplastic deformity. The aim of this narrative review was to summarize techniques for inducing hip dysplasia, the associated morphologic and histopathologic changes, and the ability of surgical correction to mitigate joint degeneration in order to guide future research using the rabbit as a model of hip dysplasia. We identified 21 studies that induced dysplastic deformity in the rabbit hip. The most common method to induce dysplastic deformity was immobilization of the knee in extension in skeletally immature rabbits. Immobilization initiated at a younger age and for longer duration resulted in more severe dysplasia. In the few studies that assessed surgical treatment of the dysplastic hip, cartilage degeneration was reduced with correction of dysplastic deformity. We concluded that immobilizing skeletally immature rabbit knees in extension reliably causes dysplastic deformity of the hip, replicating a shallow and abnormally oriented acetabulum, which can progress to full dislocation more characteristic of hip dysplasia in infants and children, or be present without complete femoral head dislocation more characteristic of human hip dysplasia that presents in young adults. This model thereby offers the opportunity to assess the tissue level effects of hip dysplasia and the effects of surgical correction across the age spectrum.
Clinical trials number
: Not applicable.