Potential pathogenic mechanisms of periodontitis associated pregnancy complications.

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 PGE(2) and IL-1-beta 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-PGE(2) 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-PGE(2) levels at P = 0.023. These data suggest a dose-response relationship for increasing GCF-PGE(2) 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 microbial burden are associated with current PLBW.

Identifying losing sites at periodontal reevaluation.

Our present method for clinical evaluation of marginal periodontal tissues involves examination for bleeding and suppuration and the measurement of probing depth. There is little doubt that this method provides useful guidelines for evaluation of the overall periodontal status of dentitions. On an individual-site basis, however, it has limitations in the identification of locations prone to disease progression. So far, there is no reliably clinical, microbiologic, or other method to predict or identify sites with disease activity (i.e., ongoing loss of attachment). Therefore, there are no clear guidelines for distinguishing between active and arrested lesions. A treatment resulting in a plaque-free mouth with nonbleeding and shallow probing depths throughout the dentition will reduce the risk of residual, active disease. Such a result, although desirable, is not realistic for many patients. Therefore, the clinician is faced with the delicate task of evaluating sites with various grades of involvement using current clinical methods of examination.