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Preterm birth (PTB), accompanied by low birth weight (LBW) or not, is a syndrome with tremendous risk factors and long-term health consequences for children. In recent decades, overwhelming studies have shown that periodontitis contributes to prematurity and LBW. This study was conducted to determine the link between maternal periodontitis and the pathogenesis of PTB and/or LBW through a rat infection model induced by Porphyromonas gingivalis, an important periodontopathic bacterium. The murine model was established by surgically ligating the left mandibular first molars and inoculating with P. gingivalis, and then all female rats initiated mating 6 weeks post infection. The gestational day and birth weight were recorded, and blood, amniotic fluid, and placental specimens were collected. Rats with a PTB and LBW newborns were observed in the P. gingivalis-infected group. Additionally, P. gingivalis infection significantly increased the maternal serum levels of interferon-γ and interleukin-1β, whereas no significant difference in the cytokine response was observed in the amniotic fluid. Moreover, with the translocation of P. gingivalis to placentas, remarkable changes in gestational tissues were found, followed by significantly enhanced expression of Toll-like receptor 2 (TLR2) as well as Fas and Fas ligand (FasL). These results support the concept that severe cases of periodontitis caused by P. gingivalis infection may be indicative of rats being more susceptible to PTB/LBW, probably through the activation of the TLR2 and Fas/FasL pathways within the placental tissues. This study gave us new insight into how maternal periodontopathogens might be linked to placental damage and premature pathogenesis.

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