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A Novel Method for Involving Women of Color at High Risk for Preterm Birth in Research Priority Setting
Published on: January 12, 2018
Periodontal infection with Porphyromonas gingivalis induces preterm birth and lower birth weight in rats
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.
Abstract:
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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