Porphyromonas gingivalis OMVs promoting endothelial dysfunction via the STING pathway in periodontitis

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Zhenwei Chen1,2, Ye Cao1,2, Wenxiu Jiang1,2

  • 1Department of Orthodontics, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing, China.

Oral Diseases
|May 2, 2024
PubMed
Abstract

Insights

Porphyromonas gingivalis outer membrane vesicles (Pg-OMVs) induce endothelial dysfunction and activate the cGAS-STING-TBK1 pathway, leading to impaired bone formation and alveolar bone loss in periodontitis.

Area of Science:

  • Oral microbiology
  • Periodontology
  • Cell biology

Background:

  • Chronic periodontitis is a prevalent inflammatory disease.
  • Porphyromonas gingivalis (Pg) is a key pathogen in periodontitis.
  • Outer membrane vesicles (OMVs) mediate bacterial pathogenesis.

Purpose of the Study:

  • To investigate the effects of Pg-OMVs on endothelial cells and osteogenesis.
  • To elucidate the underlying molecular mechanisms involving the cGAS-STING-TBK1 pathway.
  • To assess the in vivo impact of Pg-OMVs on alveolar bone mass.

Main Methods:

  • In vitro incubation of Pg-OMVs with endothelial cells (Ea.hy926) and osteoblast-like cells (MG63).
  • Assessment of endothelial function and osteoblast migration/differentiation.
  • In vivo micro-CT and immunofluorescence staining for alveolar bone, STING, and Runx2+ cells.

Main Results:

  • Pg-OMVs induced endothelial dysfunction via cGAS-STING-TBK1 pathway activation.
  • Endothelial dysfunction inhibited MG63 cell migration and osteogenic differentiation.
  • In vivo, Pg-OMVs promoted alveolar bone resorption and increased STING levels.

Conclusions:

  • Pg-OMVs contribute to periodontitis pathogenesis by causing endothelial dysfunction.
  • The cGAS-STING-TBK1 pathway is a critical mediator of Pg-OMV-induced damage.
  • Pg-OMVs impair bone regeneration and promote bone loss through vascular alterations.
Keywords:
Porphyromonas gingivalisendothelial dysfunctionouter membrane vesiclesperiodontitisstimulator of interferon genes

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