Background Recent studies suggest that periodontal disease, as a source of subclinical and persistent infection, may induce systemic inflammatory responses that increase the risk of adverse pregnancy outcomes. Objectives To examine the existing evidence on the relationship between periodontal disease and adverse pregnancy outcomes. Search strategy Published studies identified via searches of the MEDLINE, EMBASE, CINAHL, and Current Contents full‐text databases. Selection criteria We identified and selected observational studies (i.e. case–control, cross‐sectional, and cohort) and nonrandomised controlled studies or randomised controlled trials that examined periodontal disease as a risk factor for adverse pregnancy outcomes. Data collection and analysis Odds ratios (OR) or risk ratios (RR) were extracted or calculated from the studies’ data. We calculated pooled effect size for two clinical controlled trials but not for the observational studies due to the heterogeneity in definitions for periodontal disease and adverse pregnancy outcomes across studies. Main results Twenty‐five studies (13 case–control, 9 cohort, and 3 controlled trials) were identified. The studies focused on preterm low birthweight, low birthweight, preterm birth, birthweight by gestational age, miscarriage or pregnancy loss, and pre‐eclampsia. Of the chosen studies, 18 suggested an association between periodontal disease and increased risk of adverse pregnancy outcome (ORs ranging from 1.10 to 20.0) and 7 found no evidence of an association (ORs ranging from 0.78 to 2.54). Three clinical trial studies suggest that oral prophylaxis and periodontal treatment can lead to a 57% reduction in preterm low birthweight (pooled RR 0.43; 95% CI 0.24–0.78) and a 50% reduction in preterm births (RR 0.5; 95% CI 0.20–1.30). Author's conclusions Periodontal disease may be associated with an increased risk of adverse pregnancy outcome. However, more methodologically rigorous studies are needed for confirmation.
Specific conditions predispose to GDM which itself is associated with a significantly increased risk of maternal and fetal morbidity.
Background The empirical literature on the effects of disaster on pregnancy and the postpartum period is limited. The objective of this review was to examine the existing evidence on the effect of disasters on perinatal health. Methods A systematic review was conducted by searching electronic databases (MEDLINE, EMBASE, Cinahl, PsycInfo), including literature on disasters and pregnancy outcomes (e.g., preterm birth, low birthweight, congenital anomalies), mental health, and child development. 110 articles were identified, but many published reports were anecdotes or recommendations rather than systematic studies. The final review included 49 peer-reviewed studies that met inclusion criteria. Results Studies addressing the World Trade Center disaster of September 11th and other terrorist attacks, environmental/chemical disasters, and natural disasters such as hurricanes and earthquakes were identified. Disasters of various types may reduce fetal growth in some women, though there does not appear to be an effect on gestational age at birth. Severity of exposure is the major predictor of mental health issues among pregnant and postpartum women. The mother's mental health after a disaster may more strongly influence on child development than any direct effect of disaster-related prenatal stress. Conclusions There is evidence that disaster impacts maternal mental health and some perinatal health outcomes, particular among highly-exposed women. Future research should focus on under-studied outcomes such as spontaneous abortion. Relief workers and clinicians should concentrate on the most exposed women, particularly with respect to mental health.
The predominant etiologic theory of preeclampsia is that reduced uteroplacental perfusion is the unique pathogenic process in the development of preeclampsia. Decreased uteroplacental blood flow would result in lower birth weights. To date, no study has assessed the effect of preeclampsia on birth weight by gestational age. Thus, the authors conducted a retrospective cohort study based on 97,270 pregnancies that resulted in delivery between 1991 and 1996 at 35 hospitals in northern and central Alberta, Canada. Differences in mean birth weight between women with preeclampsia and normotensive women ranged from -547.5 g to 239.5 g for gestational age categories ranging from < or = 32 weeks to > or = 2 weeks. The birth weights were statistically significantly lower among mothers with preeclampsia who delivered at < or = 37 weeks, with an average difference of -352.5 g. However, the birth weights were not lower among preeclamptic mothers who delivered after 37 weeks (average difference of 49.0 g). In Alberta, 61.2% of preeclamptic patients gave birth after 37 weeks of gestation. The authors conclude that babies born to mothers with preeclampsia at term have fetal growth similar to that of babies born to normotensive mothers. This finding does not endorse the currently held theory that reduced uteroplacental perfusion is the unique pathophysiologic process in preeclampsia.
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