Dankof Anja, Krenn Veit
Institute of Pathology, Humboldt-University, University Hospital Charité, Schumannstrasse 20/21, 10117 Berlin, Germany.
Virchows Arch. 2006 Aug;449(2):230-3. doi: 10.1007/s00428-006-0221-6. Epub 2006 May 4.
Although the frequent occurrence of meniscal degeneration is a well-known fact and its consequences include rupture and even loss of the meniscus, the pathogenetic factors are established insufficiently. Because complement factors and leukocytes are present in synovial fluid, we tried to detect complement deposits and macrophages in menisci, which displayed degenerative changes. We therefore performed a retrospective analysis by immunohistochemical staining of C4d and CD68 in meniscal tissue derived from patients (n=15) who underwent meniscectomy because of meniscal tears and from three autopsy cases (n=3). In this study, focal C4d deposits in the meniscal extracellular matrix in areas of mucoid degeneration or fibrillation were demonstrated for the first time, while no C4d deposits in the avascular zone of menisci without signs of degeneration or injury could be detected. In addition, colocalization of C4d and CD68+ cells was found at sites of meniscal tissue disintegration in five cases. These results represent the first evidence for an involvement of complement and macrophages in meniscal tissue disintegration, indicating a complement mediated reaction at the site of tissue alteration.
尽管半月板退变频繁发生是一个众所周知的事实，其后果包括半月板破裂甚至缺失，但发病机制尚不明确。由于滑膜液中存在补体因子和白细胞，我们试图检测显示退变改变的半月板中的补体沉积和巨噬细胞。因此，我们对因半月板撕裂接受半月板切除术的患者（n = 15）和三例尸检病例（n = 3）的半月板组织进行了C4d和CD68免疫组化染色的回顾性分析。在本研究中，首次证实在黏液样变性或纤维状变区域的半月板细胞外基质中有局灶性C4d沉积，而在无退变或损伤迹象的半月板无血管区未检测到C4d沉积。此外，在五例病例的半月板组织崩解部位发现C4d与CD68 +细胞共定位。这些结果首次证明补体和巨噬细胞参与了半月板组织崩解，表明在组织改变部位存在补体介导的反应。
