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Authordc.contributor.authorCavalla Ruiz, Ian Franco 
Authordc.contributor.authorBiguetti, Claudia C. 
Authordc.contributor.authorDionisio, Thiago J. 
Authordc.contributor.authorAzevedo, Michelle C. S. 
Authordc.contributor.authorMartins, Walter, Jr. 
Authordc.contributor.authorSantos, Carlos F. 
Authordc.contributor.authorTrombone, Ana Paula F. 
Authordc.contributor.authorSilva, Renato M. 
Authordc.contributor.authorLetra, Ariadne 
Authordc.contributor.authorGarlet, Gustavo P. 
Admission datedc.date.accessioned2018-08-01T16:37:22Z
Available datedc.date.available2018-08-01T16:37:22Z
Publication datedc.date.issued2018
Cita de ítemdc.identifier.citationCytokine, 103 (2018): 142–149es_ES
Identifierdc.identifier.other10.1016/j.cyto.2017.09.022
Identifierdc.identifier.urihttp://repositorio.uchile.cl/handle/2250/150529
Abstractdc.description.abstractChronic and aggressive periodontitis are infectious diseases characterized by the irreversible destruction of periodontal tissues, which is mediated by the host inflammatory immune response triggered by periodontal infection. The chemokine receptor CCR5 play an important role in disease pathogenesis, contributing to pro inflammatory response and osteoclastogenesis. CCR5 Delta 32 (rs333) is a loss-of-function mutation in the CCR5 gene, which can potentially modulate the host response and, consequently periodontitis outcome. Thus, we investigated the effect of the CCR5 Delta 32 mutation over the risk to suffer periodontitis in a cohort of Brazilian patients (total N = 699), representative of disease susceptibility (chronic periodontitis, N = 197; and aggressive periodontitis, N-= 91) or resistance (chronic gingivitis, N = 193) phenotypes, and healthy subjects (N = 218). Additionally, we assayed the influence of CCR5 Delta 32 in the expression of the biomarkers TNFa, IL-10, IL-6, IFN-y and T-bet, and key periodontal pathogens P. gingivalis, T. forsythia, and T. denticola. In the association analysis of resistant versus susceptible subjects, CCR5 Delta 32 mutant allele-carriers proved significantly protected against chronic (OR 0.49; 95% CI 0.29-0.83; p-value 0.01) and aggressive (OR 0.46; 95% CI 0.22-0.94; p-value 0.03) periodontitis. Further, heterozygous subjects exhibited significantly decreased expression of TNFa in periodontal tissues, pointing to a functional effect of the mutation in periodontal tissues during the progression of the disease. Conversely, no significant changes were observed in the presence or quantity of the periodontal pathogens P. gingivalis, T. forsythia, and T. denticola in the subgingival biofilm that could be attributable to the mutant genotype.es_ES
Patrocinadordc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) 2014/03276-0 2014/17886-4es_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherElsevieres_ES
Type of licensedc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile*
Link to Licensedc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/*
Sourcedc.sourceCytokinees_ES
Keywordsdc.subjectPeriodontitises_ES
Keywordsdc.subjectCCR5 Delta 32es_ES
Keywordsdc.subjectInflammationes_ES
Keywordsdc.subjectPathogenses_ES
Títulodc.titleCCR5 Delta 32 (rs333) polymorphism is associated with decreased risk of chronic and aggressive periodontitis: a case control analysis based in disease resistance and susceptibility phenotypeses_ES
Document typedc.typeArtículo de revistaes_ES
Catalogueruchile.catalogadortjnes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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Attribution-NonCommercial-NoDerivs 3.0 Chile
Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs 3.0 Chile