Role of Maternal Periodontitis in Preterm Birth

Abstract

In the last two decades, many studies have focused on whether periodontitis is a risk factor for preterm birth (PTB). However, both epidemiological investigation and intervention trials have reached contradictory results from different studies. What explains the different findings, and how should future studies be conducted to better assess this risk factor? This article reviews recent epidemiological, animal, and in vitro studies as well as intervention trials that evaluate the link between periodontitis and PTB. Periodontitis may act as a distant reservoir of microbes and inflammatory mediators and contribute to the induction of PTB. Animal studies revealed that maternal infections with periodontal pathogens increase levels of circulating IL-1β, IL-6, IL-8, IL-17, and TNF-α and induce PTB. In vitro models showed that periodontal pathogens/byproducts induce COX-2, IL-8, IFN-γ, and TNF-α secretion and/or apoptosis in placental tissues/cells. The effectiveness of periodontal treatment to prevent PTB is influenced by the diagnostic criteria of periodontitis, microbial community composition, severity of periodontitis, treatment strategy, treatment efficiency, and the period of treatment during pregnancy. Although intervention trials reported contradictory results, oral health maintenance is an important part of preventive care that is both effective and safe throughout pregnancy and should be supported before and during pregnancy. As contradictory epidemiological and intervention studies continue to be published, two new ideas are proposed here: (1) severe and/or generalized periodontitis promotes PTB and (2) periodontitis only promotes PTB for pregnant women who are young or HIV-infected or have preeclampsia, pre-pregnancy obesity, or susceptible genotypes.

Keywords: low birth weight; periodontitis; pregnancy; preterm birth; risk factor.

Figure 1

Periodontal disease is a highly prevalent infectious and inflammatory disease of tooth-supporting tissues. (A) The arrowheads indicate periodontal disease. (B) Periodontal disease includes gingivitis and periodontitis. Gingivitis is the presence of gingival inflammation without loss of connective tissue attachment. Periodontitis is the presence of gingival inflammation at sites where there has been apical migration of the epithelial attachment onto the root surfaces accompanied by the loss of connective tissue and alveolar bone. (C) Clinical attachment loss is measured with a periodontal probe and is the distance from the base of the probeable crevice to the cementoenamel junction. Probing depth is defined as the distance between the bottom of the periodontal pocket and the gingival margin.

Figure 2

Potential biological mechanisms linking periodontal disease to preterm birth. In periodontitis, gingival ulceration in the periodontal pocket enables egress and systemic bacterial dissemination, and locally produced proinflammatory cytokines can enter systemic circulation and induce an acute-phase response in the liver that is characterized by an increased level of C-reactive protein.