Abstract: Objective: To study the effect of Porphyromonas gingivalis on human extravillous trophoblast cell line (HTR-8) and the role of p-Akt in this process. Methods: HTR-8 cells were infected with Porphyromonas gingivalis ATCC 33277 at a multiplicity of infection (MOI) of 200 or 0. The target siRNA was chosen to inactivate PI3K, inverted microscope and confocal microscope were used to record the morphological changes of HTR-8 cells, flow cytometry was used to detect the apoptosis of HTR-8 cells after infection with Porphyromonas gingivalis, and real time-PCR was used to test the inactivation of siRNA whose target was PI3K. Results: When HTR-8 cells were infected with Porphyromonas gingivalis for 12 hours, there was no statistical significance of the apoptosis rate in MOI 200 group compared with MOI 0 group. HTR-8 cells were infected for 24 hours, the number of apoptotic cells in MOI 200 group significantly increased (P<0.01). Infected for 48 hours, the extent of apoptosis was more obvious compared with control group MOI 0 group (P<0.001). When HTR-8 cells were pretreated with siRNA and then co-cultured with Porphyromonas gingivalis for 48 hours (SI 200 Group), the relative amounts of PI3K mRNA in SI 200 group was much lower than that in interference group (C 200 group) (P<0.01). At the same time, the apoptosis rate of SI 200 group was greater than 45%, which was significantly higher than that of MOI 200 group (P<0.01); and there was no statistical difference of apoptosis rate between MOI 200 group and C 200 group. Conclusion: Porphyromonas gingivalis does induce apoptosis in human extravillous trophoblast cells and p-Akt is activated to inhibit the apoptosis of HTR-8 cells to some extent in this process. All of these suggest that the mechanism by which periodontitis promotes preterm low birth weight is that Porphyromonas gingivalis induced human extravillous trophoblastic cells apoptosis.

Key words: Periodontitis, Porphyromonas gingivalis, Preterm low birth weight, Apoptosis