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牙周疾病进展的一种新范式:牙龈结缔组织重塑伴胶原降解与纤维增粗同时发生。

A new paradigm in the periodontal disease progression: gingival connective tissue remodeling with simultaneous collagen degradation and fibers thickening.

作者信息

Lorencini M, Silva J A F, Almeida C A, Bruni-Cardoso A, Carvalho H F, Stach-Machado D R

机构信息

Department of Microbiology and Immunology, Institute of Biology, State University of Campinas (UNICAMP), Campinas, SP, Brazil.

出版信息

Tissue Cell. 2009 Feb;41(1):43-50. doi: 10.1016/j.tice.2008.07.001. Epub 2008 Sep 17.

DOI:10.1016/j.tice.2008.07.001
PMID:18801546
Abstract

Bacterial dental plaque is considered to be the main cause of periodontal diseases, but progression of the disease is also related to the host inflammatory response. The earliest affected tissue is the gingiva, but the specific mechanisms involved in the onset of this condition remain unclear. Frequently, collagen degradation is pointed as the main marker of periodontal disease progression, but the organization of the fibers in the gingival tissue is still unknown. The aim of the present study was to investigate the gingival extracellular matrix in a model of ligature-induced periodontal disease. Analysis of the microbiota indicated a progressive increase in the ratio of Gram-negative/Gram-positive microorganisms. There was no difference in the organization of reticulin fibers next to the epithelial basement membrane, whereas the arrangement of collagen fibers in the gingival connective tissue was significantly affected. Animals with inflammation presented a reduction of 35% in the total area occupied by collagen fibers. However, these fibers were thicker and more densely packed. These alterations involve type I, type III and type VI collagens as determined by immunohistochemistry. The results demonstrated the occurrence of marked reorganization of the gingival extracellular matrix in response to the inflammatory process, indicating a new paradigm in the periodontal disease progression: collagen degradation and fibers thickening, simultaneously.

摘要

细菌牙菌斑被认为是牙周疾病的主要病因,但疾病的进展也与宿主炎症反应有关。最早受影响的组织是牙龈,但其发病的具体机制仍不清楚。通常,胶原蛋白降解被认为是牙周疾病进展的主要标志,但牙龈组织中纤维的排列情况仍不清楚。本研究的目的是在结扎诱导的牙周疾病模型中研究牙龈细胞外基质。微生物群分析表明革兰氏阴性菌/革兰氏阳性菌的比例逐渐增加。上皮基底膜旁网状纤维的排列没有差异,而牙龈结缔组织中胶原纤维的排列受到显著影响。有炎症的动物胶原纤维所占总面积减少了35%。然而,这些纤维更粗且排列更紧密。免疫组织化学检测确定这些改变涉及I型、III型和VI型胶原蛋白。结果表明,牙龈细胞外基质在炎症过程中发生了显著的重组反应,这表明牙周疾病进展存在一种新的模式:胶原蛋白降解和纤维增粗同时发生。

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