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The avascular necrosis associated with LCPD also triggers a chronic synovitis which is characterized by perivascular aggregation of lymphocytes and plasma cells with elevated levels of IgG and IgM in the serum. This suggests that immunological mechanisms may be involved in mediating the synovitis. Elevated interleukin-6 levels in the synovial fluid have also been noted . Muscle spasm induced by the synovitis is partly responsible for the initial reduction in the range of hip motion. Hypertrophy of the ligamentum teres and femoral and acetabular articular cartilage occurs early in the disease. These soft tissue changes predispose to the femoral head extruding from under the margin of the acetabulum. When the femoral head extrudes, the avascular segment of the epiphysis is exposed to weight-bearing stress and muscular forces across the acetabular margin. Maximal extrusion tends to coincide with the period when the bone is inherently weak due to the imbalance between bone resorption and new bone deposition. The weakened avascular bone of the extruded epiphysis cannot withstand the physiologic stresses of weight-bearing and irreversible deformation of the femoral head ensues. Extrusion in excess of 20% is associated with a high risk of permanent deformation of the femoral head . Extrusion tends to be more severe with more extensive epiphyseal avascularity and it invariably develops in children over the age of seven.