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Polymorphisms in the +252(A/G) lymphotoxin‐alpha and the −308(A/G) tumor necrosis factor‐alpha genes and susceptibility to chronic periodontitis in a Czech population
Author(s) -
Fassmann Antonin,
Holla Lydie Izakovicova,
Buckova Dana,
Vasku Anna,
Znojil Vladimir,
Vanek Jiri
Publication year - 2003
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.1600-0765.2003.00661.x
Subject(s) - lymphotoxin alpha , lymphotoxin , alpha (finance) , tumor necrosis factor alpha , lymphotoxin beta receptor , periodontitis , chronic periodontitis , gene , population , immunology , biology , genetics , medicine , environmental health , construct validity , nursing , patient satisfaction
Background: Periodontitis is an inflammatory disease that leads to irreversible attachment loss, bone destruction and eventually tooth loss. Tumor necrosis factor (TNF), a pluripotent proinflammatory cytokine that is able to induce tissue destruction and bone resorption, has been implicated in the pathogenesis of periodontal disease. Methods: In this study, we investigated an association between chronic periodontitis and two previously described bi‐allelic polymorphisms in the TNF locus: a G to A transition at position −308 in the 5′promoter region of the TNF‐α gene and an Nco I restriction fragment length polymorphism (RFLP) in the first intron (position +252A/G) of the lymphotoxin α (LT‐α) gene. Genomic DNA was obtained from 132 patients with chronic periodontitis together with 114 age‐ and gender‐matched unrelated control subjects. Results: The TNF‐α (−308G/A) polymorphism itself showed no association with chronic periodontitis, whereas the frequency distribution of the LT‐α (+252A/G) genotypes showed statistically significant differences between patients and the reference group. The proportion of individuals carrying the LT‐α 1/1 genotype was significantly lower in the group of patients with chronic periodontitis (0.8%) than in the control group (8.8%) ( P < 0.0094, P corr < 0.05). However, the significant differences in the frequencies of the combined genotypes (TNF‐α and LT‐α) between the control and the patient groups were found using a simulation by applying the Monte‐Carlo method ( P < 0.01). Conclusion: Our data suggest that combined genotypes composed of the TNF‐α and LT‐α gene polymorphisms may influence the susceptibility to chronic periodontitis. We also showed that, comparing the two genes, the 1/1 genotype of the Nco I polymorphism in the first intron of the LT‐α gene is a more informative marker and it may be one of the protective genetic factors against chronic periodontitis in our population.