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Host response to periodontopathic microorganisms can be modulated by genetic factors. Accumulated evidence highlighted the role of renin-angiotensin system (RAS) in inflammatory response thus potential implication of this molecular system in the pathogenesis of periodontitis can be suggested. The present study investigated common genetic variants of molecules within the RAS family namely angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II type 1 receptor (AT1R) in relation to generalized aggressive periodontitis (G-AgP).DNA was obtained from peripheral blood of 103 G-AgP patients and 100 periodontally healthy subjects. ACE I/D, AGT M235T and AT1R A1166C polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism method. Chi-square, ANOVA and logistic regression were used in statistical analyses.Both ACE I/D and AT1R polymorphisms were similar in G-AgP and healthy groups (p0.05). G-AgP subjects exhibited decreased AGT TT genotype and T allele frequency as compared to healthy subjects (p0.05). The same trend was also observed in the nonsmoker subgroup regarding investigated RAS polymorphisms.Present findings suggest that AGT M235T TT genotype and T allele might be associated with decreased risk for G-AgP in Turkish population.

Aim: Evidence suggests that the ultimate product of the renin-angiotensin system (RAS), angiotensin II, exerts inflammatory actions. The present study aimed to evaluate the inter-relation between gene polymorphisms of the RAS components; angiotensin converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II type-I receptor (AT1R), and severe chronic periodontitis (CP). Material and Methods: DNA was obtained from peripheral blood of 90 CP patients and 126 periodontally healthy subjects, and the clinical parameters were recorded. ACE I/D, AGT M235T and AT1R A1166C polymorphisms were genotyped by the PCR-RFLP method. Chi-square, ANOVA and logistic regression methods were used in statistical analyses. Results: The frequency of the ACE D allele was significantly lower in the CP group than the healthy group (p corr = 0.015). CP subjects exhibited increased C allele carriage and C allele frequency of the AT1R gene (p corr = 0.03 and p corr = 0.03, respectively). All clinical parameters of CP patients were found to be similar in variant allele-carrying and non-carrying subjects (p>0.05). Conclusions: The present findings suggest that ACE I/D and AT1R polymorphisms might be associated with susceptibility to CP but not with disease severity. The D allele of ACE I/D might be associated with decreased, whereas the C variant of AT 1R A1166C might be associated with an elevated risk for CP in Turkish population.

Aim Matrix metalloproteinases (MMPs) are involved in periodontal tissue remodeling and degradation. MMP polymorphisms could alter transcription and function of these enzymes. The aim of this study was to investigate MMP-2 , MMP-9 and MMP-12 gene polymorphisms in relation to susceptibility to severe chronic periodontitis (CP). Methods Genomic DNA was obtained from peripheral blood of 87 severe CP patients and 107 periodontally healthy subjects. MMP-2 − 735C / T , MMP-9 − 1562C / T and MMP − 12 357Asn / Ser gene polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism. Probing depth, clinical attachment loss, supragingival plaque accumulation and bleeding on probing were recorded. The data were analyzed by chi-square, logistic regression and Mann–Whitney- U -tests. Results The genotype distributions and allele frequencies of MMP-2 , MMP-9 and MMP-12 genes were similar in CP and healthy subjects ( p > 0.05). Differences between rare allele carriage rates of CP and healthy groups regarding MMP-2 , MMP-9 and MMP-12 gene polymorphisms were not significant ( p > 0.05). However, T allele carriers of MMP-9 − 1562 gene had less risk for CP (OR = 0.36; 95% CI = 0.16–0.81). Conclusion These data suggest that MMP-2 − 735C / T , MMP-9 − 1562C / T and MMP-12 357Asn / Ser polymorphisms are not associated with susceptibility to severe CP in Turkish population. However, T allele of MMP-9 − 1562 gene might be associated with decreased susceptibility to severe CP.

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.

Toll-like receptors (TLRs) recognize exogenous ligands such as lipopolysaccharide and bacterial lipoprotein during the immune responses to pathogens. The aim of the present study was to investigate whether TLR2 and TLR4 gene polymorphisms are related to susceptibility to generalized aggressive periodontitis (GAgP).A total of 245 subjects were included in the present study. Genomic DNA was obtained from the peripheral blood of 90 patients with GAgP and 155 periodontally healthy subjects. Probing depth, clinical attachment loss, plaque accumulation, and bleeding on probing were recorded. The TLR2 gene Arg753Gln and Arg677Trp polymorphisms and TLR4 gene Asp299Gly and Thr399Ile polymorphisms were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method. The data were analyzed by chi2 and Mann-Whitney U tests and logistic regression analysis.There was no significant difference in the distribution of TLR2 and TLR4 genotypes and allele frequencies between GAgP patients and healthy subjects (P0.05). The TLR2 753Gln allele was found in 3.9% of the GAgP patients compared to 6.1% in the healthy group. The GAgP patients and healthy subjects did not show homozygosity for the TLR2 mutant alleles. The TLR2 677Trp mutant allele was not found in any of the subjects; 2.2% of the GAgP patients and 2.9% of the periodontally healthy subjects were identified as having the TLR4 299Gly polymorphic allele. With regard to the TLR4 399Ile polymorphic allele, 1.1% of the GAgP patients and 2.3% of the periodontally healthy subjects had this allele.The present study failed to find any significant association between the TLR polymorphisms and GAgP, potentially because of the small sample size. To the best of our knowledge, this was the first study to examine the prevalence of these polymorphisms in a Turkish population with aggressive periodontitis.

Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) are involved in the pathogenesis of periodontitis by controlling proteolytic events in the extracellular matrix. This study was designed to investigate the association of t-PA and PAI-1 gene polymorphisms with chronic periodontitis (CP).One hundred eighty-nine subjects were included. Genomic DNA was obtained from the peripheral blood of 84 patients with CP and 105 periodontally healthy subjects. Polymerase chain reaction and endonuclease digestion was used to genotype the 4G/5G polymorphism in the promoter region of the PAI-1 gene and the Alu-repeat insertion (I)/deletion (D) polymorphism in intron 8 of the t-PA gene.The genotype distributions and allele frequencies of t-PA polymorphism were not different between patients with CP and healthy subjects (24.7% I/I, 45.7% I/D, and 29.6% D/D and 30.3% I/I, 45.5% I/D, and 24.2% D/D, respectively; P0.05). The t-PA D allele frequency was similar in patients with CP (52.4%) and healthy subjects (46.5%). PAI-1 genotype distribution in patients with CP (30.9% 4G/4G, 35.8% 4G/5G, and 33.3% 5G/5G) and healthy subjects (36.2% 4G/4G, 41.9% 4G/5G, and 21.9% 5G/5G) was also similar. The 4G allele frequency was not different between patients with CP (48.8%) and healthy subjects (57.1%) (P0.05). The 4G allele frequency in non-smoking CP patients was significantly lower than in non-smoking, healthy subjects (chi(2) = 4.201; P = 0.040). Non-smoking CP patients also had a significantly lower percentage of 4G-positive genotypes compared to non-smoking healthy subjects (chi(2) = 5.046; P = 0.025).t-PA or PAI-1 genotypes are not associated with susceptibility to CP in Turkish subjects. Conversely, the 4G allele of the PAI-1 gene could be related to a decreased susceptibility to CP in non-smokers.

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 χ2 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