COX-1 and COX-2 expression in osteoid osteomas

COX-1 and COX-2 expression in osteoid osteomas
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DOI:
10.1016/s0736-0266(01)00065-1
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发表时间:
2002-01-01
影响因子:
2.8
通讯作者:
Schwarz, EM
Schwarz, EM
中科院分区:
医学3区
文献类型:
--
作者:
Mungo, DV;Zhang, XP;Schwarz, EM

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骨样骨瘤是一种良性骨形成肿瘤,其特点是体积小(小于2厘米)、自限性生长,并且容易引起邻近组织广泛的反应性变化。这种病变通常会在夜间出现剧烈疼痛,但非甾体抗炎药可显着缓解疼痛。该肿瘤已被证明表达非常高水平的前列腺素,特别是 PGE2 和 PG12。这些前列腺素的局部高水平被认为是患有这种病变的患者出现剧烈疼痛的原因。一种普遍接受的治疗方式是长期使用非甾体抗炎药。由于环氧合酶被认为是这些前列腺素的来源,也是 NSAID 的中心靶标,因此我们评估了手术后患者骨样骨瘤组织中环氧合酶-1 (COX-1) 和环氧合酶-2 (COX-2) 的表达。在检查的 12 个标本中,我们发现肿瘤成骨细胞对 COX-2 具有很强的免疫组织化学染色,而反应性骨中周围宿主成骨细胞的染色很少。在肿瘤和宿主成骨细胞中也检测到显着的 COX-1 染色。为了进行比较,我们检查了人类骨折愈伤组织、纤维异常增殖症、成骨细胞瘤、骨纤维异常增殖症和骨化性肌炎中的 COX 表达。除骨折愈伤组织外,在这些组织中可以检测到非常有限的 COX-2。综上所述,我们得出结论,骨样骨瘤产生的前列腺素增加表明 COX-2 是这种情况的介质之一。这些发现表明,新的选择性 COX-2 抑制剂可用于更安全地治疗骨样骨瘤。 (C) 2002 年骨科研究学会。由爱思唯尔科学有限公司出版。保留所有权利。
Osteoid osteoma is a benign bone forming neoplasm that is characterized by its small size (less than 2 cm), self-limited growth, and the tendency to cause extensive reactive changes in the adjacent tissue. The lesion classically presents with severe pain at night that is dramatically relieved by NSAIDs. The tumor has been shown to express very high levels of prostaglandins, particularly PGE2 and PG12. The high local levels of these prostaglandins are presumed to be the cause of the intense pain seen in patients with this lesion. One generally accepted form of treatment is the prolonged use of NSAIDs. Since the cyclooxygenases are thought to be the source of these prostaglandins, and the central target of NSAIDs, we evaluated the expression of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in osteoid osteoma tissues from patients following surgery. In the 12 specimens examined we found that the tumor osteoblasts had strong immunohistochemical staining for COX-2, while the staining in the surrounding host osteoblasts in the reactive bone was scant. Significant COX-1 staining was also detected in both tumor and host osteoblasts. For comparison we examined the COX expression in human fracture callus, fibrous dysplasia, osteoblastoma, osteofibrous dysplasia, and myositis ossificans. With the exception of fracture callus, very limited amounts of COX-2 could be detected in these tissues. Taken together, we conclude that the increased production of prostaglandins by osteoid osteomas implicates that COX-2 is one of the mediators of this condition. These findings suggest that the newly selective COX-2 inhibitors could be used to more safely treat osteoid osteomas. (C) 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.