Monocyte chemotactic protein-3: possible involvement in apical periodontitis chemotaxis

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Monocyte chemotactic protein-3: possible involvement in apical periodontitis chemotaxis

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Monocyte chemotactic protein-3: possible involvement in apical periodontitis chemotaxis

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Title: Monocyte chemotactic protein-3: possible involvement in apical periodontitis chemotaxis
Author: Dezerega Piwonka, Andrea Patricia; Osorio A., Constanza; Mardones Peñailillo, Jeannette Isabel; Dutzan, Nicolás; Franco, María Eugenia; Gamonal, Jorge; Oyarzún Droguett, Alejandro; Overall, M. C.; Hernández, Marcela
Abstract: Aim  To study the expression of monocyte chemotactic protein-3 (MCP-3, also known as chemokine CCL-7) in tissue from apical lesions (AL) and to associate MCP-3 expression with symptomatic or asymptomatic apical periodontitis. Methodology  To determine the expression of MCP-3 in AL, biopsies obtained during tooth extraction procedures were fixed, subjected to routine processing and diagnosed as apical granuloma (AG) (n = 7) or radicular cyst (RC) (n = 5). As controls, apical periodontal ligament (PDL) specimens from healthy premolars extracted for orthodontics reasons were included (n = 7). All specimens were immunostained for MCP-3 and examined under a light microscope. In addition, homogenates from AL (n = 14) and healthy PDL samples (n = 7) were studied through immunowestern blot. Finally, periapical exudates samples were collected from root canals of teeth having diagnosis of symptomatic (n = 14) and asymptomatic apical periodontitis (n = 14) during routine endodontic treatments and analysed by immunowestern blot and densitometry. Results  MCP-3 was detected in AG and RC and localized mainly to inflammatory leucocytes, whereas no expression was observed in healthy PDLs. MCP-3 was also detected in periapical exudate, and its levels were significantly higher in symptomatic than in asymptomatic apical periodontitis. Conclusions  MCP-3 was expressed in AL and its levels associated with clinical symptoms. MCP-3 might play a role in disease pathogenesis, possibly by stimulating mononuclear chemotaxis.
URI: http://www.captura.uchile.cl/handle/2250/14688
Date: 2010-10
dc.identifier.citation: International Endodontic Journal 2010: 43(10) 902–908


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