Background: Periodontal diseases originate from a group of oral inflammatory infections initiated by oral pathogens. Among these pathogens, Gram-negative bacteria such as p. gingivalis play a major role in chronic periodontitis. P. gingivalis harbours lipopolysaccharide (LPS) which enables it to attach to TLR2.
Objectives: Evaluating the effects of P. gingivalis and E. coli LPS on the gene expression of TLRs and inflammatory cytokines in human dental pulp stem cells (hDPSCs).
Methods: We evaluated the expression level of TLR2, TLR4, IL-6, IL-10, and 1L-18 in hDPSCs treated with 1μg/mL of P. gingivalis lipopolysaccharide and E. coli LPS at three different exposure times using Real-time RT-PCR.
Result: The test group treated with P. gingivalis LPS showed a high level of TLR4 expression in 24 hours exposure period and the lowest expression in 48 hours of exposure time. In the case of IL-10, the lowest expression was in the 24 hours exposure period. Although in the E.coli LPS treated group, IL-10 showed the highest expression in 24 and lowest in 48 hours exposure period. Moreover, IL-18 in P. gingivalis LPS treated group showed a significant difference between 6, 24, and 48-time periods of exposure, but not in the E. coli LPS treated group.
Conclusion: Both types of LPS stimulate inflammation through TLR4 expression. P. gingivalis LPS performs more potentially than E. coli in terms of stimulating inflammation at the first 24 hours of exposure. Nevertheless, our study confirmed that increasing P. gingivalis and/or the E.coli LPS exposure time, despite acting as an inflammatory stimulator, apparently showed anti-inflammatory properties.