Potential Pathogenic Mechanisms of Periodontitis‐Associated Pregnancy Complications

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 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.

Periodontal Disease and Preterm Birth, is There any Relationship?

“…This association is highly significant with odds ratio of 5.8 (p=0.04). These findings are in agreement with many other studies that found a positive correlation [4,[6][7][8][9][10].…”

Influence of diltiazem in combination with a sucrose-rich diet on gingival alterations in rats

“…Microscopically, there was only a mild infl ammation in the animals (Figure 1), which is particularly relevant because the diet followed by the animals was expected to cause gingivitis. Based on previous studies 11,12,18 that described the sucroserich diet as a model to induce periodontal disease (gingivitis and periodontitis), we aimed to promote natural accumulation of supragingival plaque on the dentogingival area and consequently experimental gingivitis. However, our result was similar to that of Galvão et al 19 (2003), who reported that a sucroserich diet was not capable of promoting more infl ammation than that seen in rats treated with standard rat lab chow.…”

“…Diltiazem was administered orally in daily doses of 5, 25, 50 or 100 mg/kg body weight during 40 or 60 days, using a hypodermic needle and an injector device assembled manually. The animals were fed daily a sucrose-rich diet composed of 56% refi ned sugar, 30% integral powdered milk and 14% standard ground chow, 11,12 which were weighed in an electronic balance and mixed manually. The food was prepared daily by adding a small amount of water to obtain a pasty consistence.…”

Can Oral Anaerobic Bacteria cause Adverse Pregnancy Outcomes?/ Дали Оралните Анаеробни Бактерии Можат Да Доведат До Лоши Опстетрички Исходи?

“…The systemic dissemination via the haematogenous route of inflammatory mediators and prostaglandins such as IL-6, IL-8, and TNF-a, PGE2 originating from the periodontal inflammatory process are not dissimilar to those associated with the onset of labor [19]. Therefore, is the on set of labor a single or cumulative effect of the increased levels of inflammatory process originating from the infected periodontium that acts as a reservoir for microbial products and inflammatory mediators.…”