Department of Orthopaedics, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, 107 West Yanjiang Road, Guangzhou, 510120, People's Republic of China.
Inflammation. 2017 Dec;40(6):1815-1824. doi: 10.1007/s10753-017-0616-3.
Macrophage-related inflammatory response is one of the main biological factors resulting in failure of anterior cruciate ligament (ACL) reconstruction, although the specific pathomechanism remains to be clarified. Our aim was to investigate the association between graft loosening and macrophage-related inflammation in cases of loosening of reconstructed ACL autografts. Tissue samples were obtained from 21 patients who underwent a second-look arthroscopy within the first year after arthroscopic ACL reconstruction using single-bundle hamstring tendon autografts. Possible biological factors of graft loosening were analyzed using polymerase chain reaction, Western blot, and hematoxylin/eosin and immunohistochemical staining of graft tissue samples obtained during the second-look arthroscopy. Graft loosening was closely related to increased gene and protein expression of inflammatory cytokines (TNF-α, IL-6, and IL-8) and activation of the inflammation-related toll-like receptor (TLR) signaling (TLR2 and TLR4). The molecular expression of TGF-β and type I and III collagen was also inhibited to varying degrees, with decreased vascularization of the graft due to an inhibition of VEGF. iNOS, a marker of M1 macrophage activation, was highly expressed in cases of graft loosening, with no effect of M2 macrophages identified. The activation of M1 macrophages and aseptic inflammation signaling is an important biological factor of graft loosening after ACL reconstruction, affecting ligamentization and the health of grafts.
巨噬细胞相关炎症反应是导致前交叉韧带 (ACL) 重建失败的主要生物学因素之一，尽管其具体发病机制仍需阐明。我们的目的是研究在重建 ACL 自体移植物松动的情况下，移植物松动与巨噬细胞相关炎症之间的关系。从 21 例接受关节镜 ACL 重建后 1 年内再次关节镜检查的患者中获得组织样本。使用聚合酶链反应、Western blot 和苏木精/伊红及免疫组织化学染色分析取自再次关节镜检查的移植物组织样本中可能导致移植物松动的生物学因素。移植物松动与炎症细胞因子（TNF-α、IL-6 和 IL-8）的基因和蛋白表达增加以及炎症相关 toll 样受体（TLR）信号（TLR2 和 TLR4）的激活密切相关。TGF-β 和 I 型和 III 型胶原的分子表达也受到不同程度的抑制，由于 VEGF 的抑制，导致移植物血管化减少。在移植物松动的情况下，M1 巨噬细胞激活的标志物 iNOS 高度表达，而 M2 巨噬细胞则没有作用。M1 巨噬细胞的激活和无菌性炎症信号是 ACL 重建后移植物松动的重要生物学因素，影响韧带化和移植物的健康。
