In addition, miR-22-3p also upregulated the expression levels of the inflammatory cytokines tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-8 in PDLSC through SIRT1 pathway and downregulated the expression of TLR-2 and TLR-4. miR-22-3p is a new target either for the treatment of periodontitis or the improvement of inflammation caused by orthodontics.
The objective of this study was to investigate the role of TLR-2 in inflammation and alveolar bone loss in a murine model of ligature-induced peri-implantitis and to compare it with ligature-induced periodontitis.
Naringin-carrying CHC-β-GP-glycerol hydrogel sites showed significantly reduced periodontal bone loss (P <0.05) and inflammatory infiltration (P <0.01) as well as significantly downregulated TLR2 (P <0.05), RAGE (P <0.01), and TNF-α (P <0.05) relative to the sites with experimental periodontitis alone.
Our data shows potential interaction between IFN-γ and TLR2 responses in hPDLSCs, which might be involved in regulation of immune response in inflammatory diseases, and particularly periodontitis.
The expression of TLR2 and CD14 was greatest in the periodontitis group that was classified as severe grade, followed by moderate and mild grades, which suggests a role of TLR2 and CD14 in the pathogenesis of chronic periodontitis.
We investigated the effects of a synthetic GAG, GM-0111, on various molecular events associated with periodontitis: growth of Porphyromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) pathogenic bacteria associated with periodontitis; activation of pro-inflammatory signaling through TLR2 and TLR4 in mouse macrophage RAW 264.7 cells and heterologously expressed HEK 293 cells; osteoclast formation and bone matrix resorption in cultured mouse pre-osteoclasts.
In conclusion, these novel findings indicate that baicalin inhibits the TLR2 and TLR4 expression and the downstream signaling and mitigates inflammatory responses and the alveolar bone loss in rat experimental periodontitis.
We conclude that Lipid 654 and Lipid 430 have the potential to promote TLR2-dependent bone loss as is reported in experimental periodontitis following oral infection with P. gingivalis.
Although periodontitis might significantly increase TLR-2 and TLR-4 gene expression in gingival tissues, smoking habit in periodontitis subjects could selectively potentiate TLR-4 gene expression.
The meta-analysis showed no association between periodontitis and the TLR2 753Arg allele (Odds ratio [OR]=0.962, 95% confidence interval [CI]=0.662-1.400, p=0.841).
The aim of study was to evaluate the methylation status and the expression of TLR2 gene in gingival samples from individuals with and without periodontitis.
The aim of this study was to comprehensively investigate TLR2 linkage disequilibrium (LD) regions for their potential associations with periodontitis in two large analysis populations of aggressive (AgP) and chronic periodontitis (CP) of North West European descent.
In conclusion, although no significant role of the TLR2 gene in periodontitis was found, our results indicate that TLR9 haplotypes may be associated with susceptibility to CP.
Although there was no association of the TLR2 polymorphism Arg753Gln with periodontitis, heterozygous carriers (Arg/Gln) were at a higher risk for colonization with bacteria of the 'red complex' (corrected p-value = 0.042).
The TLR2 Arg753Gln mutant allele was not found in periodontitis patients, while a heterozygous frequency of 6% (6 of 100) was detected in the controls.
Because Toll-like receptor 2 and Toll-like receptor 4 have been shown to play an important role in the recognition of periodontal pathogens, we investigated the relevance of genetic variations in TLR2 and TLR4 to susceptibility to periodontitis.