Background: The repair response that follows ischemic necrosis of the immature femoral head and the biological processes that are responsible for the development of femoral head deformity and fragmentation have not been clearly defined. A piglet model was used to study the radiographic and histopathologic changes that occur prior to and during the development of femoral head deformity and fragmentation following ischemic necrosis.

Methods: Twenty-five male piglets were studied. A nonabsorbable ligature was placed tightly around the femoral neck to disrupt the blood supply to the capital femoral epiphysis. The animals were killed three days to eight weeks following the induction of ischemia. Radiographs of whole and sectioned femoral heads were made, and the radiographic findings were correlated with the histopathologic changes observed in the specimens.

Results: Mild femoral head flattening was observed by four weeks after the induction of ischemia, and severe flattening and fragmentation were observed by eight weeks. The predominant repair response observed following revascularization was osteoclastic bone resorption. Prior to the development of flattening, a large area of osteoclastic bone resorption was observed in the central region of the femoral head. Many osteoclasts were present along the revascularization front, which we believe were responsible for active resorption of the necrotic trabecular bone. Appositional new-bone formation, the hallmark of the repair response in adult ischemic necrosis, was not observed in the area of bone resorption. Instead, the areas of resorbed bone were replaced with a fibrovascular tissue that persisted for up to eight weeks. Appositional new-bone formation was observed, but it was limited to small areas in which revascularization was not followed by osteoclastic bone resorption and in which necrotic trabecular bone was still present. The simultaneous presence of the areas of bone resorption and new-bone formation contributed to the fragmented radiographic appearance of the femoral head.

Conclusions: The predominant repair response observed in the piglet model of ischemic necrosis was osteoclastic bone resorption. The early bone loss, the lack of new-bone formation, and the persistence of fibrovascular tissue in the areas of bone resorption compromised the structural integrity of the femoral head and produced progressive femoral head flattening over time. The repair response was different from that observed in femoral heads removed from adult patients with ischemic necrosis and from that observed in the adult rabbit model of ischemic necrosis.

Clinical Relevance: The piglet model of ischemic necrosis may be useful for the investigation of the biological processes that lead to the development of femoral head deformity following ischemic necrosis of the immature femoral head.