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Background: Matrix metalloproteinases (MMPs) are involved in periodontal tissue remodeling and degradation. Polymorphisms in the promoter region of the MMP-2 and -9 genes and in the coding region of the MMP-12 gene could affect transcription and the function of these enzymes. The aim of the present study was to determine the association between the aforementioned MMP polymorphisms and generalized aggressive periodontitis (GAgP)., Methods: Genomic DNA was obtained from the peripheral blood of 92 subjects with GAgP and 157 periodontally healthy subjects. MMP-2 -735C/T, MMP-9 -1562C/T, and MMP-12 357Asn/Ser 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(2), logistic regression, and Mann-Whitney U tests., Results: The genotype distributions, allele frequencies, and rare allele carriage of MMP-2 and MMP-12 genes were similar in GAgP and healthy subjects (P >0.05). T allele frequency and T allele carriage of the MMP-9 -1562 C/T polymorphism were significantly lower in the GAgP group than in the healthy group (P <0.05). In addition, logistic regression analysis revealed a protective effect for MMP-9 -1562 T allele carriers (odds ratio = 0.52; P = 0.04)., Conclusions: MMP-2 -735C/T and MMP-12 357Asn/Ser polymorphisms are not related to GAgP. Conversely, the MMP-9 -1562 gene T allele might be associated with a decreased risk for GAgP in the Turkish population.

Background: 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)., Methods: 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., Results: There was no significant difference in the distribution of TLR2 and TLR4 genotypes and allele frequencies between GAgP patients and healthy subjects (P > 0.05). 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., Conclusions: 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.

Background: 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)., Methods: 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., Results: 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; P >0.05). 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%) (P >0.05). 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)., Conclusions: 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.