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Abstract Objectives Nickel (Ni) is one of the main metal elements in orthodontic and prosthetic devices. Different effects of Ni are described ranging from an induction of local inflammation to allergy and cancerous/mutagenic properties. Inflammatory reactions are frequently observed in the oral cavity, but the interrelationship of Ni with those events is still unknown. Therefore, we focused on the impact of Ni on inflammation in vitro. Methods In accordance to previous immersion tests of our lab, human gingival fibroblasts (HGFs) ( n = 6) were exposed to a pro-inflammatory environment using interleukin-1 beta (IL-1β) and additionally stimulated with different Ni(II) concentrations (400 and 4000 ng/ml). At varying time points the expression of pro- and anti-inflammatory as well as matrix degeneration proteins, i.e. MMPs, were analyzed. Furthermore, proliferation assays, wound healing tests and the detection of NF-κB activation were conducted. Unstimulated HGFs served as control. Results Our experiments showed that low clinical average Ni(II) levels did not alter pro-inflammatory cytokines significantly compared to control ( p > 0.05). Instead, a 10-fold higher dose up-regulated these mediators significantly in a time-dependent manner ( p < 0.01). This was even more pronounced combining both Ni(II) concentrations with an inflammatory condition ( p < 0.001), MMP expressions were in line with our findings ( p < 0.001). The mRNA data were supported by proliferation and wound closure assays ( p < 0.001). However, the combination of both stimuli induced contradictory results. Analyzing NF-κB activation revealed that our results may be in part attributed to NF-κB. Significance Our in vitro study implicated that Ni(II) has various modifying effects on IL-1β-induced inflammatory processes depending on the concentration.