α-Smooth muscle actin containing contractile fibroblastic cells in human knee arthrofibrosis tissue -: Winner of the AGA-DonJoy Award 2003
α-Smooth muscle actin containing contractile fibroblastic cells in human knee arthrofibrosis tissue -: Winner of the AGA-DonJoy Award 2003
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DOI：
10.1007/s00402-004-0742-x
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发表时间：
2004-11-01
影响因子：
2.3
通讯作者：
Weiler, A
中科院分区：
文献类型：
--
作者：
Unterhauser, FN;Bosch, U;Weiler, A
简介：原发性关节纤维化是关节创伤或膝关节韧带手术后的主要问题。详细的潜在机制仍不清楚。高度分化的成纤维细胞，所谓的肌成纤维细胞，表达肌动蛋白同种型α-平滑肌肌动蛋白（ASMA），并已被发现在伤口愈合和器官纤维化期间的组织收缩中起主要作用。因此，我们研究了人原发性膝关节纤维化组织中肌成纤维细胞的表达。材料与方法：从9名前交叉韧带（ACL）重建后因关节纤维化接受翻修手术的患者（研究组）的髌下脂肪垫和髁间区域采集组织样本。对照组织取自5名接受初次ACL重建的患者（对照组I）和8名在初次ACL重建后接受二次关节镜检查的患者（对照组II）。用单克隆抗体对含有ASMA的成纤维细胞进行免疫染色。对总细胞量、含ASMA的成纤维细胞和血管横截面进行组织形态计量学分析。结果：关节纤维化组中含有肌成纤维细胞的ASMA含量（23.4%）是对照组I的10倍（2.3%）。与对照组I相比，总细胞计数显著升高，血管密度显著降低。对照组II显示肌成纤维细胞的上调几乎是对照组I的五倍;然而，没有瘢痕形成或组织纤维化的证据。结论：肌成纤维细胞是创伤愈合过程中瘢痕组织收缩的主要原因。在关节纤维化中，组织成纤维细胞收缩可能参与组织纤维化和收缩，并伴有连续的运动丧失。我们发现肌成纤维细胞在关节纤维化组织中表达上调。ACL重建本身引起肌成纤维细胞含量的上调。然而，这些患者没有表现出任何关节纤维化的临床或组织学体征。因此，我们有理由认为结缔组织中肌成纤维细胞和总细胞数量的比例是关节纤维化发生的原因。因此，解决这种高度分化的细胞类型的表达可能为未来的治疗干预提供靶点。
Introduction: Primary arthrofibrosis is of major concern after joint trauma or knee ligament surgery. The underlying mechanism in detail remains unclear. Highly differentiated fibroblastic cells, so-called myofibroblasts, express the actin isoform alpha-smooth muscle actin (ASMA) and have been found to play a major role in tissue contraction during wound healing and organ fibrosis. We therefore studied the expression of myofibroblasts in human primary knee arthrofibrosis tissue. Materials and methods: Tissue samples were taken from the infrapatellar fat pad and intercondylar region of nine patients who underwent revision surgery due to arthrofibrosis after anterior cruciate ligament (ACL) reconstruction (study group). Control tissue was taken from five patients who underwent primary ACL reconstruction (control group I) and from eight patients, who underwent second-look arthroscopy after primary ACL reconstruction (control group II). ASMA containing fibroblasts were immunostained with a monoclonal antibody. Histomorphometry was performed for total cell amount, ASMA containing fibroblasts, and vessel cross-sections. Results: The arthrofibrosis group showed a tenfold higher amount of ASMA containing myofibroblasts (23.4% vs. 2.3%) than in control group I. There was a significantly higher total cell count and lower vessel density than in control group I. Control group II showed an upregulation of myofibroblasts almost five times that in control group I; nevertheless there was no evidence of scar formation or tissue fibrosis. Conclusions: Myofibroblasts are responsible for scar tissue contraction during wound healing. In arthrofibrosis tissue fibroblast contraction may be involved in tissue fibrosis and contraction with consecutive loss of motion. We found that myofibroblasts are upregulated in arthrofibrosis tissue. ACL reconstruction itself caused an up regulation of myofibroblast content. Nevertheless these patients did not show any clinical or histological signs of arthrofibrosis. Thus it is reasonable to assume that the ratio of myofibroblasts and total cell amount in connective tissue are responsible for the onset of arthrofibrosis. Address the expression of this highly differentiated cell type may therefore present a target for future therapeutic interventions.