Badalamente M A, Stern L, Hurst L C
J Hand Surg Am. 1983 May;8(3):235-43. doi: 10.1016/s0363-5023(83)80150-6.
The role of myofibroblasts in the pathogenesis of Dupuytren's contracture was investigated by light and electron microscopic histochemical methods. Dupuytren's myofibroblasts contain an intracellular contractile mechanism that is driven by the dephosphorylation of adenosine triphosphate. Our study of calcium adenosinetriphosphatase (ATPase) activities verifies that the site of this energy system is on the myofilaments of the myofibroblasts. The degree of ATPase activity, as determined by cell counts, appeared to correlate with the residual contracture as predicted by the Legge and McFarlane Outcome Standard Formula. Further, alcian blue staining on the ultrastructural level indicates that the myofibroblasts are associated with each other and with surrounding collagen by a glycosaminoglycan matrix 300 to 1000 A thick. Collagen fibrils are attached by a similar matrix comprised of 100 A thick fibrils. The dynamic cellular architecture of the multiple adjacent myofibroblasts with their connections to surrounding collagen may be partially responsible for the residual clinical deformities seen in this disease.
通过光镜和电镜组织化学方法研究了肌成纤维细胞在掌腱膜挛缩症发病机制中的作用。掌腱膜挛缩症的肌成纤维细胞含有一种细胞内收缩机制，该机制由三磷酸腺苷的去磷酸化驱动。我们对钙三磷酸腺苷酶（ATP酶）活性的研究证实，这个能量系统的位点位于肌成纤维细胞的肌丝上。通过细胞计数确定的ATP酶活性程度，似乎与Legge和McFarlane结果标准公式预测的残余挛缩相关。此外，超微结构水平的阿尔辛蓝染色表明，肌成纤维细胞通过厚度为300至1000埃的糖胺聚糖基质相互连接，并与周围的胶原相连。胶原纤维通过由100埃厚的纤维组成的类似基质连接。多个相邻肌成纤维细胞的动态细胞结构及其与周围胶原的连接可能是导致该疾病中所见残余临床畸形的部分原因。
