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The cause of interruption of blood flow to the capital epiphysis is unknown but it is clear that the vascular insult results in infarction of part or all of the femoral epiphysis. When partial epiphyseal infarction occurs, the medial and posterior parts of the epiphysis are most commonly spared. The vascular occlusion may involve the medial circumflex femoral artery or its lateral epiphyseal branches and the site of vascular occlusion determines the extent and location of the infarcted segment in the epiphysis. There is some evidence to suggest that more than one episode of infarction occurs . Reparative processes begin soon after the bone infarction commences. Initially, there is a robust osteoclastic response to resorb the necrotic bone. However, replacement of the resorbed trabeculae with new bone does not proceed in tandem because of a relatively poor initial osteoblastic response . This imbalance between bone resorption and new bone formation renders the bone trabeculae weak and susceptible to collapse. Over a period of time the osteoblasts lay down new bone on the periphery of the infracted epiphysis. This new woven bone is also vulnerable to deformation as the trabeculae are laid down haphazardly and not in directions that resist deformation by weight bearing stresses seen in lamellar bone. There is thus a period during the evolution of the disease when the femoral epiphysis is inherently prone to deformation. Once the woven bone is replaced by lamellar bone the normal strength of the epiphysis is restored and no further deformation of the epiphysis occurs . The entire process of repair takes 2–4 years.