Evidence of periopathogenic microorganisms in placentas of women with preeclampsia
- PMID: 17397314
- DOI: 10.1902/jop.2007.060362
Evidence of periopathogenic microorganisms in placentas of women with preeclampsia
Abstract
Background: Periodontal disease is a chronic inflammatory infectious disease that may act as a focus of infection. Preeclampsia is a pregnancy-specific hypertensive disorder that often leads to maternal morbidity and mortality. Acute atherosis, the placental lesion of preeclampsia, shares many histopathological features with atherosclerosis. Recently, chronic infection was linked to the initiation of atherosclerosis. Oral pathogens have been detected in atherosclerotic plaques, where they may play a role in the development and progression of atherosclerosis. The purpose of the present study was to explore the possibility that periopathogenic bacteria may translocate into the placental tissues of women with preeclampsia.
Methods: Samples were taken from 16 placentas obtained from cesarean sections of women with preeclampsia and from 14 age-matched healthy pregnant women. Polymerase chain reaction was used to detect Actinobacillus actinomycetemcomitans, Fusobacterium nucleatum ssp., Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythensis, and Treponema denticola.
Results: Eight of the 16 (50%) placenta specimens were positive for one or more periopathogenic bacteria in the preeclampsia group, compared to only two of the 14 samples (14.3%) from controls. Bacterial counts were statistically significantly higher in the preeclampsia group for all of the periopathogenic bacteria examined (P <or=0.0055). Although all of the target periopathogenic bacteria were found in the preeclampsia group, only three (P. gingivalis, T. forsythensis, and T. denticola) were found in the control group.
Conclusion: The significant presence of periopathogenic microorganisms or their products in human placentas of women with preeclampsia may suggest a possible contribution of periopathogenic bacteria to the pathogenesis of this syndrome.
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