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Induction of cyclooxygenase‐2 mRNA and protein expression by dentin bonding agents in human gingival fibroblasts
Author(s) -
Huang FuMei,
Chang YuChao
Publication year - 2004
Publication title -
journal of biomedical materials research part b: applied biomaterials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.665
H-Index - 108
eISSN - 1552-4981
pISSN - 1552-4973
DOI - 10.1002/jbm.b.30045
Subject(s) - dentin , cyclooxygenase , messenger rna , chemistry , dentin bonding agents , inflammation , gene expression , microbiology and biotechnology , enzyme , dentistry , biochemistry , gene , immunology , bond strength , medicine , biology , adhesive , organic chemistry , layer (electronics)
An ideal dentin bonding agent should be nonirritating to surrounding tissues. Unfortunately, all histological investigations have demonstrated that dentin bonding agents can induce mild to severe inflammatory alterations. However, there is little information on the precise mechanisms about dentin bonding agents‐induced inflammatory reaction. Cyclooxygenase‐2 (COX‐2) is an inducible enzyme believed to be responsible for prostaglandin synthesis at the site of inflammation. The aim of the present study was to investigate the effects of three dentin bonding agents, Clearfil SE Bond, Prime & Bond NT, and Single Bond on the expression of COX‐2 mRNA gene and protein in cultured human gingival fibroblasts. The exposure of quiescent human gingival fibroblasts to dentin bonding agents resulted in the induction of COX‐2 mRNA expression. The investigations of the time‐dependent on COX‐2 mRNA expression in dentin bonding agent‐treated human gingival fibroblasts revealed different patterns. The influence of COX‐2 mRNA depended on the tested materials. In addition, all dentin bonding agents also induced COX‐2 protein expression in human gingival fibroblasts. Taken together, the activation of COX‐2 expression may be one of the potential mechanisms of dentin bonding agent‐induced gingival inflammation. © 2004 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 70B: 297–302, 2004