Synopsis
There is early evidence supporting the association between periodontitis and adverse pregnancy outcomes including preterm birth, low birth weight and preeclampsia.
There are several factors proposed to explain the association including:
- 1. Inflammatory mediators
- 2. Oral bacterial dissemination
Information
Oral microbial imbalance is associated with adverse pregnancy outcomesi. These include preterm birth, low birth weight and preeclampsia. The bacterial imbalance in the mother’s oral cavity is thought to be linked to maternal immunity and infant health leading to some studies hypothesising this imbalance to be the link between the mouth and the adverse pregnancy outcomes.
Pregnancy related pathology in the oral cavity is most commonly found in gingival tissueii. Gingival inflammation is plaque induced but modified by oestrogen and progesterone during pregnancyi, iii. Studies have identified that these hormones can alter subgingival microbiota, compromise periodontal ligament cells and change the maternal immune response. Gingivitis typically precedes periodontitis. The evidence base between periodontal disease and adverse pregnancy outcomes have been controversial with some supporting the link and others finding contradictions. This article will focus on what is known regarding the mechanisms between periodontal disease and pregnancy.
Dental treatment during pregnancy is safe. People planning to become pregnant should have dental treatment done ideally beforehand to minimise the impact that hormonal fluctuations have on oral health.
During pregnancy, there is overproduction of oestrogen and progesterone with the values shifting depending on the stage of reproduction. Some studies have suggested that these hormones can affect the species of bacteria present in the periodontium. One study assessing the oral microbiota differences in pregnancy determined an increase in pathogenic A. actinomycetemcomitans, S. mutans and P. gingivalis in pregnant women than in non-pregnant women. The same study noted an increase of periodontal pathogens in preterm delivery and showed that women with pre-eclampsia who had an adverse pregnancy outcome had higher rates of periodontal pathogensiv. Another study demonstrated that hormones could act as an essential growth factor for some of the pathogensii.
The hormones are also attributed to affecting periodontal ligament cells by either changing the effectiveness of the epithelium as a barrier to bacterial insult or by affecting the capacity of collagen repair. Oestrogen and progesterone have also been shown to increase the rate of folate metabolism in gingival tissue thereby, leaving insufficient quantities for tissue repair. Oestrogen has also been shown to reduce collagen production when introduced to gingival fibroblasts in vitro. Hormones have also been involved in the immune response to oral pathogens.
Immune responses also change during pregnancy with neutrophil function being impaired. This may increase the susceptibility of pregnant women to gingival inflammation. Pregnancy hormones increase levels of prostaglandins however, their influence on leukocytes has not been consolidated with some showing an increase in chemotaxis and proliferation but others contradicting these views.
The mechanisms by which periodontal disease is linked to adverse pregnancy outcomes has been categorized into direct and indirect pathways. The direct pathway involves the translocation of oral microorganisms to the placenta through haematogenous spread or through the genitourinary tract. The presence of this bacteria may lead to development of amniochorionic infection causing uterine contractility and cervical ripening contributing to an increased risk of preterm birth. One study determined that foetal immunoglobulin to oral microbes was associated with an increased risk of preterm birthii, v.
Indirectly, the association is thought to occur due to an increase in pro-inflammatory cytokines. These inflammatory mediators circulate and lead to early contractions when in the fetoplacental unit or can enhance cytokine production when reaching the liver that then influences the fetoplacental unitiii.
Further research is required to ascertain the links between oral health and adverse pregnancy outcomes but there is sufficient evidence to indicate that monitoring and management of oral health diseases in pregnant patients is vital in reducing the adverse outcomes from occurring.
i Ye C, Kapila Y. Oral microbiome shifts during pregnancy and adverse pregnancy outcomes: Hormonal and Immunologic changes at play. Periodontology 2000. 2021; 87: 267-281
ii Yenen Z, Ataçağ T. Oral care in pregnancy. J Turk Ger Gynecol Assoc. 2019 Nov 28;20(4):264-268.
iii Raju K, Berens L. Periodontology and pregnancy: An overview of biomedical and epidemiological evidence. Periodontology 2000 2021. 87:132-142
iv Jang H, Patoine A, Wu TT, Castillo DA, Xiao J. Oral microflora and pregnancy: a systematic review and meta-analysis. Sci Rep. 2021 Aug 19;11(1):16870.
v Daalderop LA, et al. Periodontal Disease and Pregnancy Outcomes: Overview of Systematic Reviews. JDR Clinical & Translational Research. 2018; 3(1):1 0-27.