In vitro IL‐1β release from gingival fibroblasts in response to pure metals, dental alloys and ceramic

Abstract

Little information is available on the immunological basis for side-effects of dental materials. The objective of this study is to evaluate effects of pure metals, dental alloys and ceramic on cell viability and interleukin-1 beta (IL-1beta) release in three-dimensional human gingival fibroblast cultures as an indicator of their biological performance in gingival tissues. The gingival fibroblast cultures were exposed to test specimens fabricated from nickel, iron, molybdenum, copper, indium, gold, Ni-Cr-Mo alloy (Remanium CS), Au-Pt-In alloy (Pontostar) and a dental ceramic (In-ceram). Cell viability was determined by the MTT method 24 and 48 h after exposure. Assays for IL-1beta were carried out by ELISA. Statistical analysis was performed applying the non-parametric Mann-Whitney pairwise test. Dental ceramic and gold did not influence cell viability after 24 and 48 h. Cell viability was determined after 24 and 48 h to nickel (79-77%), iron (92-90%), molybdenum (86-83%), copper (48-36%), indium (90-90%), Remanium CS (83-80%), Pontostar (94-91%) compared with control cultures. Dental ceramic, Pontostar and gold had no significant influence on IL-1beta secretion. The highest amounts of IL-1beta (10-fold) levels were determined in cell cultures exposed to copper. Indium, molybdenum and iron induced twofold IL-1beta levels compared with untreated control cultures. These results support that some metals may alter immune responses and thereby contribute to a variety of dental pathological conditions and three-dimensional cell culture models for gingival fibroblasts appear to be suitable for in vitro studies.

Orthodontic Attachments and Chlorhexidine-Containing Varnish Effects on Gingival Health

“…2 Some investigations are dealing with the possible impact of materials on gingival health. 35,36 Plaque was also found on the banded teeth, so this last hypothesis may have a secondary rather than a primary influence.…”

Induction of lactoferrin and IL‐8 release from human neutrophils by tryptic enzymes via proteinase activated receptor‐2

“…Among them, PAR-1 is a receptor of thrombin and trypsin (Vu et al, 1991); PAR-2 is a receptor of trypsin, tryptase (Molino et al, 1997) and elastase (Uehara et al, 2003); PAR-3 (Schmidt et al, 1998) and PAR-4 (Xu et al, 1998) are receptors of thrombin. Activation of PARs could profoundly alter the secretion ability of numerous cell types, such as histamine release from human mast cells (He et al, 2004), IL-6 release from airway epithelial cells (Asokananthan et al, 2002), IL-1 release from fibroblasts (Ozen et al, 2005), and IL-8 release from human oral epithelial cells (Uehara et al, 2004).…”

Possible implications of Ni(II) on oral IL-1β-induced inflammatory processes

“…Different authors analyzed Ni-induced mechanism in vitro and in vivo using several cell types (immune cells like dendritic cells (DCs) or monocytes, cancer cell lines or epithelial cells of the lung, dermis or gingival) various Ni(II) concentrations and analysis methods [5,[14][15][16][17][18][19][20]39]. In almost every cell line, Ni(II) induced dose-and time-dependent changes of proand anti-inflammatory cytokines or other mediators such as prostaglandins or MMPs [5,[14][15][16][17][18][19][20]39].…”

“…In almost every cell line, Ni(II) induced dose-and time-dependent changes of proand anti-inflammatory cytokines or other mediators such as prostaglandins or MMPs [5,[14][15][16][17][18][19][20]39]. The present data support these findings showing that higher but not clinical relevant Ni(II) concentrations led to a significant increase of NF-B activation followed by an up-regulation of pro-inflammatory cytokines (p < 0.001) and MMPs (p < 0.001) compared to control.…”

“…Thereby, biocompatibility is related to the duration and route of exposure, form and concentration of this metal. Several studies investigated the impact of Ni(II) on cell metabolism using immune cells like monocytes and dendritic cells (DCs) as well as human dermal or gingival epithelial cells [5,[14][15][16][17][18][19][20]. The authors detected dose-and time-depended cytotoxic and pro-inflammatory reactions.…”