Schmalz G, Krifka S, Schweikl H
Department of Operative Dentistry and Periodontology, University Medical Centre Regensburg, Germany.
Adv Dent Res. 2011 Jul;23(3):302-6. doi: 10.1177/0022034511405391.
Unreacted monomers released from dental resin-based composites at non-cytotoxic concentrations cause a depletion of glutathione and an increase of reactive oxygen species (ROS), leading to, e.g., DNA damage and apoptosis. ROS-sensitive MAP-kinases are activated by HEMA and TEGDMA. MAP-kinases are also involved in the bacteria-triggered cell responses of the innate immune system, e.g., after bacterial lipopolysaccharide (LPS) binding to the Toll-like receptor (TLR) 4. Therefore, both bacteria and monomers imply environmental stress to pulp tissue, and they may influence the target cell reactions in a combined way. In macrophages, cell-surface antigens and cytokines were up-regulated after exposure to LPS, but TEGDMA caused a significant down-regulation. Regulation was dependent on exposure time, indicating that LPS and TEGDMA act differently on MAP-kinases. Furthermore, the cell type played a decisive role. Inhibition of the immune response may result in a decrease in inflammatory symptoms and/or a reduced defense capacity against bacteria.
牙科树脂基复合材料释放出的处于无细胞毒性浓度的未反应单体，会导致谷胱甘肽耗竭和活性氧（ROS）增加，进而引发例如DNA损伤和细胞凋亡等情况。对ROS敏感的丝裂原活化蛋白激酶（MAP激酶）会被甲基丙烯酸羟乙酯（HEMA）和三乙二醇二甲基丙烯酸酯（TEGDMA）激活。MAP激酶也参与先天免疫系统的细菌触发细胞反应，例如在细菌脂多糖（LPS）与Toll样受体（TLR）4结合之后。因此，细菌和单体都会给牙髓组织带来环境压力，并且它们可能以一种联合的方式影响靶细胞反应。在巨噬细胞中，暴露于LPS后细胞表面抗原和细胞因子会上调，但TEGDMA会导致显著下调。这种调节取决于暴露时间，表明LPS和TEGDMA对MAP激酶的作用不同。此外，细胞类型起着决定性作用。免疫反应的抑制可能会导致炎症症状减轻和/或对细菌的防御能力降低。
