实验性牙周炎大鼠牙龈胶原纤维质变的组织病理学研究。用picrosirius偏振法检测I型和III型胶原的重塑。

M Kamata, K Kamoi
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引用次数: 2

摘要

本研究的目的是证明I型和III型胶原的运动伴随牙龈炎症破坏。以3周龄Wistar大鼠为研究对象,采用致结石性饮食和高糖粪便饮食诱导实验性边缘性牙周炎。采用小螺旋偏振法和电子显微镜对牙周组织病理变化进行观察。1. 饮食5周后,发现轻度牙龈炎。可见少量由中性粒细胞组成的炎性细胞。第2周开始出现各种牙槽嵴骨吸收。第10周,观察到上皮细胞生长下降。第64周可见上皮附着迁移至半尖,浆细胞高度浸润炎性细胞。2. 偏光显微镜下观察显示,横断纤维变粗,I型胶原减少,中间III型胶原增加。而在水平束新形成时,ⅰ型总是占优势。在牙间水平纤维和牙槽嵴之间,III型增加。3.电镜下观察到胶原原纤维被破坏和消失的部位,在降解成纤维细胞周围可见微原纤维。相反,在脱离炎症细胞浸润的部位可见小束的微原纤维。我们认为,在破坏性胶原结构的区域,III型的相对增加和微原纤维的出现是由i型的减少引起的。同时,在与病变脱离的部位,III型的完全生长和微原纤维的出现被发现,并被认为是新形成的幼年胶原结构。此外,还得出结论,胶原纤维类型的质变涉及分解和新形成的平衡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Histopathological study on qualitative changes in gingival collagen fibers for experimental periodontitis in rats. Remodeling of type I and III collagens detected by the Picrosirius-polarization method].

The objective of this study was to demonstrate the movement of type I and III collagens accompanying gingival inflammatory destruction. Experimental marginal periodontitis was induced by a calculogenic diet and a high-sucrose diet with feces in 3-week-old Wistar rats. We observed the changes in the interdental periodontium histopathologically by using the picrosirius-polarization method and an electron microscope. 1. After 5 weeks of eating the calculogenic diet, mild gingivitis was found. A small number of inflammatory cells consisting of neutrophils were seen. At the 2nd week, a variety of bone resorptions of alveolar crests began to appear. At the 10th week, an epithelial downgrowth was observed. At the 64th week, migration of epithelial attachment to half of the apex and a high degree of inflammatory cell infiltration of plasma cells could be seen. 2. Observations under the polarization microscope showed that interdantal horizontal fibers became coarse and type I collagen decreased but at the middle type III increased. However when the horizontal fasciculus were newly formed, type I was always dominant. Between interdental horizontal fibers and the alveolar crest, type III was increased. 3. Under the electron microscope microfibrils were found around adjacent degraded fibroblasts at the locations where collagen fibrils were destroyed and disappeared. In contrast, at the locations detached from inflammatory cell infiltration small bundles of microfibrils were seen. It is suggested that at the areas of destructive collagen structures the relative increase in type III and the appearance of microfibrils were caused by the reduction of type I. At the same time at the sites of detachment from the lesions, complete growth of type III and the appearance of microfibrils were found and were considered to be newly formed juvenile collagen structures. Moreover it is concluded that a balance proceeds with the qualitative changes in the types of collagen fibers involving breakdown and new formation.

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