Tarpey S G, White F H
J Cancer Res Clin Oncol. 1984;107(3):183-94. doi: 10.1007/BF01032605.
Stereological point-counting methods were used to determine the volumetric alterations in collagen from the lamina propria immediately beneath the epithelial-connective tissue junction in hamster check-pouch mucosa treated with the chemical carcinogen DMBA. In addition, a non-neoplastic inflammatory control was evaluated in which a delayed hypersensitivity reaction was induced by the contact-sensitising agent DNCB. DMBA-treated tissues were assigned to histopathologically defined hyperplasia, dysplasia and carcinoma stages. The volume densities of collagen present in unit volume of extracellular lamina propria were found to decrease progressively and significantly in DMBA-treated tissues when compared with values obtained from normal untreated mucosa. Values from the inflammatory control were comparable with those from the dysplasia stage of carcinogenesis. The mechanisms responsible for these decreases in collagen volume density are unknown, but contributory factors might include collagen destruction by enzymes originating in either the epithelium or the cells of the inflammatory infiltrate, dilution of collagen produced by inflammatory oedema or alterations in the synthetic capabilities of fibroblasts.
采用体视学点计数法，来确定用化学致癌物二甲基苯并蒽（DMBA）处理的仓鼠颊囊黏膜上皮-结缔组织连接处正下方固有层中胶原蛋白的体积变化。此外，还评估了一个非肿瘤性炎症对照，其中通过接触致敏剂二硝基氯苯（DNCB）诱导迟发型超敏反应。将经DMBA处理的组织分为组织病理学定义的增生、发育异常和癌阶段。与从未经处理的正常黏膜获得的值相比，发现经DMBA处理的组织中单位体积细胞外固有层中存在的胶原蛋白的体积密度逐渐且显著降低。炎症对照的值与致癌作用发育异常阶段的值相当。胶原蛋白体积密度降低的原因尚不清楚，但促成因素可能包括上皮或炎症浸润细胞产生的酶对胶原蛋白的破坏、炎症水肿产生的胶原蛋白稀释或成纤维细胞合成能力的改变。
