Diabetic conditions such as HG induce IL-1β and sIL-6R production from macrophages in inflammatory periodontal tissues and may exacerbate the periodontitis synergistically via MMP-1 production from HGFs.
I found that macrophage-like cells, fibroblast-like cells, vascular endothelial cells and gingival epithelial cells were stained more intensely for MMP-1 and were observed more frequently in the periodontitis affected group than in the control group.
Our results revealed that although studies of the association between MMP-8 -799 C/T variant and the susceptibility to periodontitis have not yielded consistent results, MMP-1 (-1607 1G/2G, -519 A/G, and -422 A/T), MMP-2 (-1575 G/A, -1306 C/T, -790 T/G, and -735 C/T), MMP-3 (-1171 5A/6A), MMP-8 (-381 A/G and +17 C/G), MMP-9 (-1562 C/T and +279 R/Q), and MMP-12 (-357 Asn/Ser), as well as MMP-13 (-77 A/G, 11A/12A) SNPs are not related to periodontitis risk.Conclusions.
The pooled results showed significant association between periodontitis susceptibility and MMP-1g.-1607dupG polymorphism in homozygote (2G/2G versus 1G/1G, OR = 1.50, 95% CI = 1.02-2.20) and dominant model analysis (2G/2G+2G/1G versus 1G/1G, OR = 1.28, 95% CI = 1.04-1.57).
The current study demonstrated that the Matrix metalloproteinase-1-1607 1G-to-2G polymorphism was associated with susceptibility to periodontitis, apparently, severe periodontitis.
This meta-analysis demonstrates a lack of association between the TLR2 Arg753Gln, TLR4 Asp299Gly, Thr399Ile, MMP-9 -1562 C/T polymorphisms and periodontitis, but shows an association between the MMP-1 -1607 G2G2 genotype and periodontitis in Asians.
Nonsmoker subjects with periodontitis had statistically significantly higher MMP-1, lower MMP-9 and TIMP-1 expression and higher MMP-1/TIMP-1 ratio than smokers; and higher MMP-8 expression and MMP-8/TIMP-1 and MMP-1/TIMP-1 ratios than healthy nonsmokers.
Our data demonstrate a limited role for MMP1-1607 SNP in periodontitis, where the extensive chronic antigenic challenge exposure overcomes the genetic control and plays a major role in the determination of MMP-1 expression.
The ratios of MMP-1/TIMP-2 (P <0.01), MMP-3/TIMP-2 (P <0.05), MMP-9/TIMP-2 (P <0.05), and MMP-1/TIMP-3 (P <0.01) from periodontitis lesions were significantly higher than those in the control tissues.
Analysis of polymorphisms showed no differences in distribution of the -1607 1G/2G and -519 A/G variants in the MMP-1 gene between the healthy and periodontitis group (p > 0.05).
Our data did not support the hypothesis that MMP-1 and/or MMP-3 gene promoter polymorphisms influenced the susceptibility to periodontitis in Japanese patients, indicating MMP-1 and MMP-3 expressions were regulated by complex processes such as cytokine network in periodontal disease rather than gene polymorphisms.
Sections of tissue biopsies obtained from advanced, destructive periodontitis were compared with minimally inflamed periodontal tissues in relation to the distribution of type I (interstitial) collagenase.