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1.
Arch Oral Biol ; 57(9): 1256-63, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22425265

RESUMO

OBJECTIVE: Three single nucleotide polymorphisms (SNPs), -1082, -819 and -592, located on the promoter region of IL10 gene have been associated with high in vitro IL-10 production and autoimmune diseases. We aim to investigate whether polymorphisms in the IL10 gene would influence dental implant loss. METHODS: We evaluated a total of 277 unrelated patients, including 185 individuals presenting at least one osseointegrated implant in function for six months or more and with no implant failure, and 92 individuals presenting at least one implant loss. DNA was extracted from buccal mucosa cells and SNPs were genotyped using TaqMan(®) probes-based assays. RESULTS: Multiple logistic regression showed association between dental implant failure with -819(C/T) genotype (OR=3.27; 95% CI=1.02-10.46; p=0.0334). However, considering the statistical significance level α=0.004 (adjusted by Bonferroni correction of multiple comparisons), these results lost their significance. No association of dental implant loss with genotypes and alleles of the -1082 and -592 SNPs, as well as IL10 haplotypes in genotype/allele forms were found (p=0.9400; p=0.8861). CONCLUSIONS: Neither the IL10 gene polymorphisms, nor haplotypes or other covariates were associated with susceptibility to dental implant failure in the studied population.


Assuntos
Implantes Dentários , Falha de Restauração Dentária , Interleucina-10/genética , Polimorfismo de Nucleotídeo Único/genética , Adenina , Alelos , Anti-Inflamatórios/uso terapêutico , Anti-Inflamatórios não Esteroides/uso terapêutico , Doenças Cardiovasculares/complicações , Estudos de Casos e Controles , Citosina , Feminino , Predisposição Genética para Doença/genética , Genótipo , Guanina , Haplótipos/genética , Humanos , Hipertensão/complicações , Desequilíbrio de Ligação/genética , Masculino , Pessoa de Meia-Idade , Osseointegração/fisiologia , Regiões Promotoras Genéticas/genética , Doenças Reumáticas/complicações , Fumar , Timina
2.
Int J Oral Maxillofac Implants ; 23(3): 409-16, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18700362

RESUMO

The observation that clinical factors alone do not explain why some patients develop implant loss; the understanding of the osseointegrated implant failure as a complex, multifactorial process; and the observed aggregation of repetitive failure in certain individuals raise interesting questions related to host susceptibility to dental implant failure. Genetic analysis applied to dental implants began in the late 1990s, and since then, increased interest in genetic susceptibility to the phenotype has been demonstrated by several studies. These studies, however, have been based on and limited to candidate gene association analysis and were intended to find associations between specific alleles and/or genotypes of genetic markers and susceptibility to implant failure. The aim of this review is to provide a brief description of the current methodology for genetic analysis of complex traits, followed by a comprehensive review of the literature related to genetic susceptibility to dental implant failure and a discussion of different aspects of the applied methodology. Moreover, a novel approach of genome wide, case-control analysis is discussed as an alternative method to access genetic influence to dental implant failure mechanisms. Advances toward the elucidation of the genetic basis of dental implant loss may contribute to the understanding of why some patients do not respond to currently available treatments while others do and provide potential targets for effective screening, prevention, and treatment. For example, clinicians might be able to estimate, before the elective surgical procedure, the risk of a given patient to develop a negative individual host response.


Assuntos
Implantação Dentária Endóssea , Implantes Dentários , Falha de Restauração Dentária , Osseointegração/genética , Humanos , Interleucinas/genética , Metaloproteinases da Matriz/genética , Herança Multifatorial , Polimorfismo Genético , Fator de Necrose Tumoral alfa/genética
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