ANIMAL MODELS

DEVELOPMENT OF FEMORAL HEAD DEFORMITY IN SWINE MODEL, OF ISCHEMIC NECROSIS OF FEMORAL HEAD

H.K.W. Kim, P.-H. Su
Center for Research in Skeletal Development and Pediatric Orthopaedics, Shriners Hospital for Children, Tampa, Florida

In many instances, ischemic necrosis of femoral head (INFH) in children produces a femoral head deformity (FHD) that persists and leads to premature degenerative arthritis in adulthood. Immature swine model, of ischemic necrosis was used to study the reliability of this model to produce FHD and to study the pathogenesis of the FHD. 30 male piglets weighing between 5-10 kgs were used. A suture ligature was placed tightly around the femoral neck to disrupt the blood supply to the femoral head. Animals were sacrificed 3 days to 8 wks following the surgery. Histologic, radiographic, and microangiographic (Microfil infusion) assessments were performed. A complete absence of perfusion dye was observed in the femoral head following the placement of the suture ligature. Radiographically, all 8 animals sacrificed at 8 wks showed flattening of the femoral head. In some animals, the femoral head revealed severe fragmentation and irregular appearance, similar to Legg-Perthes disease. A time study showed, that appearance of osteolytic area m the infarcted femoral head preceded the development of the FHD. Histologically, the lytic area correlated with an area of revascularization with active bone resorption by osteoclasts. Bone resorption was not closely linked to new bone formation. We conclude that the immature swine model reliably produced FHD and that one of the mechanisms involved in the development of the FHD is the loss of bone structure and volume due to osteoclastic resorption of the necrotic bone following revascularization.