title: Induction of cyclooxygenase-2 expression in human pulp cells stimulated by dentin bonding agents.
abstract: OBJECTIVE
  Histological investigations have demonstrated that dentin bonding agents can induce pulpal inflammation. However, there is little information on the precise mechanisms about dentin bonding agent-induced pulpal inflammation. Cyclooxygenase-2 (COX-2) is an inducible enzyme believed to be responsible for prostaglandin synthesis at the site of inflammation. The aim of this study was to investigate the effects of dentin bonding agents on the expression of COX-2 in human pulp cells.
  
  
  METHODS
  Human pulp cells were cultured from extracted impacted third molars using an explant technique. Patients gave informed consent. The reverse-transcriptase polymerase chain reaction and Western blot assays were used to investigate the effects of cultured human pulp cells exposed to dentin bonding agents. In addition, NS-398 (a selective COX-2 inhibitor) was added to test how it modulated the cytotoxic effects of dentin bonding agents.
  
  
  RESULTS
  The exposure of quiescent human pulp cells to dentin bonding agents resulted in the induction of COX-2 mRNA and protein expression. The expression of COX-2 signals depended on the materials tested. In addition, NS-398 at noncytotoxic dose was not able to prevent dentin bonding agent-induced cytotoxicity (P > .05).
  
  
  CONCLUSIONS
  The activation of COX-2 expression may be one of the pathogenesis of dentin bonding agent-induced pulpal inflammation. In addition, dentin bonding agent-induced cytotoxicity is not directly via the induction of COX-2 expression.
authors.affiliation: Oral Medicine Center, Chung Shan Medical University Hospital, Taichung, Taiwan.
authors.forename: Fu-Mei
authors.initials: FM
authors.lastname: Huang
authors.forename: Chung-Hung
authors.initials: CH
authors.lastname: Tsai
authors.forename: Shinn-Jyh
authors.initials: SJ
authors.lastname: Ding
authors.forename: Yu-Chao
authors.initials: YC
authors.lastname: Chang
mesh_terms: D000096:Acetone / Q000633:toxicity; D000704:Analysis of Variance; D015153:Blotting, Western; D002478:Cells, Cultured; D051546:Cyclooxygenase 2 / Q000096:biosynthesis*; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology; D003782:Dental Pulp / Q000166:cytology / Q000187:drug effects / Q000201:enzymology*; D017220:Dentin-Bonding Agents / Q000633:toxicity*; D004790:Enzyme Induction / Q000187:drug effects; D006801:Humans; D009578:Nitrobenzenes / Q000494:pharmacology; D011109:Polymethacrylic Acids / Q000633:toxicity; D011671:Pulpitis / Q000139:chemically induced* / Q000517:prevention & control; D012333:RNA, Messenger / Q000032:analysis; D019279:Resin Cements / Q000633:toxicity; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013449:Sulfonamides / Q000494:pharmacology
chemical_list: C438313:Clearfil SE Bond; D052246:Cyclooxygenase 2 Inhibitors; D017220:Dentin-Bonding Agents; D009578:Nitrobenzenes; D011109:Polymethacrylic Acids; D012333:RNA, Messenger; D019279:Resin Cements; D013449:Sulfonamides; C444444:prime and bond 2.1; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D000096:Acetone; D051546:Cyclooxygenase 2