Charles C R, Cooper P H, Helwig E B
Lab Invest. 1977 Apr;36(4):444-51.
The necrobiotic disease granuloma annulare was studied with the electron microscope in an effort to develop a theory for the mechanism of development of necrobiotic connective tissue. That mechanism must provide for the disappearance of nuclei, the tinctorial change in collagen, and the retention of connective tissue outlines characteristic of necrobiosis. Our observations suggest that necrosis of histiocytes and fibroblasts with release of lysosomal enzymes is an important early event in the development of necrobiosis. Increased quantities of extracellular hyaluronic acid are also present in the earliest recognizable lesions. The combination of lysosomal enzymes and abundant hyaluronic acid in the interstitium results in swelling of collagen. Necrotic cellular debris is deposited about many collagen fibrils. This material seems to protect collagen from further destruction and may account for the preservation of connective tissue outlines observed at the light microscopic level. Some collagen fibrils not protected by cellular debris appear to be disrupted into constituent filaments. Crossbanded filamentous aggregates that resemble fibrous long spaced collagen were also observed and may represent an abnormal reassembly of disrupted collagen.
采用电子显微镜对渐进性坏死性疾病环状肉芽肿进行了研究，旨在建立一种关于渐进性坏死性结缔组织发病机制的理论。该机制必须解释细胞核的消失、胶原蛋白的染色变化以及渐进性坏死所特有的结缔组织轮廓的保留。我们的观察结果表明，组织细胞和成纤维细胞坏死并释放溶酶体酶是渐进性坏死发展过程中的一个重要早期事件。在最早可识别的病变中也存在大量细胞外透明质酸。间质中溶酶体酶与丰富的透明质酸相结合导致胶原蛋白肿胀。坏死的细胞碎片沉积在许多胶原纤维周围。这种物质似乎可保护胶原蛋白免受进一步破坏，并且可能是在光学显微镜水平观察到的结缔组织轮廓得以保留的原因。一些未被细胞碎片保护的胶原纤维似乎被分解成组成细丝。还观察到了类似纤维性长间距胶原的交叉带状丝状聚集体，它们可能代表了被破坏的胶原的异常重新组装。
