Interactions of lymphotoxin alpha (TNF-beta), angiotensin-converting enzyme (ACE), and endothelin-1 (ET-1) gene polymorphisms in adult periodontitis

• Published in: Journal of periodontology (1970) Vol. 72; no. 1; p. 85
• Main Authors: Hollá, L I, Fassmann, A, Vasků, A, Znojil, V, Vanek, J, Vácha, J
• Format: Journal Article
• Language: English
• Published: United States 01.01.2001
• Subjects: Adult; Alleles; Case-Control Studies; Chi-Square Distribution; Chromosome Mapping; DNA Transposable Elements - genetics; Endothelin-1 - genetics; Female; Gene Frequency; Genetic Predisposition to Disease; Genotype; Homozygote; Humans; Lymphotoxin-alpha - genetics; Male; Middle Aged; Odds Ratio; Peptidyl-Dipeptidase A - genetics; Periodontitis - genetics; Polymorphism, Genetic - genetics; Risk Factors; Sequence Deletion - genetics; Statistics as Topic
• ISSN: 0022-3492; 1943-3670
• DOI: 10.1902/jop.2001.72.1.85

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. 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. 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. 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.