Periodontal disease, oxidative stress, and risk for preeclampsia.
BACKGROUND
Maternal periodontal infection is associated with an increased risk for preeclampsia. Periodontal infection is also associated with increased oxidative stress. Our objective was to determine the relationship among maternal periodontal disease, maternal oxidative stress, and the development of preeclampsia.


METHODS
A secondary analysis of prospectively collected data from the Oral Conditions and Pregnancy Study was performed. A cohort of healthy women enrolled at <26 weeks of gestation underwent an oral examination, serum sampling, and delivery follow-up. A periodontal infection was categorized by clinical parameters as healthy or mild or moderate/severe periodontal infection. Preeclampsia was defined by the American Congress of Obstetricians and Gynecologists criteria as blood pressure >140/90 mmHg and >or=1+ proteinuria on a catheterized specimen. Maternal blood was assayed for 8-isoprostane concentrations using an enzyme-linked immunosorbent assay and stratified as elevated (>or=75th percentile) or not elevated (<75th percentile). Odds ratios (ORs) for preeclampsia were calculated and stratified by periodontal disease and the level of 8-isoprostane concentration.


RESULTS
A total of 34 (4.3%) of 791 women developed preeclampsia. Women with an 8-isoprostane concentration >or=75th percentile at enrollment were more likely to develop preeclampsia compared to women with an 8-isoprostane concentration <75th percentile (38.2% versus 24.4%, respectively; P = 0.07; OR: 1.91; 95% confidence interval [CI]: 0.94 to 3.90). Among women with moderate/severe periodontal disease, an elevated 8-isoprostane concentration (>or=75th percentile) did not significantly increase the likelihood for preeclampsia (adjusted OR: 2.08; 95% CI: 0.65 to 6.60).


CONCLUSIONS
Women with oxidative stress early in pregnancy, as measured by an 8-isoprostane concentration >or=75th percentile, were at an increased risk for developing preeclampsia. The presence of periodontal disease did not appear to modify this risk.
Horton
Amanda L
AL
Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of North Carolina, Chapel Hill, NC 27599-7516, USA. horton.alm@gmail.com
Boggess
Kim A
KA
Moss
Kevin L
KL
Beck
James
J
Offenbacher
Steven
S
D000328:Adult; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D015237:Dinoprost / Q000031:analogs & derivatives* / Q000097:blood; D005260:Female; D006801:Humans; D016017:Odds Ratio; D018384:Oxidative Stress; D010510:Periodontal Diseases / Q000097:blood / Q000150:complications*; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000097:blood*; D011446:Prospective Studies; D012016:Reference Values; D012307:Risk Factors; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D055815:Young Adult
D015415:Biomarkers; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost