Interactions of lymphotoxin alpha (TNF-beta), angiotensin-converting enzyme (ACE), and endothelin-1 (ET-1) gene polymorphisms in adult periodontitis
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Alleles MeSH
- Peptidyl-Dipeptidase A genetics MeSH
- Adult MeSH
- Endothelin-1 genetics MeSH
- Gene Frequency MeSH
- Genetic Predisposition to Disease MeSH
- Genotype MeSH
- Homozygote MeSH
- Middle Aged MeSH
- Humans MeSH
- Lymphotoxin-alpha genetics MeSH
- Chromosome Mapping MeSH
- Odds Ratio MeSH
- Periodontitis genetics MeSH
- Polymorphism, Genetic genetics MeSH
- Risk Factors MeSH
- Chi-Square Distribution MeSH
- Sequence Deletion genetics MeSH
- Statistics as Topic MeSH
- Case-Control Studies MeSH
- DNA Transposable Elements genetics MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Peptidyl-Dipeptidase A MeSH
- Endothelin-1 MeSH
- Lymphotoxin-alpha MeSH
- DNA Transposable Elements MeSH
BACKGROUND: Adult periodontitis is a complex multifactorial disease whose etiology is not well defined. To investigate whether the genes encoded within the HLA class III region may confer susceptibility to periodontitis, polymorphisms in the ET-1 and TNF-beta genes were analyzed together with the I/D polymorphism of the ACE gene. METHODS: We determined allele and genotype frequencies of the NcoI bi-allelic polymorphism of the TNF-beta gene, the I/D (insertion/deletion) polymorphism of the ACE gene, and the TaqI polymorphism of the ET-1 gene in 63 Caucasian patients with adult periodontitis and 95 orally healthy controls. RESULTS: We found a significant difference in a 3 locus combination of genotypes between patients and controls (P<0.05). In the next analyses, no significant differences were found in allele frequencies of single genes, but we did find a significant difference in the genotype distribution between cases and controls for TNF-beta (P<0.03). Differences were also observed for 2 locus combinations of ACE and TNF-beta genotypes (P<0.03), and the ET-1 and TNF-beta (P<0.05) genes. Evidence of deviation from Hardy-Weinberg equilibrium was observed in the periodontitis group for TNF-beta, with an absence of the B1B1 homozygotes in patients. CONCLUSIONS: This study is of an exploratory nature. Considering the number of significant results, however, at least a part of the observed associations may obviously be real and our findings suggest that interactions of the TNF-beta, ET-1, and ACE genes may be involved in susceptibility to adult periodontitis.
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