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Genetic polymorphism of the tumor necrosis factor (TNF)‐α promoter region in families with localized early‐onset periodontitis
Author(s) -
Shapira Lior,
Stabholz Ayala,
Rieckmann Peter,
Kruse Niels
Publication year - 2001
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2001.360307.x
Subject(s) - genotype , tumor necrosis factor alpha , promoter , allele , biology , periodontitis , proinflammatory cytokine , allele frequency , gene polymorphism , aggressive periodontitis , gene , immunology , microbiology and biotechnology , genetics , medicine , gene expression , inflammation
Tumor necrosis factor (TNF)‐α is a potent proinflammatory cytokine that is able to induce tissue destruction and bone resorption. A G‐to‐A polymorphism at the −308 position of the TNF‐α promoter region was suggested to influence TNF‐α production. We had previously shown that monocytes of patients with localized early‐onset periodontitis (EOP) secrete high levels of TNF‐α compared to matched controls. The aim of the present study was to investigate the possible link between the −308 polymorphism in the TNF‐α gene and EOP. Genomic DNA was extracted from the blood of 64 individuals from 11 nuclear families with EOP. The TNF‐α polymorphism at −308 was assessed using allele‐specific polymerase chain reaction. 77% of the tested adolescents were found to have the G/G genotype, and 23% had the A/G genotype. In the diseased subjects, 81% were with G/G genotype and 19% with A/G genotype. The healthy children had 74% G/G genotype, while 26% had A/G genotype. The differences between the disease group and the healthy group were not statistically significant. In summary, the present results could not demonstrate any link between EOP and genetic polymorphism in the −308 position of the TNF‐α promoter.