TORONTO — A combination of maternal periodontal disease and high levels of maternal C-reactive protein is associated with significantly more risk of preeclampsia than either risk factor alone, according to a new analysis of the Oral Conditions and Pregnancy Study.
“There seems to be some type of synergy when both are combined,” said Dr. Michael S. Ruma, who presented the findings at the annual meeting of the Society for Gynecologic Investigation.
A secondary analysis of 775 healthy pregnant women who had oral examinations and C-reactive protein (CRP) levels measured at enrollment (less than 26 weeks' gestation) found that preeclampsia was more common in those with high CRP levels alone (OR 2.6), and those with moderate to severe periodontal disease (PD) alone (OR 2.0)—but a combination of high CRP levels and moderate to severe PD increased the odds ratio to 7.0.
A total of 31 women (4%) developed preeclampsia in the cohort. The rate of preeclampsia was greater among women with a high CRP level (above the 75th percentile) than for women with a low CRP level (at or below the 75th percentile): 7% and 3%, respectively. The addition of mild PD to the elevated CRP level significantly increased the risk of preeclampsia from an odds ratio of 2.6 to 6.0 and moderate to severe PD increased it further (OR 7.0).
“Maternal systemic inflammation may be in the causal pathway between periodontal disease and the development of preeclampsia,” said Dr. Ruma of the University of North Carolina at Chapel Hill. However, he said, future research is required to further understand this phenomenon. “Both periodontitis and preeclampsia are multifactorial, but the implication is that inflammation in the mother is leading to systemic disease,” he said in an interview.
A separate study presented at the meeting suggests that such maternal inflammation may also be transferred to the fetus—particularly in the setting of maternal smoking.
In a study of 277 women, Dr. John P. Newnham of the Women and Infants Research Foundation at King Edward Memorial Hospital in Perth, Western Australia, and his colleagues found that 12% of women with PD had babies who were small for gestational age (SGA), compared with 2% of women who had healthy gums (“Gum Disease Again Tied to Pregnancy Outcomes,” FAMILY PRACTICE NEWS, Sept. 1, 2005, p. 50). Further analysis of this study, which was presented at the meeting, found this effect is significantly increased (25%) in women who smoke. Additionally, the researchers found that in smokers, both with and without PD, inflammatory markers (CRP and tumor necrosis factor-α) were significantly elevated in umbilical cord blood, indicating an inflammatory response in the fetus.
“The thing I found absolutely fascinating was this marked inflammation in the fetus at birth as a result of the woman smoking in pregnancy—and PD added further to it,” Dr. Newnham said in an interview. “Smoking not only increases the risk of PD, which everyone has known for a long time, but smoking increased the inflammatory markers in the cord blood and PD added to this.”
Although the absence of PD is associated with better obstetric outcomes, it is not known whether treating PD during pregnancy is beneficial or harmful, said Dr. Newnham. “We are in equipoise. We know inflamed periodontal tissue can release cytokines and prostaglandins,” he said, leading some to hypothesize that the treatment of PD could temporarily increase maternal systemic inflammation.