Periodontitis & preeclampsia: were outer membrane vesicles a potential connection?

Abstract

Introduction

Preeclampsia (PE) is gestation-specific hypertension coupled by systemic multiple organ damages, remaining the leading causes of maternal and infant death worldwide.

Materials and methods

Though numerous pathogenetic mechanisms have been engaged in this disorder and several methods have been undertaken to treat PE, few clinical strategies are effective in PE management, suggesting more studies from novel perspective being in great need to decipher the underlying mechanisms of PE.

Results

Growing evidence shows that women with periodontitis, an oral microflora-induced chronic inflammation of the periodontal tissues, are more inclined to suffer PE, which may be tightly associated with microflora-derived outer membrane vesicles (OMVs). Latest studies reveal that OMVs are spherical membrane-enclosed entities released by bacteria and can gain free access to the circulation of the host and therefore reach the remote tissue of the host, participating the interaction among oral bacterial with the host and contribute to some systemic disease with carried bioactive materials.

Conclusions

OMVs may be the underlying mechanism linking oral flora-induced periodontitis with dysfunction trophoblast and finally contributes to the pathogenesis of in PE. Here we provide evidence to support the potential roles of OMVs linking periodontal disease between PE.

Keywords:

• Preeclampsia
• periodontitis
• trophoblast
• outer membrane vesicles

Disclosure statement

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Additional information

Funding

This work was supported by National Natural Science Foundation of China 82071670 (Jinjun Liu), 81771616 (Jinjun Liu), Grant for A-level Department (Oral Microflora Involved in the Pathogenesis of Pre-eclampsia through Outer Membrane Vesicles, 2022) and Shaanxi Key Research and Development Program [2022SF-102] to Chunfang Li.