TEGDMA reduces mineralization in dental pulp cells.
Direct application of dentin bonding agents onto the exposed pulp has been advocated, but in vivo studies indicate a lack of reparative dentin formation. Our objective was to investigate the role of triethylene glycol dimethacrylate (TEGDMA), a commonly used compound in dentin bonding agents, as a potential inhibitor of mineralization. Human pulp cells were exposed to different concentrations of TEGDMA, and expression of the mineralization-related genes collagen I, alkaline phosphatase, bone sialoprotein, osteocalcin, Runx2, and dentin sialophosphoprotein was analyzed. Gene expression studies by real-time polymerase chain-reaction revealed a concentration- and time-dependent decrease of mineralization markers. A subtoxic TEGDMA concentration (0.3 mM) reduced expression levels by 5 to 20% after 4 hrs and by 50% after 12 hrs. Furthermore, alkaline phosphatase activity and calcium deposition were significantly lower in dental pulp cells treated with TEGDMA over 14 days. These findings indicate that even low TEGDMA concentrations might inhibit mineralization induced by dental pulp cells, thus impairing reparative dentin formation after pulp capping with dentin bonding agents.
Department of Operative Dentistry and Periodontology, University of Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg, Germany.
K M
KM
Galler
H
H
Schweikl
K-A
KA
Hiller
A C
AC
Cavender
C
C
Bolay
R N
RN
D'Souza
G
G
Schmalz
D000469:Alkaline Phosphatase / Q000096:biosynthesis / Q000235:genetics; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured / Q000187:drug effects; D024042:Collagen Type I / Q000096:biosynthesis / Q000235:genetics; D050659:Core Binding Factor Alpha 1 Subunit / Q000096:biosynthesis / Q000235:genetics; D003782:Dental Pulp / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D003809:Dentin, Secondary / Q000187:drug effects* / Q000378:metabolism; D017220:Dentin-Bonding Agents / Q000633:toxicity*; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis / Q000235:genetics; D015870:Gene Expression / Q000187:drug effects; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D058574:Integrin-Binding Sialoprotein / Q000096:biosynthesis / Q000235:genetics; D015675:Osteocalcin / Q000096:biosynthesis / Q000235:genetics; D010750:Phosphoproteins / Q000096:biosynthesis / Q000235:genetics; D011092:Polyethylene Glycols / Q000633:toxicity*; D011109:Polymethacrylic Acids / Q000633:toxicity*; D057872:Pulp Capping and Pulpectomy Agents / Q000633:toxicity*; D012795:Sialoglycoproteins / Q000096:biosynthesis / Q000235:genetics; D018709:Statistics, Nonparametric; D014074:Tooth Calcification / Q000187:drug effects*; D000099311:Dentin Sialophosphoprotein
D000469:Alkaline Phosphatase; D024042:Collagen Type I; D050659:Core Binding Factor Alpha 1 Subunit; D017220:Dentin-Bonding Agents; D016326:Extracellular Matrix Proteins; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D058574:Integrin-Binding Sialoprotein; D015675:Osteocalcin; D010750:Phosphoproteins; D011092:Polyethylene Glycols; D011109:Polymethacrylic Acids; D057872:Pulp Capping and Pulpectomy Agents; D012795:Sialoglycoproteins; D000099311:Dentin Sialophosphoprotein; C493709:RUNX2 protein, human; C020946:triethylene glycol dimethacrylate