Sequential changes in histologic pattern and extracellular matrix deposition during the healing of chronic venous ulcers.
Sequential changes in histologic pattern and extracellular matrix deposition during the healing of chronic venous ulcers.
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慢性静脉溃疡愈合过程中组织学模式和细胞外基质沉积的连续变化。
DOI：
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发表时间：
1992
影响因子：
6
通讯作者：
Mark W. J. Ferguson
中科院分区：
文献类型：
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作者：
S. Herrick;P. Sloan;M. McGurk;L. Freak;Charles McCollum;Mark W. J. Ferguson
作为一项重要临床试验的一部分，在下肢静脉溃疡愈合期间，从溃疡边缘连续进行活检。愈合过程中组织结构和细胞外基质合成的变化模式进行了记录组织学和免疫细胞化学。最初的活检在外观上相似：突出的纤维蛋白袖口，可变炎症，含铁血黄素和红细胞外渗。所谓的“纤维蛋白袖口”是由层粘连蛋白、纤连蛋白、腱生蛋白和胶原蛋白以及捕获的白细胞和纤维蛋白组成的高度组织化的结构。纤维连接蛋白是缺席的溃疡组织，虽然胶原蛋白丰富。压力绷带治疗2周后观察到主要的组织学变化;含铁血黄素、急性炎症和肉芽组织伴纤维连接蛋白沉积均增加，上皮细胞迁移开始。完全上皮化是频繁的第四周的治疗，但基底膜不完整。此时，含铁血黄素和红细胞外渗减少，尽管慢性炎症仍然存在，但几乎不存在“纤维蛋白袖套”。所谓的“纤维蛋白袖口”的复杂组织除了先前认为的引起组织缺血的作用之外，还可以抑制血管生成（但提供针对静脉压增加的保护）。
As part of a major clinical trial, sequential biopsies were taken from the margins of venous leg ulcers during their healing. The changing patterns of tissue architecture and extracellular matrix synthesis during healing were documented histologically and immunocytochemically. Initial biopsies were similar in appearance: prominent fibrin cuffs, variable inflammation, hemosiderin, and red blood cell extravasation. So called "fibrin cuffs" were highly organized structures composed of laminin, fibronectin, tenascin, and collagen as well as trapped leukocytes and fibrin. Fibronectin was absent from the ulcer tissue although collagen was abundant. Major histologic changes were observed after 2 weeks' pressure bandage therapy; hemosiderin, acute inflammation, and granulation tissue with the deposition of fibronectin had all increased and epithelial migration had commenced. Complete epithelialization was frequent by the fourth week of treatment, but the basement membrane was incomplete. At this time, hemosiderin and red blood cell extravasation had decreased and "fibrin cuffs" were virtually absent although chronic inflammation remained. The complex organization of the so-called "fibrin cuffs" may inhibit angiogenesis (but offer protection against increased venous pressure) in addition to their previously ascribed role in causing tissue ischemia.