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Erschienen in:
01.05.2014 | Original article
Effects of mechanical and bacterial stressors on cytokine and growth-factor expression in periodontal ligament cells
Erschienen in: Journal of Orofacial Orthopedics / Fortschritte der Kieferorthopädie | Ausgabe 3/2014
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Objectives
The goal of the study was to examine the effects of a mechanical (orthodontic force simulation by static compressive loading) and a bacterial (endotoxins from a heat-inactivated gram-negative periodontal pathogen) stressor on the expression patterns of factors that are key to regulating osteoclastogenesis and bone remodeling.
Materials and methods
Three experimental groups were formed with fifth-passage periodontal ligament (PDL) fibroblasts treated by the static application of compressive force (2 g/cm2), heat-inactivated aggregatibacter actinomycetemcomitans (1 × 107 cells), or both of these stressors combined. Real-time polymerase chain reaction (RT-PCR) was used to study gene expression of IL-6, IL-8, COX-2, IGF-1, VEGF, and MMP-13 in the 3 groups. Protein levels of COX-2, prostaglandin E2 (PGE2), and IL-8 production were quantified using immunoblotting and enzyme-linked immunosorbent assay (ELISA).
Results
The mechanical stressor upregulated the genes of COX-2, IL-8, IGF-1, and MMP-13 in PDL fibroblasts and the bacterial stressor upregulated IL-6, IL-8, COX-2 and MMP-13. Both stressors in combination upregulated VEGF and caused COX-2 gene expression to increase further; the latter effect was also detected at the protein level and indirectly via the enhanced production of PGE2. We noted that the posttranscriptional regulation of IL-8 was induced by the mechanical stressor and influenced by PGE2.
Conclusion
While mechanical-stressor application increased the gene expression of COX-2, IL-8, and VEGF in the presence of the bacterial stressor, IL-8 production was posttranscriptionally regulated by the mechanical stressor, whereas COX-2 expression correlated with enhanced production of the inflammatory tissue hormone PGE2, which exerted a suppressive effect on endotoxin-induced IL-8 production.