In the present study, we have demonstrated the presence of P. gingivalis antigens on trophoblasts, decidual cells, amniotic epithelial cells, and vascular cells, suggesting a possible route of transmission from the vasculature to placental tissue.
Although the staining was present in both normal placentas and placentas affected by chorioamnionitis, the extent to which the latter were positive was 30% higher compared with the normal. The difference in staining between the two groups was statistically significant. As far as we know, this is the first report that documents increased expression of P. gingivalis antigens in human placental cells affected by chorioamnionitis.
is a Gram-negative anaerobe that can invade and survive within epithelial cells (Lamont and Jenkinson, 1998
). Infection by P. gingivalis
disrupts cytokine expression and increases cell proliferation while suppressing apoptosis (Mao et al., 2007
). All of these properties could potentially disrupt homeostasis in the placental tissues. It is also potentially important that, during the first 10-12 wks of gestation, the placenta is in a state of physiological hypoxia (James et al., 2006
), which would facilitate growth of anaerobes such as P. gingivalis
Preterm delivery of low-birthweight infants is a major public health concern that contributes to infant mortality and short- and long-term morbidity. Preterm delivery occurs in about 12% of births, although rates are higher (more than 20%) among poor and minority pregnant women. Despite dramatic advances in reproductive and neonatal medicine in general, the rate of preterm delivery is not decreasing in either developed or developing countries. While several risk factors for preterm delivery have been identified, their predictive power is limited, and there are no effective treatments to prolong pregnancy once preterm labor commences.
Our present findings show that P. gingivalis antigens are more frequent and more intense in the chorioamnionitis placenta compared with the normal placenta. This is in accordance with some epidemiological studies that have associated severe periodontal disease with subsequently increased bacterial load and preterm delivery.
We chose to focus on P. gingivalis
, since this organism is the predominant pathogen in severe cases of periodontal disease, is epidemiologically associated with preterm delivery, and expresses appropriate virulence properties in animal models. However, it is possible, and indeed likely, that other species—such as F. nucleatum, A. actinomycetemcomitans, P. intermedia. T. forsythia
, and T. denticola
—are present (Barak et al., 2007
). Other relevant factors are immune system competency, as well as the physical integrity of placental tissues and their ability to resist bacterial intrusion. It is important to note that the reactivity to P. gingivalis
antibodies does not confirm the presence of whole bacteria, but rather their antigens.
In conclusion, accumulating evidence implicates a role for periodontal pathogens such as P. gingivalis
in pregnancy complications, including preterm delivery. To date, this evidence is based on epidemiological studies and the pathogenic attributes of the organism in animal placentas following infection and in human amniotic fluid (Lin et al., 2003
; Leon et al., 2007
). Analysis of our data confirms the results of another study (Barak et al., 2007
) showing that P. gingivalis
antigens can be present in the normal asymptomatic human placenta. The significance of this finding remains to be determined, although asymptomatic tissue colonization of bacteria is well-documented. The hypothesis is that P. gingivalis
bacteremia spreads to the placenta, and infection becomes common. Disease would then occur when there was a change in the overall host-microbe balance, much as in periodontal disease.
Disease outcome following P. gingivalis colonization of the placenta may therefore be dependent on many factors, including bacterial genotype and load, host physiology, genetics, and environmental factors.