Periodontal health and pregnancy

This article discusses factors that affect periodontal (gum) health and implications associated with delay in conception and reported adverse pregnancy outcomes. Periodontal disease is the result of a host/parasite response in a susceptible group of people whose immune response is hyper-responsive to microbial colonisation of the subgingival (gum) tooth interface. The oral cavity is naturally colonised by more than 500 species of bacteria, some of which are pathognomonic for periodontal disease in patients with susceptibility. These bacteria trigger the immune response resulting in release of pro-inflammatory cytokines (promoters of inflammatory response) not just at the point of microbial infection but also throughout the body. This general up-regulation of the immune response is implicated as the mechanism involved in other systemic conditions, such as atherosclerotic cardiovascular disease, rheumatoid arthritis, aspiration pneumonia and chronic obstructive pulmonary disease (Hajishengallis, 2015). Pregnant women do not seem to harbour different groups of microbes, but preterm mothers have been shown to have higher levels of subgingival bacteria compared to mothers who go to term (Borgo et al, 2014). The acute phase inflammatory marker, C-reactive protein, has been found to be up to 65% higher during pregnancy where periodontal disease is present, indicating a general increase in the systemic inflammatory pathways (Pitiphat et al, 2006). Bacteraemia following chewing/tooth brushing may result in periodontal pathogens and their by-products reaching the placenta and spreading to fetal circulation and amniotic fluid. This may trigger immune/inflammatory responses in the placental/fetal compartment that have been linked to miscarriage, premature birth, pre-eclampsia and low birth weight. Fetal inflammatory tissue damage may also increase the risk for perinatal morbidity/mortality (Bobetsis et al, 2006; Clothier et al, 2007; Genco and Williams, 2010; Madianos et al, 2013).