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Clinical Oral Investigations
Published in: Clinical Oral Investigations 1/2015

01-01-2015 | Original Article

TEGDMA and filler particles from dental composites additively attenuate LPS-induced cytokine release from the macrophage cell line RAW 264.7

Authors: Gro H. Mathisen, Vibeke Ansteinsson, Jan T. Samuelsen, Rune Becher, Jon E. Dahl, Anette K. Bølling

Published in: Clinical Oral Investigations | Issue 1/2015

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Abstract

Objectives

Due to incomplete curing and material degradation, cells in the oral cavity may be exposed to monomers and filler particles from dental composite fillings. The objective of the present study was to investigate if combined exposures to particles and a methacrylate monomer from composite fillings resulted in additive effects on the macrophage immune response.

Material and methods

Two filler particles, Nanosilica (12 nm) and Quartz (1 μm), were studied at concentrations 0.5–4 μg/cm2, while the methacrylate monomer triethyleneglycol dimethacrylate (TEGDMA) was applied at 5 and 50 μM. RAW 264.7 macrophages were exposed to monomers and/or particles for 24 h, with a subsequent 24 h combined exposure to monomers and/or particles and the bacterial factor lipopolysaccharide (LPS) to stimulate an immune response. Release of the pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) were measured as well as the cellular viability.

Results

Co-exposure to Nanosilica and Quartz resulted in an additive attenuation of the LPS-induced IL-1β release. Moreover, co-exposure to TEGDMA and both types of filler particles also resulted in an additive attenuation, although with a weak synergistic trend. The cellular viability and TNF-α release were not significantly affected by the exposures.

Conclusion

The present findings emphasize the necessity of considering effects of combined exposure to dental degradation products in future risk assessments.

Clinical relevance

Attenuated cytokine release could have implications for the macrophage immune response and result in impaired bacterial clearance. Further studies are necessary to determine implications for formation of dental biofilms and caries development.
Literature
1.
Madianos PN, Bobetsis YA, Kinane DF (2005) Generation of inflammatory stimuli: how bacteria set up inflammatory responses in the gingiva. J Clin Periodontol 32(Suppl 6):57–71PubMedCrossRef
2.
Ara T, Kurata K, Hirai K, Uchihashi T, Uematsu T, Imamura Y, Furusawa K, Kurihara S, Wang PL (2009) Human gingival fibroblasts are critical in sustaining inflammation in periodontal disease. J Periodontal Res 44:21–27PubMedCrossRef
3.
Roberts HC, Moseley R, Sloan AJ, Youde SJ, Waddington RJ (2008) Lipopolysaccharide alters decorin and biglycan synthesis in rat alveolar bone osteoblasts: consequences for bone repair during periodontal disease. Eur J Oral Sci 116:207–216PubMedCentralPubMedCrossRef
4.
Sun Y, Shu R, Li CL, Zhang MZ (2010) Gram-negative periodontal bacteria induce the activation of Toll-like receptors 2 and 4, and cytokine production in human periodontal ligament cells. J Periodontol 81:1488–1496PubMedCrossRef
5.
Glauser MP (1996) The inflammatory cytokines. New developments in the pathophysiology and treatment of septic shock. Drugs 52(Suppl 2):9–17PubMedCrossRef
6.
Sun Y, Li H, Yang MF, Shu W, Sun MJ, Xu Y (2012) Effects of Aging on Endotoxin Tolerance Induced by Lipopolysaccharides derived from Porphyromonas gingivalis and Escherichia coli. PloS ONE 7:e39224PubMedCentralPubMedCrossRef
7.
8.
Mizgerd JP, Spieker MR, Doerschuk CM (2001) Early response cytokines and innate immunity: essential roles for TNF receptor 1 and type I IL-1 receptor during Escherichia coli pneumonia in mice. J Immunol 166:4042–4048PubMedCrossRef
9.
Fortin D, Vargas MA (2000) The spectrum of composites: new techniques and materials. J Am Dent Assoc 131(Suppl):26S–30SPubMedCrossRef
10.
11.
Van Landuyt KL, Nawrot T, Geebelen B, De Munck J, Snauwaert J, Yoshihara K, Scheers H, Godderis L, Hoet P, Van Meerbeek B (2011) How much do resin-based dental materials release? A meta-analytical approach. Dent Mater 27:723–747PubMedCrossRef
12.
Pelka M, Distler W, Petschelt A (1999) Elution parameters and HPLC-detection of single components from resin composite. Clin Oral Investig 3:194–200PubMedCrossRef
13.
Shin MA, Drummond JL (1999) Evaluation of chemical and mechanical properties of dental composites. J Biomed Mater Res 48:540–545PubMedCrossRef
14.
Beyth N, Bahir R, Matalon S, Domb AJ, Weiss EI (2008) Streptococcus mutans biofilm changes surface-topography of resin composites. Dent Mater 24:732–736PubMedCrossRef
15.
Helmis CG, Tzoutzas J, Flocas HA, Halios CH, Stathopoulou OI, Assimakopoulos VD, Panis V, Apostolatou M, Sgouros G, Adam E (2007) Indoor air quality in a dentistry clinic. Sci Total Environ 377:349–365PubMedCrossRef
16.
Krifka S, Petzel C, Hiller KA, Frank EM, Bosl C, Spagnuolo G, Reichl FX, Schmalz G, Schweikl H (2010) Resin monomer-induced differential activation of MAP kinases and apoptosis in mouse macrophages and human pulp cells. Biomaterials 31:2964–2975PubMedCrossRef
17.
Noda M, Wataha JC, Lockwood PE, Volkmann KR, Kaga M, Sano H (2003) Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes. Dent Mater 19:101–105PubMedCrossRef
18.
Bolling AK, Samuelsen JT, Morisbak E, Ansteinsson V, Becher R, Dahl JE, Mathisen GH (2013) Dental monomers inhibit LPS-induced cytokine release from the macrophage cell line RAW264.7. Toxicol Lett 216:130–138PubMedCrossRef
19.
Amakawa K, Terashima T, Matsuzaki T, Matsumaru A, Sagai M, Yamaguchi K (2003) Suppressive effects of diesel exhaust particles on cytokine release from human and murine alveolar macrophages. Exp Lung Res 29:149–164PubMedCrossRef
20.
Mundandhara SD, Becker S, Madden MC (2006) Effects of diesel exhaust particles on human alveolar macrophage ability to secrete inflammatory mediators in response to lipopolysaccharide. Toxicol In Vitro 20:614–624PubMedCrossRef
21.
Eckhardt A, Harorli T, Limtanyakul J, Hiller KA, Bosl C, Bolay C, Reichl FX, Schmalz G, Schweikl H (2009) Inhibition of cytokine and surface antigen expression in LPS-stimulated murine macrophages by triethylene glycol dimethacrylate. Biomaterials 30:1665–1674PubMedCrossRef
22.
Krifka S, Hiller KA, Bolay C, Petzel C, Spagnuolo G, Reichl FX, Schmalz G, Schweikl H (2012) Function of MAPK and downstream transcription factors in monomer-induced apoptosis. Biomaterials 33:740–750PubMedCrossRef
23.
Zheng D, Wang N, Wang X, Tang Y, Zhu L, Huang Z, Tang H, Shi Y, Wu Y, Zhang M, Lu B (2012) Effects of the interaction of TiO2 nanoparticles with bisphenol A on their physicochemical properties and in vitro toxicity. J Hazard Mater 199–200:426–432PubMedCrossRef
24.
Altenburger R, Scholz S, Schmitt-Jansen M, Busch W, Escher BI (2012) Mixture toxicity revisited from a toxicogenomic perspective. Environ Sci Technol 46:2508–2522PubMedCrossRef
25.
Allouni ZE, Cimpan MR, Hol PJ, Skodvin T, Gjerdet NR (2009) Agglomeration and sedimentation of TiO2 nanoparticles in cell culture medium. Colloids Surf B: Biointerfaces 68:83–87PubMedCrossRef
26.
Kocbach A, Totlandsdal AI, Lag M, Refsnes M, Schwarze PE (2008) Differential binding of cytokines to environmentally relevant particles: a possible source for misinterpretation of in vitro results? Toxicol Lett 176:131–137PubMedCrossRef
27.
Laetz CA, Baldwin DH, Collier TK, Hebert V, Stark JD, Scholz NL (2009) The synergistic toxicity of pesticide mixtures: implications for risk assessment and the conservation of endangered Pacific salmon. Environ Health Perspect 117:348–353PubMedCentralPubMedCrossRef
28.
Heil TL, Volkmann KR, Wataha JC, Lockwood PE (2002) Human peripheral blood monocytes versus THP-1 monocytes for in vitro biocompatibility testing of dental material components. J Oral Rehabil 29:401–407PubMedCrossRef
29.
Hornung V, Bauernfeind F, Halle A, Samstad EO, Kono H, Rock KL, Fitzgerald KA, Latz E (2008) Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. Nat Immunol 9:847–856PubMedCentralPubMedCrossRef
30.
Becker S, Mundandhara S, Devlin RB, Madden M (2005) Regulation of cytokine production in human alveolar macrophages and airway epithelial cells in response to ambient air pollution particles: further mechanistic studies. Toxicol Appl Pharmacol 207:269–275PubMedCrossRef
31.
Guo B, Zebda R, Drake SJ, Sayes CM (2009) Synergistic effect of co-exposure to carbon black and Fe2O3 nanoparticles on oxidative stress in cultured lung epithelial cells. Part Fibre Toxicol 6:4 doi:10.​1186/​1743-8977-6-4
32.
Berg JM, Ho S, Hwang W, Zebda R, Cummins K, Soriaga MP, Taylor R, Guo B, Sayes CM (2010) Internalization of carbon black and maghemite iron oxide nanoparticle mixtures leads to oxidant production. Chem Res Toxicol 23:1874–1882PubMedCrossRef
33.
Christen V, Crettaz P, Oberli-Schrammli A, Fent K (2012) Antiandrogenic activity of phthalate mixtures: validity of concentration addition. Toxicol Appl Pharmacol 259:169–176PubMedCrossRef
34.
Hehlgans T, Pfeffer K (2005) The intriguing biology of the tumour necrosis factor/tumour necrosis factor receptor superfamily: players, rules and the games. Immunology 115:1–20PubMedCentralPubMedCrossRef
35.
Barksby HE, Nile CJ, Jaedicke KM, Taylor JJ, Preshaw PM (2009) Differential expression of immunoregulatory genes in monocytes in response to Porphyromonas gingivalis and Escherichia coli lipopolysaccharide. Clin Exp Immunol 156:479–487PubMedCentralPubMedCrossRef
Metadata
Title
TEGDMA and filler particles from dental composites additively attenuate LPS-induced cytokine release from the macrophage cell line RAW 264.7
Authors
Gro H. Mathisen
Vibeke Ansteinsson
Jan T. Samuelsen
Rune Becher
Jon E. Dahl
Anette K. Bølling
Publication date
01-01-2015
Publisher
Springer Berlin Heidelberg
Published in
Clinical Oral Investigations / Issue 1/2015
Print ISSN: 1432-6981
Electronic ISSN: 1436-3771
DOI
https://doi.org/10.1007/s00784-014-1212-7

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