Evidence for eicosanoids within the reparative front in avascular necrosis of human femoral head.

Abstract

Eicosanoids, including prostaglandins and leukotrienes, are important mediators of inflammation. To observe inflammation after necrosis, the histology and the changes of eicosanoid levels were compared in the subchondral cortex and spongy bone of femoral head of sixteen patients with Ficat III or IV idiopathic avascular necrosis (AVN). Neither inflammatory cells nor elevation of eicosanoid levels were observed in the necrotic subchondral cortex or osteochondral junction, whereas infiltration of lymphocytes and plasma cells, fibrosis, and fat emboli were present in the reparative front of necrotic spongy bone. Biochemical analysis in this region revealed significant increases of prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2 (TXB2), leukotriene B4 (LTB4), and LTC4. The increased eicosanoids due to initial necrosis become aggravating factors by increasing vascular permeability, which leads to marrow edema and intraosseous hypertension; it ultimately develops into a cycle of inflammation and AVN.