Interleukin-2 -330 and 166 gene polymorphisms in relation to aggressive or chronic periodontitis and the presence of periodontopathic bacteria.
OBJECTIVE
As a pro-inflammatory cytokine, interleukin-2 mediates the activation, growth and differentiation of T and B lymphocytes and natural killer cells. Promoter polymorphisms of the interleukin-2 gene have been associated with altered interleukin-2 production or identified as prognostic markers for various infectious diseases. Therefore, the aim of this study was to evaluate two polymorphisms at positions -330 T/G and 166 G/T in patients with generalized chronic periodontitis (n = 58) or generalized aggressive periodontitis (n = 73) in comparison with periodontitis-free controls (n = 69).


METHODS
Both interleukin-2 polymorphisms were analyzed using the polymerase chain reaction with sequence-specific primers. Distributions of single alleles, genotypes and haplotypes were calculated using the chi-square test. Risk factor analyses were carried out by logistic regression with respect to established cofactors for periodontitis. The presence of subgingival bacteria in an individual were analyzed using a molecular biological method (the micro-Ident test).


RESULTS
The interleukin-2 genotype -330 TG occurred less frequently in patients with chronic periodontitis (25.9% vs. 49.3%). Moreover, this genotype decreased the adjusted odds ratio for chronic periodontitis (odds ratio = 0.394), whereas the interleukin-2 genotype 166 TT and the haplotype combination interleukin-2 -330,166 TT : TT were associated with an increased adjusted odds ratio (odds ratio = 2.82 or 2.97). For the latter interleukin-2 combination, a positive association for the subgingival presence of Porphyromonas gingivalis (81.3% vs. 59.5%) and bacteria of the 'red complex' (78.1% vs. 56.0%) was shown.


CONCLUSIONS
The interleukin-2 genotypes -330 TG and 166 TT, as well as the combination genotype interleukin-2 TT : TT, could be putative prognostic factors for chronic periodontitis.
Reichert
S
S
University School of Dental Medicine, Department of Operative Dentistry and Periodontology, Martin-Luther University Halle-Wittenberg, Halle (Saale), Germany. stefan.reichert@medizin.uni-halle.de
Machulla
H K G
HK
Klapproth
J
J
Zimmermann
U
U
Reichert
Y
Y
Gläser
C
C
Schaller
H-G
HG
Schulz
S
S
D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000502:physiology; D010520:Aggressive Periodontitis / Q000276:immunology* / Q000382:microbiology; D000483:Alleles; D001439:Bacteroides / Q000502:physiology; D055113:Chronic Periodontitis / Q000276:immunology* / Q000382:microbiology; D005260:Female; D005787:Gene Frequency / Q000235:genetics; D005838:Genotype; D006147:Guanine; D006239:Haplotypes / Q000235:genetics; D006801:Humans; D007376:Interleukin-2 / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D017622:Periodontal Attachment Loss / Q000276:immunology / Q000382:microbiology; D010514:Periodontal Pocket / Q000276:immunology / Q000382:microbiology; D011110:Polymorphism, Genetic / Q000235:genetics*; D016966:Porphyromonas gingivalis / Q000502:physiology*; D018713:Prevotella intermedia / Q000502:physiology; D011401:Promoter Regions, Genetic / Q000235:genetics; D013941:Thymine; D048373:Treponema denticola / Q000502:physiology
C508594:IL2 protein, human; D007376:Interleukin-2; D006147:Guanine; D013941:Thymine