Potential Pathogenic Mechanisms of Periodontitis‐Associated Pregnancy Complications

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Abstract
During normal pregnancy, maternal hormones and locally acting cytokines play a key role in regulating the onset of labor, cervical ripening, uterine contraction, and delivery. Maternal infections during pregnancy have been demonstrated to perturb this normal cytokine and hormone‐regulated gestation, sometimes resulting in preterm labor, preterm premature rupture of membranes, and preterm low birth weight (PLBW), i.e., < 2,500 g and < 37 weeks of gestation. Our research focus has been to determine whether periodontal infections can provide sufficient challenge to the mother to trigger PLBW. New experiments from 48 case‐control subjects have measured gingival crevicular fluid (GCF) levels of PGE2 and IL‐1β to determine whether mediator levels were related to current pregnancy outcome. In addition, the levels of 4 periodontal pathogens were measured by using microbe‐specific DNA probes. Results indicate that GCF–PGE2 levels are significantly higher in PLBW mothers, as compared with normal birth weight (NBW) controls (131.4 ± 21.8 vs. 62.6 ± 10.3 [mean ± SE ng/mL], respectively, at P = 0.02). Furthermore, within primiparous PLBW mothers, there was a significant inverse association between birth weight (as well as gestational age) and GCF–PGE2 levels at P = 0.023. These data suggest a dose‐response relationship for increasing GCF–PGE2 as a marker of current periodontal disease activity and decreasing birth weight. Microbial data indicate that 4 organisms associated with mature plaque and progressing periodontitis—Bacteroides forsythus, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Treponema denticola—were detected at higher levels in PLBW mothers, as compared to NBW controls. These data suggest that biochemical measures of maternal periodontal status and oral microbiol burden are associated with current PLBW. Ann Periodontol 1998;3:233—250.