Abstract

Aims: Periodontal disease is associated with adverse pregnancy outcome, but the underlying pathophysiologic mechanism is still unknown. In this prospective, longitudinal, non-interventional case-control study, 45 women with preterm premature rupture of membranes and 26 controls with uncomplicated pregnancies were examined at three time-points (T1: 20–34 weeks of gestations; T2: within 48 h after delivery; T3: 4–6 weeks post partum). Examinations included subgingival, blood, vaginal, and placenta sampling for microbiologic, cytokine, and histology assessment. Objective of this study was to test the hypothesis that systemic inflammatory changes and not specific bacteria are predominantly involved in the association between periodontal disease and adverse pregnancy outcome.Results: Demographic data and gestational age at T1 were comparable between groups. While there was no correlation between vaginal and gingival fluid microbiome, cytokine levels in the assessed compartments differed between cases, and controls. Vaginal smears did not show a higher rate of abnormal flora in the cases at the onset of preterm premature rupture of membranes. Number and variety of bacteria in the case group placental membranes and vagina were higher, but these bacteria were not found in membranes at birth.Conclusions: On the basis of our results we speculate that an inflammatory pathway sequentially involving periodontal tissue, maternal serum, and finally vaginal compartment contributes to the underlying pathomechanism involved in preterm premature rupture of membranes associated with periodontitis.

Highlights

  • Preterm birth (PTB) is the leading cause of perinatal morbidity and mortality in developed countries [1]

  • Albeit this is believed to be the primary cause of prelabor rupture of membranes (PPROM) [1, 6, 7], to what extent remote infections contribute to PTB and PPROM is not known [1, 8, 9]

  • Seventy-one women were included in the study analysis of whom 45 were PPROM-cases and 26 controls

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Summary

Introduction

Preterm birth (PTB) is the leading cause of perinatal morbidity and mortality in developed countries [1]. Ascending (asymptomatic) intrauterine infections cause an inflammatory decidual activation resulting in preterm labor or PPROM [3,4,5]. Albeit this is believed to be the primary cause of PPROM [1, 6, 7], to what extent remote infections contribute to PTB and PPROM is not known [1, 8, 9]. Many of the risk factors for PTB culminate in increased systemic inflammation which might as well result in decidual activation [1]

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