Please use this identifier to cite or link to this item:
Type: Artigo de periódico
Title: Changes in MMPs and inflammatory cells in experimental gingivitis
Author: Lorencini, M
Silva, JAF
de la Hoz, CLR
Carvalho, HF
Stach-Machado, DR
Abstract: In periodontal disease, extensive disorganization of the extracellular matrix promotes the loss of adhesion between the teeth and periodontium. A previous study suggested a reduction in the area occupied by collagen in the gingiva, during the first week of periodontal disease induction, however, the remaining fibers were more compact and thicker. Therefore, it was decided to investigate which of the MMP-2, -9, -14 and RECK, an MMP inhibitor, were involved in these modifications taking place in early gingivitis induced by ligature. The results of gene expression analysis indicated no changes for RECK. MMP-14 showed a reduction at 7 days of inflammation, and there was an immediate increase in MMP-2 gene expression and enzymatic activity, apparently by the stimulation of resident cells such as fibroblasts. A peak of MMP-9 expression 5 days after ligature followed after the peak of enzymatic activity found two days earlier. This pattern was consistent with the kinetics of macrophage and neutrophil recruitment. Immunohistochemistry suggested that MMP-9 was produced by both resident and inflammatory cells. Based on this evidence, it is suggested that extracellular matrix remodeling is related to MMP-2 and -9 production and activation. This allowed us to conclude that the host inflammatory response represents a significant factor for the advance of periodontal diseases.
Subject: Matrix metalloproteinases
Inflammatory cells
Periodontal disease
Experimental model
Country: Espanha
Editor: F Hernandez
Citation: Histology And Histopathology. F Hernandez, v. 24, n. 2, n. 157, n. 166, 2009.
Rights: fechado
Date Issue: 2009
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File Description SizeFormat 
WOS000261696900004.pdf3.96 MBAdobe PDFView/Open

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.