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Histochemical study of periodontitis in MRL/* mice with immunological disorder

免疫紊乱MRL/*小鼠牙周炎的组织化学研究

基本信息

批准号：
03670859
负责人：
TANAKA Akio
金额：
$ 1.28万
依托单位：
Osaka Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1992
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-03670859/
关键词：
Autoimmune MRL * mouse Periodontitis Histochemistry 歯周組織マウス

项目摘要

The unequivocal main cause of periodontitis is bacterial plaque present in the gingival sulcus, and it is widely accepted that Gram-negative anaerobic rods in dental plaque are essentially responsible for the onset and progression of this disease. In addition however, there are many other factors, local and systemic, that effect the onset and progression of periodontitis. Systemic factors include nutritional deficiency, metabolic disturbance, endocrinopathy, allergy, and autoimmune diseases. In the latter case, vasculitis is often evident, and its presence in periodontal tissue is thought to result in more severe tissue destruction. In order to elucidate this process, periodontitis was induced by ligature in MRL/MPJ-lpr/lpr mice with autoimmune disease, and studied histochemically. The gingival sulcular epithelium (GSE) became ulcerated and polymorphonuclear leukocytes (PMNs) were found to infiltrate the GSE. Macrophages, lymphocytes and PMNs were observed beneath the GSE and junctional epithelium (JE). The PMNs were ultrastructurally evident in the intercellular spaces of the epithelium, and PMNs, macrophages with large dense bodies and lymphocytes also were seen adjacent to the GSE and JE. The 1-positive were observable immunohistochemically in and beneath the GSE and JE. Cells with intense acid phosphatase activity accumulated beneath the GSE and JE. These cells were considered to be macrophages. This cellular accumulation beneath the GSE and JE indicates that the destruction of periodontal tissue due to inflammation is exacerbated by the coexistence of vasculitis.

牙周炎的明确的主要原因是存在于龈沟中的细菌菌斑，并且广泛认为牙菌斑中的革兰氏阴性厌氧杆菌是该疾病的发病和进展的主要原因。然而，除此之外，还有许多其他因素，局部和全身，影响牙周炎的发病和进展。全身因素包括营养缺乏、代谢紊乱、内分泌疾病、过敏和自身免疫性疾病。在后一种情况下，血管炎通常是明显的，并且它在牙周组织中的存在被认为会导致更严重的组织破坏。为了阐明这一过程，牙周炎的结扎诱导MRL/MPJ-lpr/lpr小鼠自身免疫性疾病，并进行了组织化学研究。牙龈沟上皮（GSE）溃疡，发现多形核白细胞（PMN）浸润GSE。在GSE和交界上皮（JE）下观察到巨噬细胞、淋巴细胞和中性粒细胞。电镜下可见嗜中性粒细胞分布于上皮细胞间隙，在GSE和JE附近可见嗜中性粒细胞、巨噬细胞和淋巴细胞。免疫组化结果显示，1-阳性细胞位于GSE和JE内及下方。酸性磷酸酶活性强的细胞聚集在GSE和JE下方。这些细胞被认为是巨噬细胞。GSE和JE下方的细胞积聚表明，由于炎症引起的牙周组织破坏因血管炎的共存而加剧。