ABSTRACT
AIM: Toll-like receptor (TLR) gene polymorphisms could affect the host's ability to respond to microbial pathogens. In this case-control study, the association of TLR2 and TLR4 gene polymorphisms with chronic periodontitis (CP) was investigated. MATERIALS AND METHODS: Genomic DNA was obtained from the peripheral blood of 83 patients with CP and 106 periodontally healthy subjects. The TLR2 Arg753Gly, Arg677Trp and TLR4 Asp299Gly, Thr399Ile gene polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. The data were analysed by a chi2 test, logistic regression analysis and the Mann-Whitney U test. RESULTS: The 753Gln allele was found in 6.1% of the CP patients as compared with 6.6% in the control group (p>0.05). The frequency of the 299Gly and 399Ile allele was 2.4% and 1.8% in CP patients. For the healthy subjects, the frequency was 2.8% for the 299Gly and 2.5% for the 399Ile allele (p>0.05). None of the CP patients or healthy subjects showed homozygosity for the TLR2 and TLR4 alleles. Percentage of sites with bleeding on probing and plaque were significantly higher in 299Gly-positive patients compared with 299Gly-negative patients (p<0.05). CONCLUSION: These results showed that the TLR2 and TLR4 gene polymorphisms studied are not associated with susceptibility to CP in Turkish patients.
Subject(s)
Arginine/genetics , Aspartic Acid/genetics , Glycine/genetics , Isoleucine/genetics , Periodontitis/genetics , Polymorphism, Genetic/genetics , Threonine/genetics , Toll-Like Receptor 2/genetics , Toll-Like Receptor 4/genetics , Adult , Aged , Alleles , Case-Control Studies , Chronic Disease , DNA/genetics , Dental Plaque/genetics , Female , Gene Frequency/genetics , Genotype , Gingival Hemorrhage/genetics , Humans , Male , Middle Aged , TurkeyABSTRACT
AIM: Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) have important roles in proteolytic events in periodontitis. The aim of this study was to investigate TPA and PAI-1 gene polymorphisms in relation to susceptibility to generalized aggressive periodontitis (G-AgP). METHODS: Genomic DNA was obtained from peripheral blood of 90 G-AgP patients and 154 periodontally healthy subjects. 4G/5G polymorphism in the promoter region of the PAI-1 gene and Alu-repeat insertion/deletion (I/D) polymorphism in intron 8 of the TPA gene were genotyped by polymerase chain reaction and endonuclease digestion. RESULTS: The genotype distributions of TPA and PAI-1 genes were similar between G-AgP and healthy subjects (p>0.05). The distribution of TPA genotypes in G-AgP patients was 33.4% D/D, 44.4% I/D, and 22.2% I/I and was 26.3% D/D, 40.4% I/D, and 33.3% I/I in healthy subjects. The D allele was 55.6% in G-AgP and 46.6% in healthy subjects. There was a significant difference among study groups in D allele frequencies (p=0.044). The PAI-1 genotype distribution in G-AgP was 29.1% 4G/4G, 43.0% 4G/5G, and 27.9% 5G/5G, while it was 35.7% 4G/4G, 43.8% 4G/5G, and 20.5% 5G/5G in healthy subjects. CONCLUSION: These data suggest that the D polymorphic allele of TPA gene polymorphism could be associated with susceptibility to G-AgP in Turkish subjects.
