We hypothesize (I) PD-driven endotoxemia may increase the host responsiveness to autoantigens via TLR4 activation and (II) this participates in development and propagation of RA (III) circulating PD-derived bacterial DNA is taken up by phagocytes, activates TLR9, and thus increases the responsiveness to autoantigens.
Carriage of the TLR4-rs7873784 was associated with higher odds for periodontitis (GG versus CC and GC, P = 0.05, OR 2.30, 95% CI 1.00-5.63; GG versus GC, P = 0.05, OR 2.46, 95% CI 1.01-5.99).
On the other hand, while the sTLR-2 and the paired epithelial cell associated TLR-2 mRNA exhibited a direct correlation (r2 = 0.62), that of sTLR4 and TLR-4 mRNA exhibited an inverse correlation (r2 = 0.53) in the periodontitis cohort.
The involvement of TLR4 gene in the inflammatory response of periodontitis results in periodontitis, and its mechanism may be that it activates TLR4, so as to affect the expression of T-bet, GATA3 and Foxp3.
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.
Three SNPs of TLR4, i.e., rs1927911 (TT/CC+CT), rs2149356 (TT/GG+GT) and rs2737190 (GG/AA+AG), were associated with moderate/severe chronic periodontitis in Chinese population infected with <i>P. gingivalis</i>.<i>P. gingivalis</i>, which interacted with TLR4 gene plays an important role in the pathogenesis of periodontitis.
CONCLUSIONS Taken together, our results revealed that SAC effectively attenuates LPS-induced inflammation and apoptosis via the TLR4/NF-kappaB pathway and that SAC is effective in treating periodontitis.