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Vaginal and oral microbes, host genotype and preterm birth

Usha Srinivasan1, Dawn Misra, Mary L Marazita

  • 1Department of Epidemiology, School of Public Health, University of Michigan, Ann Arbor, MI, USA. usha@umich.edu

Medical Hypotheses
|November 28, 2009
PubMed

Insights

Infections and inflammation are key causes of preterm birth (PTB). Bacterial imbalances in the mouth and vagina may increase PTB risk, potentially influenced by host genetics.

Area of Science:

  • Reproductive Health
  • Microbiology
  • Immunology

Background:

  • Preterm birth (PTB) is a major global cause of infant mortality and morbidity.
  • Infection and inflammation are significant contributors to PTB, accounting for approximately 40% of cases.
  • Emerging evidence points to infections distant from the uterus as potential PTB initiators.

Purpose of the Study:

  • To review the current understanding of PTB risk associated with bacterial flora disruptions in oral and vaginal sites.
  • To explore the role of host genetics in modulating the risk of infection-related PTB.
  • To investigate potential shared pathophysiological mechanisms between bacterial vaginosis, periodontitis, and PTB.

Main Methods:

  • Review of epidemiological evidence linking bacterial vaginosis and periodontitis to PTB.
  • Analysis of shared bacterial species and risk factors between oral and vaginal dysbiosis.
  • Examination of genetic polymorphisms in host inflammatory responses relevant to PTB.

Main Results:

  • Bacterial vaginosis and periodontitis, characterized by altered microflora, are epidemiologically linked to infection-associated PTB.
  • Similar bacterial species and risk factors are observed in both oral and vaginal dysbiosis.
  • Shared genetic polymorphisms in inflammatory responses suggest common pathways linking host genotype to infection-related PTB.

Conclusions:

  • Perturbations in vaginal and oral bacterial flora are associated with increased PTB risk.
  • Host genetic factors likely interact with abnormal bacterial colonization to influence PTB.
  • Bacterial species common to dysbiotic oral and vaginal environments may contribute to PTB via immune system interactions.

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