Periodontal infection with Porphyromonas gingivalis induces preterm birth and lower birth weight in rats

S Liang1, H Ren2, H Guo1

  • 1The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine, Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

Insights

Maternal periodontitis, caused by Porphyromonas gingivalis, is linked to preterm birth (PTB) and low birth weight (LBW) in rats. Infection activated placental pathways, suggesting a mechanism for pregnancy complications.

Area of Science:

  • Reproductive Biology
  • Oral Health
  • Immunology

Background:

  • Periodontitis is increasingly linked to adverse pregnancy outcomes like preterm birth (PTB) and low birth weight (LBW).
  • Porphyromonas gingivalis is a key bacterium implicated in severe periodontitis.
  • The precise mechanisms connecting maternal periodontitis to PTB/LBW remain incompletely understood.

Purpose of the Study:

  • To investigate the causal relationship between maternal periodontitis induced by Porphyromonas gingivalis and the pathogenesis of PTB and/or LBW in a rat model.
  • To explore the underlying molecular mechanisms involving immune responses and placental changes.

Main Methods:

  • A rat model of periodontitis was established by ligating molars and inoculating with P. gingivalis.
  • Infected rats were mated, and gestational outcomes (gestational day, birth weight) were recorded.
  • Maternal serum, amniotic fluid, and placental tissues were analyzed for cytokine levels, bacterial translocation, and expression of TLR2, Fas, and FasL.

Main Results:

  • P. gingivalis infection in rats led to a higher incidence of PTB and LBW.
  • Maternal serum levels of interferon-γ and interleukin-1β were significantly elevated post-infection.
  • P. gingivalis translocated to placentas, causing tissue damage and upregulating TLR2 and Fas/FasL expression.

Conclusions:

  • Severe maternal periodontitis caused by P. gingivalis infection increases susceptibility to PTB and LBW in rats.
  • Activation of TLR2 and Fas/FasL pathways in placental tissues appears to mediate these pregnancy complications.
  • This study provides insights into the link between maternal periodontopathogens, placental damage, and premature birth.

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