Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes.
OBJECTIVE
The aim of this study was to investigate the hypothesis that dental material components alter cytokine secretion from monocytes if applied for several weeks at sublethal doses. The current study significantly extended exposure times of monocytes to the components over times published in previous studies. These exposure times approached the estimated average life span of monocytes in the bloodstream.


METHODS
Human THP-1 monocytes were exposed to 2-hydroxyethylmethacrylate (HEMA, 0-1.2mmol/l), triethyleneglycoldimethacrylate (TEGDMA, 0-0.75mmol/l), Hg(2+) (0-2 micromol/l), or Ni(2+) (0-20 micromol/l) for 2 weeks. The cells were then collected and additionally incubated for 24h, with or without bacterial lipopolysaccharide (LPS), a common component of dental plaque. TNF-alpha secretion from THP-1 was determined using by enzyme-linked immunosorbent assay.


RESULTS
None of the dental material components induced TNF-alpha from THP-1 by themselves, but LPS alone strongly induced TNF-alpha secretion as expected. HEMA and TEGDMA significantly suppressed (40-70%) TNF-alpha secretion from cells stimulated with LPS. Hg(2+) at 2.0 micromol/l doubled TNF-alpha secretion from THP-1s stimulated with LPS over LPS alone. Ni(2+) did not significantly affect TNF-alpha secretion, with or without LPS exposure. Significance. The results in this study suggest that sublethal, 2-week exposures of some dental material components may alter TNF-alpha secretion from THP-1 monocytes when the cells are challenged. These alterations may influence the biological response of tissues to materials in an inflammatory intraoral environment.
Noda
Mamoru
M
Department of Oral Health Sciences, Hokkaido University Graduate School of Dental Medicine, Sapporo, Japan. nodam@den.hokudai.ac.jp
Wataha
John C
JC
Lockwood
Petra E
PE
Volkmann
Keith R
KR
Kaga
Masayuki
M
Sano
Hidehiko
H
D000704:Analysis of Variance; D002478:Cells, Cultured; D003764:Dental Materials / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008628:Mercury / Q000633:toxicity; D008689:Methacrylates / Q000633:toxicity*; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D009532:Nickel / Q000633:toxicity; D011092:Polyethylene Glycols / Q000633:toxicity; D011109:Polymethacrylic Acids / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis* / Q000378:metabolism
D003764:Dental Materials; D008070:Lipopolysaccharides; D008689:Methacrylates; D011109:Polymethacrylic Acids; D014409:Tumor Necrosis Factor-alpha; C020946:triethylene glycol dimethacrylate; D011092:Polyethylene Glycols; C005044:hydroxyethyl methacrylate; D009532:Nickel; D008628:Mercury