4.5 Article

Cyclic tensile strain affects the response of human periodontal ligament stromal cells to tumor necrosis factor-α

期刊

CLINICAL ORAL INVESTIGATIONS
卷 26, 期 1, 页码 609-622

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s00784-021-04039-8

关键词

Human periodontal ligament stromal cells; Orthodontic force; Mechanical loading; Periodontitis; Inflammatory cytokine

资金

  1. Medical University of Vienna

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The study investigates the combined effect of mechanical stress and TNF-alpha on inflammatory response in human periodontal ligament stromal cells. It was found that mechanical force can differentially regulate the expression of inflammatory mediators and adhesion molecules induced by TNF-alpha, with potential anti-inflammatory or pro-inflammatory effects depending on the type of mediators and force magnitude.
Objectives Orthodontic treatment in adult patients predisposed to mild or severe periodontal disease is challenging for orthodontists. Orthodontic malpractice or hyper-occlusal forces may aggravate periodontitis-induced destruction of periodontal tissues, but the specific mechanism remains unknown. In the present study, the combined effect of mechanical stress and tumor necrosis factor (TNF)-alpha on the inflammatory response in human periodontal ligament stromal cells (hPDLSCs) was investigated. Materials and methods hPDLSCs from 5 healthy donors were treated with TNF-alpha and/or subjected to cyclic tensile strain (CTS) of 6% or 12% elongation with 0.1 Hz for 6- and 24 h. The gene expression of interleukin (IL)-6, IL-8 and cell adhesion molecules VCAM and ICAM was analyzed by qPCR. The protein levels of IL-6 and IL-8 in conditioned media was measured by ELISA. The surface expression of VCAM-1 and ICAM-1 was quantified by immunostaining followed by flow cytometry analysis. Results TNF-alpha-induced IL-6 gene and protein expression was inhibited by CTS, whereas TNF-alpha-induced IL-8 expression was decreased at mRNA expression level but enhanced at the protein level in a magnitude-dependent manner. CTS downregulated the gene expression of VCAM-1 and ICAM-1 under TNF-alpha stimulation, but the downregulation of the surface expression analyzed by flow cytometry was observed chiefly for VCAM-1. Conclusions Our findings show that mechanical force differentially regulates TNF-alpha-induced expression of inflammatory mediators and adhesion molecules at the early stage of force application. The effect of cyclic tensile strain is complex and could be either anti-inflammatory or pro-inflammatory depending on the type of pro-inflammatory mediators and force magnitude.

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