Periodontal disease and PRETERM birth

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    Anonymous
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    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.

    Researches done by Offenbacher et al at North Carolina Univeristy show that periodontitis may be linked to preterm pregnancies and low birth weight. More than 60% of mortality among infants without congenital or anatomical defects is attributable to PLBW. If periodontitis is confirmed as a risk factor for PLBW, it could provide new opportunities to reduce infant mortality.
    In a study on 124 women by Offenbacher, O’Reilly and Katz, it was shown that women with periodontitis has an almost eight fold greater chance of having PLBW infants than mothers without periodontal disease. Pre-term labor appears to be mediated by the mother’s secreted anti-inflammatory agents such as prostaglandin in response to an infection.
    Offenbacher et al found a two fold increase of prostaglandin E2 in the gum area (crevicular fluid) around the teeth of women with PLBW infants as compared to women with normal birth weight infants. This suggests a relationship between prostaglandin concentration in the gum area and inside the amniotic sac. These data suggest that biochemical measures of maternal periodontal status and oral microbial burden are associated with current PLBW.

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