The immature goat as an animal model for Legg-Calvé-Perthes disease.

Abstract

Legg-Calvé-Perthes disease (LCPD) results from avascular necrosis of the capital femoral epiphysis in growing children. This disease often yields a significant deformity of the proximal femur, which may result in osteoarthritis. Its cause is unknown, although extensive radiographic, clinical, and histologic evaluations have been performed. Attempts at developing an animal model for LCPD have been unsuccessful. Previous models have been based predominantly on determining the vascular etiology of the disease. There is a need for an animal model that mimics the growth pattern of the proximal femur seen in LCPD. Such a model would allow for the development and testing of new treatments. Thus far, no treatment strategy has been completely successful. A study involving graphic analysis of radiographs found that arrested anterolateral physeal growth with continued or accelerated perichondrial ring and posteromedial epiphyseal growth would account for the most severe morphologic changes observed in the femoral heads of patients with LCPD. A surgical procedure was performed to ablate the capital femoral physis in goat kids in an attempt to mimic the changes noted in this study. The procedure was evaluated with radiographs, gross specimens, and histopathologic slides. Graphic analysis of the radiographs revealed changes in the shape of the operated femoral head compared with the unoperated femoral head. While bone, fibrous, and fibrocartilaginous bridges were histologically observed across the physis, the resultant deformities did not mimic the changes identified in the graphic analysis study, perhaps because of inconsistencies in the surgical ablative techniques, which will require further modification. This study provides the basis for further research to develop a successful model.