Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder
Immunolocalization of cytokines and their receptors in adhesive capsulitis of the shoulder
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DOI：
10.1002/jor.1100150316
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发表时间：
1997-05-01
影响因子：
2.8
通讯作者：
Wickiewicz, TL
中科院分区：
文献类型：
--
作者：
Rodeo, SA;Hannafin, JA;Wickiewicz, TL
本研究的目的是验证特定的细胞因子参与了粘连性肩关节囊炎纤维化过程的启动和演变的假说。在机构审查委员会批准后，在肩关节镜检查中收集了19名粘连性囊炎患者的肩囊和滑膜活检组织，14名非特异性滑膜炎患者没有纤维化或粘连性滑囊炎的临床证据，以及7名接受手术的另一种病理的患者，他们的囊膜和滑膜正常。用抗转化生长因子-β及其受体、血小板衍生生长因子及其受体、碱性成纤维细胞生长因子、白介素1-β、肿瘤坏死因子-α和肝细胞生长因子的单抗进行免疫组织化学定位。细胞因子染色频率与临床诊断相关。滑膜细胞、成纤维细胞、T细胞和B细胞用特异性抗体鉴定，新合成的基质用免疫组织化学染色检测I型和III型胶原。主要细胞类型为滑膜细胞和成纤维细胞。粘连性囊炎组织中III型胶原染色显示囊内有新的胶原沉积。粘连性滑膜炎和非特异性滑膜组织中有转化生长因子-β及其受体、血小板衍生生长因子及其受体、白介素1-β和肿瘤坏死因子-α的表达，而正常滑膜组织中仅有极少量的表达。滑膜细胞的染色频率高于囊膜细胞。粘连性滑膜炎组织中转化生长因子-β、血小板衍生生长因子和肝细胞生长因子的细胞和基质染色频率高于非特异性滑膜炎患者。原发(特发性)和继发性粘连性囊炎之间的染色频率没有发现差异。本研究的结果表明，粘连性囊炎既涉及滑膜增生，也涉及囊膜纤维化。细胞因子如转化生长因子-β和血小板衍生生长因子可能参与了粘连性囊炎的炎症和纤维化过程。基质结合的转化生长因子-β可能作为一种持续性刺激，导致包膜纤维化。了解粘连性囊炎的基本病理生理机制是开发临床上有用的抗纤维化药物的重要一步，这些药物可能会成为治疗这种疾病的新方法。
The purpose of this study was to test the hypothesis that specific cytokines are involved in the initiation and evolution of the fibrotic process in adhesive capsulitis of the shoulder. After approval from the Institutional Review Board, biopsies of shoulder capsule and synovium were collected during shoulder arthroscopy from 19 patients with adhesive capsulitis, 14 patients with nonspecific synovitis and no fibrosis or clinical evidence of adhesive capsulitis, and seven patients undergoing surgery for another pathology who had a normal capsule and synovium. Immunohistochemical localization with monoclonal antibodies to transforming growth factor-beta and its receptor, platelet-derived growth factor and its receptor, basic fibroblast growth factor, interleukin-1 beta, tumor necrosis factor-alpha, and hepatocyte growth factor was performed using standard immunoperoxidase techniques. The frequency of cytokine staining was correlated with the clinical diagnosis. Synovial cells, fibroblasts, T-cells, and B-cells were identified with specific antibodies, and newly synthesized matrix was examined for type-I and type-III collagen by immunohistochemical staining. The predominant cell types present were synovial cells and fibroblasts. Staining for type-III collagen in adhesive capsulitis tissues indicated new deposition of collagen in the capsule. There was staining for transforming growth factor-beta and its receptor, platelet-derived growth factor and its receptor, interleukin-1 beta, and tumor necrosis factor-alpha in adhesive capsulitis and nonspecific synovitis tissues, compared with minimal staining in normal capsule. Staining was more frequent in synovial cells than in capsular cells. The frequency of cell and matrix staining for transforming growth factor-beta, platelet-derived growth factor, and hepatocyte growth factor was greater in adhesive capsulitis tissues than in those from patients with nonspecific synovitis. No difference in the frequency of staining between primary (idiopathic) and secondary adhesive capsulitis was found. The results of this study indicate that adhesive capsulitis involves both synovial hyperplasia and capsular fibrosis. Cytokines such as transforming growth factor-beta and platelet-derived growth factor may be involved in the inflammatory and fibrotic processes in adhesive capsulitis. Matrix-bound transforming growth factor-beta may act as a persistent stimulus, resulting in capsular fibrosis. Understanding the basic pathophysiology of adhesive capsulitis is an important step in the development of clinically useful antifibrotic agents that may serve as novel treatments for patients with this condition.