Sampson S P, Badalamente M A, Hurst L C, Seidman J
Department of Orthopaedics, School of Medicine, State University of New York, Stony Brook 11794-8181.
J Hand Surg Am. 1991 Jul;16(4):714-21. doi: 10.1016/0363-5023(91)90200-u.
Eighty-nine A1 pulleys from 65 patients with trigger digits and 20 control A1 pulleys from fresh-frozen cadavers were studied comparatively with histology, immunohistochemistry, and transmission electron microscopy. In both normal and pathologic specimens, the A1 pulley was composed of two layers: an outer, vascularized, convex layer and an inner, concave, friction, flexor tendon gliding layer. In the latter, the cells and adjacent matrix had several characteristics of fibrocartilage, including chondrocytes. In trigger digits, the number of chondrocytes and adjacent extracellular matrix was significantly increased when compared with controls. There was no evidence of a synovial cell layer on the surface of the A1 pulleys in either normal or trigger digits. We conclude that the underlying pathobiological mechanism for triggering at the A1 pulley is characterized by a fibrocartilage metaplasia.
对65例扳机指患者的89个A1滑车以及取自新鲜冷冻尸体的20个对照A1滑车进行了组织学、免疫组织化学和透射电子显微镜的比较研究。在正常和病理标本中，A1滑车均由两层组成：外层为血管化的凸层，内层为凹形的摩擦屈肌腱滑动层。在后者中，细胞和相邻基质具有纤维软骨的若干特征，包括软骨细胞。与对照组相比，扳机指中软骨细胞和相邻细胞外基质的数量显著增加。在正常或扳机指的A1滑车表面均未发现滑膜细胞层的证据。我们得出结论，A1滑车处扳机现象的潜在病理生物学机制的特征是纤维软骨化生。
