Yanagihara M, Fujita T, Shirasaki A, Ishiguro K, Kawahara K, Ueda K
Department of Dermatology, Fukui Medical School, Japan.
J Cutan Pathol. 1996 Oct;23(5):398-403. doi: 10.1111/j.1600-0560.1996.tb01429.x.
Two cases of acquired reactive perforating collagenosis with poorly controlled diabetes mellitus were studied by histochemistry and by electron microscopy. In excoriated wound the necrotic mass on the bottom of the ulcer contained the collagen bundles which were continuous with the collagen bundles in the reticular layer. In the developing stage, the epidermis regenerated between the necrotic mass and the reticular dermis, and the collagen bundles in the reticular dermis were in continuity with those in the necrotic mass through the epithelial tunnels. The collagen in the epidermal channels did not degenerate ultrastructurally. In the mature lesion, collagen bundles being eliminated through the epidermis were surrounded by the fibroblasts at the basal cell layer. Collagen fibers were seen in the cytoplasm of these fibroblasts. From these findings, the mechanisms of the formation of the eruption in acquired reactive perforating collagenosis might be as follow: 1) In the developing stage, the regeneration of epidermis progresses between the necrotic mass and the reticular dermis, and among the collagen bundles. As a result, the collagen bundles remain in the channels of the epidermis. And then, 2) the regenerated epidermis makes the thick horny layer. As a result, the necrotic masses are lifted up and the collagen bundles are pulled up from the dermis through the epidermal channels.
对两例糖尿病控制不佳的获得性反应性穿通性胶原病患者进行了组织化学和电子显微镜研究。在擦伤伤口处,溃疡底部的坏死物质中含有与网状层中的胶原束相连的胶原束。在发展阶段,表皮在坏死物质和网状真皮之间再生,网状真皮中的胶原束通过上皮通道与坏死物质中的胶原束相连。表皮通道中的胶原在超微结构上未发生退变。在成熟病变中,通过表皮排出的胶原束被基底细胞层的成纤维细胞包围。在这些成纤维细胞的细胞质中可见胶原纤维。根据这些发现,获得性反应性穿通性胶原病皮疹形成的机制可能如下:1)在发展阶段,表皮在坏死物质和网状真皮之间以及胶原束之间再生。结果,胶原束保留在表皮通道中。然后,2)再生的表皮形成厚角质层。结果,坏死物质被抬起,胶原束通过表皮通道从真皮中被拉起。