Qureshi F I, Hornigold R, Spencer J D, Hall S M
Centre for Neuroscience Research, Guy's, King's and St Thomas' School of Medicine, London, UK.
J Hand Surg Br. 2001 Aug;26(4):362-7. doi: 10.1054/jhsb.2000.0518.
We have examined biopsies of Dupuytren's contracture palmar fascia, overlying subcutis and skin, and have correlated the distribution of gross macroscopic changes in the hand, mapped pre- and intraoperatively, with light microscopic immunohistochemical findings. We report increased numbers of S100 positive Langerhans cells (an epidermal cell of dendritic lineage) and CD45 positive cells, both in "nodules" and at dermo-epidermal junctions, in the biopsied tissues. This suggests that Langerhans cells migrate from the epidermis into Dupuytren's contracture tissue, possibly in response to local changes in levels of inflammatory cytokines within the tissue. Our findings, together with other reports of increased numbers of dermal dendrocytes and inflammatory cells in Dupuytren's contracture tissue, lend circumstantial support to the "extrinsic theory" of the pathogenesis of Dupuytren's contracture. However, the earliest stages of the disease process have not been defined, and therefore the events which ultimately produce fibrosis in the palmar fascial complex in susceptible individuals could begin in the skin and/or within deeper tissues, especially where there is dysregulation of the immune system.
我们检查了掌腱膜杜普伊特伦挛缩、覆盖的皮下组织和皮肤的活检样本,并将术前和术中绘制的手部大体宏观变化分布与光镜免疫组化结果进行了关联。我们报告称,在活检组织的“结节”以及真皮-表皮交界处,S100阳性朗格汉斯细胞(一种树突状谱系的表皮细胞)和CD45阳性细胞的数量均有所增加。这表明朗格汉斯细胞可能从表皮迁移至杜普伊特伦挛缩组织,这可能是对组织内炎症细胞因子水平的局部变化做出的反应。我们的研究结果,连同其他关于杜普伊特伦挛缩组织中真皮树突状细胞和炎症细胞数量增加的报告,间接支持了杜普伊特伦挛缩发病机制的“外在理论”。然而,疾病过程的最早阶段尚未明确,因此在易感个体中最终导致掌腱膜复合体纤维化的事件可能始于皮肤和/或更深层组织,尤其是在免疫系统失调的情况下。