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|Articles|April 15, 2010
Oral Bacteria Linked to Intrauterine Infections and Pre-term Birth
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Bacteria in the mouths of pregnant women can contribute to pre-term birth according to research from Case Western Reserve University, Cleveland, Ohio, and Hathaway Brown School, Shaker Heights. The findings are published in the April 2010 issue of the journal Infection and Immunity.
Approximately 12.7 percent of births in the U.S. are pre-term deliveries, a rate that reflects a 36 percent increase over the last 25 years. Intrauterine infection is recognized as a main cause of pre-term birth as well as late miscarriage and still birth. The cause of intrauterine infections has long been attributed to bacteria ascending into the uterus from the lower genital tract, however, recent studies indicate such infections are caused not only by bacteria found in the vaginal tract, but also in the mouth.
The human mouth is home to approximately 700 bacterial species. Gingivitis, a common problem associated with pregnancy, increases bacterial concentrations in the mouth further enhancing the possibility of transmission to the placenta through the bloodstream. In the study saliva and plaque samples were injected into the tails of pregnant mice to determine what bacteria are capable of oral-uterus transmission. Researchers identified a diverse group of bacterial species colonizing the mouse placenta, of which the majority originate in the oral cavity and are associated with adverse pregnancy outcomes in humans.
"This study provides the first insight into the diversity of oral bacteria associated with intrauterine infection," say the researchers. "Based on our findings, we postulate that periodontal therapies targeted at consistently reducing the total bacterial load in the mother's oral cavity may be effective in improving birth outcomes."
Reference: Y. Fardini, P. Chung, R. Dumm, N. Joshi, Y.W. Han. 2010. Transmission of diverse oral bacteria to murine placenta: evidence for the oral microbiome as a potential source of intrauterine infection. Infection and Immunity, 78. 4: 1789-1796.
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