Introduction: Cardiovascular diseases are the leading cause of mortality worldwide. Apical periodontitis (AP) has been associated with an increased risk of cardiovascular diseases. A correlation has been shown between chronic AP and endothelial dysfunction (ED), but there is no evidence to indicate ED improves after endodontic treatment in patients with periapical lesions. The aim of this study was to investigate vascular and molecular markers of early ED before and after root canal treatment in young adults with chronic AP.
Methods: Twenty control subjects and 21 patients with AP were assessed at baseline. The AP patients were also evaluated 2 and 12 months post-treatment. Endothelial flow reserve was assessed via an endothelial function test, and enzyme-linked immunosorbent assays were used to evaluate plasma levels of proinflammatory cytokines interleukin (IL)-1, IL-6, and tumor necrosis factor alpha; vasoconstrictor ED marker endothelin (ET)-1; circulating endothelial adhesion markers intercellular adhesion molecule 1 (ICAM-1)/CD54 and soluble vascular cellular adhesion molecule (sVCAM)-1/CD106; soluble CD14; and the endothelial leukocyte adhesion molecule (E-selectin).
Results: AP was associated with increased serum levels of ET-1, ICAM-1, E-selectin, IL-1, and sCD14, suggesting early vascular ED, with no macroscopic evidence of a reduction in endothelial flow reserve. Root canal treatment ameliorated inflammation and early ED, lowering plasma levels of IL-1, sCD14, ET-1, ICAM-1/CD54, and E-selectin to those of control subjects.
Conclusions: Our findings suggest that AP may drive early vascular ED and that the endodontic therapy of AP ameliorates early ED.
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http://dx.doi.org/10.1016/j.joen.2019.01.018 | DOI Listing |
Biomarkers
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PMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Background: Growing evidence indicates that noncombustible products could be a tobacco harm reduction tool for smokers who do not quit. The Tobacco Heating System (THS) emits substantially lower levels of harmful cigarette smoke constituents, and previous randomized clinical studies showed improved levels of biomarkers of potential harm (BoPH) linked to smoking-related disease.
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Front Immunol
January 2025
Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilan-Universität (LMU) Munich, München, Germany.
Introduction: The autoantibody-driven disease pemphigus vulgaris (PV) impairs desmosome adhesion in the epidermis. In desmosomes, the pemphigus autoantigens desmoglein 1 (Dsg1) and Dsg3 link adjacent cells. Dsgs are clustered by plaque proteins and linked to the keratin cytoskeleton by desmoplakin (Dp).
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January 2025
Department of Pharmaceutics, College of Pharmacy, King Saud University, Riyadh, 11451 Saudi Arabia.
Introduction: Owing to its high prevalence, colossal potential of chemoresistance, metastasis, and relapse, breast cancer (BC) is the second leading cause of cancer-related fatalities in women. Several treatments (eg, chemotherapy, surgery, radiations, hormonal therapy, etc.) are conventionally prescribed for the treatment of BC; however, these are associated with serious systemic aftermaths.
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January 2025
Division of Immunology, Tulane National Primate Research Center, Tulane University, Covington, LA, USA.
The Bartonella genus of bacteria encompasses ubiquitous species, some of which are pathogenic in humans and animals. Bartonella henselae, the causative agent of Cat Scratch disease, is responsible for a large portion of human Bartonella infections. These bacteria can grow outside of cells, replicate in erythrocytes and invade endothelial and monocytic cells.
View Article and Find Full Text PDFNat Commun
January 2025
Biophysics Graduate Group, University of California, Davis, CA, USA.
P-cadherin, a crucial cell-cell adhesion protein which is overexpressed in numerous malignant cancers, is a popular target for drug delivery antibodies. However, molecular guidelines for engineering antibodies that can be internalized upon binding to P-cadherin are unknown. Here, we use a combination of biophysical, biochemical, and cell biological methods to demonstrate that trapping the P-cadherin extracellular region in an X-dimer adhesive conformation triggers cadherin endocytosis via an outside-in signaling mechanism.
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