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.

Numerous animal species, including the goat, have been evaluated as potential models for human Legg-Calve-Perthes disease (LCPD). These models disrupt the vasculature of the femoral head, causing it to collapse, and therefore do not mimic all the clinical patterns of the human disease. Baseline data regarding the weight and femoral length in the growing goat are not available. This study characterized the goat's normal growth for comparison with that of humans. The growth aberrations in the proximal femur created by surgically ablating the capital physis were described and compared with the aberrations observed in human LCPD cases. Age, weight, and femoral length (test and control) data were obtained for goats approximately 1 to 14 months of age. At 4 months of age, a craniolateral surgical approach was used to expose the cranial lateral capital physis so that it could be cauterized. Postoperative radiographs were evaluated by graphic analysis to assess the resultant changes in the morphology of the proximal femur. The articular cartilage of the femoral head and acetabulum was evaluated mechanically, using indentation testing, to determine the apparent modulus of elasticity, and histopathologically regarding its thickness and proteoglycan content. The proximal femurs of goats and humans exhibit similar morphology and growth patterns. There was a positive correlation between age, weight, and femoral lengths in the goat. The surgical procedure was effective in ablating the capital femoral physis as indicated by shorter femoral lengths and fragmented, flattened, and mushroomed femoral heads. The histopathological data revealed that the articular cartilage was significantly thicker in the operated hip joints at the ventrocaudal and cranial acetabula and the dorsal and ventral femoral heads. The test cartilage exhibited significantly less positive staining for proteoglycans in the dorsocaudal and the cranial acetabula as well as the ventral femoral head. The apparent modulus of elasticity, of the test cartilage was significantly lower than the control value at the dorsocaudal acetabulum. These data show that the surgical procedure produced morphological changes that mimic those in human LCPD. The increased thickness of the articular cartilage of the LCPD femoral head may account for the articular degeneration observed in older patients with LCPD, as increased cartilage thickness is associated with decreased tissue quality.