In vitro induction of hydrolytic activity in human gingival and pulp fibroblasts by triethylene glycol dimethacrylate and monocyte chemotatic protein-1
Abstract Objective Some dental resin composite materials leach the monomer triethylene glycol dimethacrylate (TEGDMA), which could contribute to the inflammatory reaction. The purpose of this study was to examine the ability of TEGDMA to alter cytokine/growth factor secretion and enzymatic activity...
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Veröffentlicht in: | Dental materials 2008-11, Vol.24 (11), p.1461-1467 |
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Sprache: | eng |
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Zusammenfassung: | Abstract Objective Some dental resin composite materials leach the monomer triethylene glycol dimethacrylate (TEGDMA), which could contribute to the inflammatory reaction. The purpose of this study was to examine the ability of TEGDMA to alter cytokine/growth factor secretion and enzymatic activity in monocyte derived macrophages (U937 cells), human gingival fibroblasts (HGFs), and human pulp fibroblasts (DPFs). Methods A human growth factor/cytokine antibody array was utilized to determine whether TEGDMA alters the expression of cytokines/growth factors from U937 cells, HGFs, and DPFs. To determine if TEGDMA alters the hydrolase activity of U937, DPF, and HGF cells, the hydrolysis of p -nitrophenyl butyrate was utilized in a spectrophotometric assay. Results TEGDMA exposure induced the expression of monocyte chemotatic protein-1 (MCP-1) from the U937 cells. Both the cell lysates and conditioned media from the HGFs showed increased hydrolase activity after exposure to a sublethal concentration of TEGDMA. MCP-1 alone increased the hydrolytic activity and the combination of MCP-1 and TEGDMA was additive in HGF conditioned media. The DPFs were also exposed to MCP-1 alone and followed by a sublethal concentration of TEGDMA. The effect of MCP-1 was greater than that of TEGDMA. Significance These results demonstrate that TEGDMA induces enzymatic activity and cytokine/growth factor expression in a cell-specific manner. |
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ISSN: | 0109-5641 1879-0097 |
DOI: | 10.1016/j.dental.2008.03.006 |