Vaginal and oral microbes, host genotype and preterm birth

Abstract

Preterm birth (PTB) is a leading cause of infant mortality and morbidity in the US and across the globe. Infection and associated inflammation are important initiators for PTB pathways; an estimated 40% of PTBs are attributed to amniochorionic-decidual or systemic inflammation. Historically, intrauterine infections have been implicated in PTB; recent evidence suggests that infections remote from the fetal site may also be causative. There is strong epidemiological evidence that bacterial vaginosis and periodontitis--two syndromes characterized by perturbations in the normal vaginal and oral bacterial microflora, respectively--are linked to infection-associated PTB. Oral and vaginal environments are similar in their bacterial microbiology; identical bacterial species have been independently isolated in periodontitis and bacterial vaginosis. Periodontitis and bacterial vaginosis also share many behavioral and sociodemographic risk factors suggesting a possible common pathophysiology. Genetic polymorphisms in host inflammatory responses to infection are shared between bacterial vaginosis, periodontitis and PTB, suggesting common mechanisms through which host genotype modify the effect of abnormal bacterial colonization on preterm birth. We review the state of knowledge regarding the risk of PTB attributable to perturbations in bacterial flora in oral and vaginal sites and the role of host genetics in modifying the risk of infection-related PTB. We posit that bacterial species that are common in perturbed vaginal and oral sites are associated with PTB through their interaction with the host immune system.

Figure 1

Hypothesized parallel potential pathways for vaginal and oral flora leading to preterm birth

Figure 2. Relative risk of preterm birth with bacterial vaginosis

11 observational studies conducted between 1986 and 2007 on populations varying in sociodemographic variables and sample size were included. Y-axis intersects x-axis at relative risk = 1.

Figure 3. Relative risk of preterm birth associated with periodontitis

25 observational studies conducted between 1996 and 2009 on populations varying in sociodemographic characteristics and sample sizes were included. Y-axis intersects X-axis at relative risk = 1.