Periodontitis exacerbates endothelial dysfunctions partly via endothelial‐mesenchymal transition in streptozotocin‐induced diabetes rats

Abstract

Objectives Periodontal infections are related to the expansion of diabetes cardiovascular problems. However, the pathological process and probable mechanism remain unexplained. This study investigated the impact of periodontitis on streptozotocin (STZ)‐induced diabetes rats' carotid artery. Methods We randomized 24 Sprague‐Dawley (SD) rats into four groups: control, chronic periodontitis (CP), diabetes mellitus (DM), and DM +CP groups. Fasting blood glucose (FBG) and hemoglobin A1c (HBA1c) were measured to verify the establishment of the DM model. After euthanasia, the maxillary was collected for further studies like hematoxylin‐eosin (HE), Masson staining, and micro‐computed tomography (micro‐CT) analysis. Immunofluorescence (IF) staining was used to detect endothelial‐mesenchymal transition (EndMT)‐related markers in carotid artery wall. We further used ELISA and quantitative real‐time PCR to investigate the effect of high glucose (HG) and Porphyromonas gingivalis lipopolysaccharide (P.g‐LPS) on human umbilical vein endothelial cells (HUVECs). Results Compared with DM and CP groups, bone resorption and pathological changes of the vascular wall were the most serious in the DM+CP group. The vascular wall of the DM+CP group had a higher level of interleukin (IL)‐6 and vascular cell adhesion molecule 1 (VCAM‐1). The carotid artery vascular wall of the DM+CP group contained more cells that expressed both mesenchymal and endothelial cell markers, along with elevated transcription factor levels. Furthermore, P.g‐LPS and HG upregulated the inflammatory cytokines expression and caused phenotypic changes of HUVECs in vitro. Conclusion Periodontitis exacerbates endothelial dysfunctions partly via endothelial‐mesenchymal transition in STZ‐induced diabetes rats.

The potential impact of periodontitis on cerebral small vessel disease

“…Another aspect of endothelial dysfunction that has been noted in in vitro and animal studies of experimental periodontitis is the inhibition of nitric oxide (NO) production in endothelial cells via proinflammatory cytokines and reactive oxygen species (Parvaneh et al, 2021;Yang et al, 2022). NO is responsible for vasodilation and changes in its production and sensitivity are a sign of endothelial dysfunction (Cyr et al, 2020).…”