Tsai C L, Liu T K
Department of Orthopaedic Surgery, School of Medicine, National Taiwan University, Taipei, Republic of China.
Clin Orthop Relat Res. 1992 Aug(281):305-12.
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.
类花生酸，包括前列腺素和白三烯，是炎症的重要介质。为观察坏死后的炎症反应，对16例Ficat III或IV期特发性股骨头缺血性坏死（AVN）患者股骨头软骨下皮质和松质骨的组织学及类花生酸水平变化进行了比较。在坏死的软骨下皮质或骨软骨交界处未观察到炎症细胞或类花生酸水平升高，而在坏死松质骨的修复前沿存在淋巴细胞和浆细胞浸润、纤维化及脂肪栓子。该区域的生化分析显示前列腺素E2（PGE2）、6-酮-前列腺素F1α（6-酮-PGF1α）、血栓素B2（TXB2）、白三烯B4（LTB4）和LTC4显著增加。初始坏死导致的类花生酸增加通过增加血管通透性成为加重因素，进而导致骨髓水肿和骨内高压；最终发展为炎症和AVN的循环。
