Cell responses to cariogenic microorganisms and dental resin materials-Crosstalk at the dentin-pulp interface?
Cell responses to cariogenic microorganisms and dental resin materials-Crosstalk at the dentin-pulp interface?
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细胞对致龋微生物和牙科树脂材料的反应——牙本质-牙髓界面的串扰？
DOI：
10.1016/j.dental.2017.02.006
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Krifka S
中科院分区：
文献类型：
--
作者：
Schweikl H;Buchalla W;Krifka S
目的从未聚合的牙科粘结剂或复合材料中释放出的树脂单体和细菌产物如脂多糖(LPS)或脂磷壁酸(LTA)同时存在于深度龋损治疗后的特定应用中。本文从致龋性微生物来源的脂多糖或脂多糖引发的免疫反应的信号通路与树脂单体激活的适应性机制之间的相互作用的证据进行综述。方法根据在线数据库中的文献，分析了临床情况下真核细胞对脂多糖刺激的龋病进展和途径的理解，以及树脂单体引起的细胞对氧化应激的反应。结果脂多糖和脂多糖激活了作为免疫活性牙髓细胞的主要调节因子的氧化还原敏感的转录因子NF-κB。氧化还原敏感的转录因子Nrf2下调了细胞对氧化应激相关的内毒素/LTA的反应。因此，通过树脂单体激活NRF2，通过增加活性氧物种(ROS)的形成而诱导氧化应激，可能是抑制内毒素刺激的反应(如促炎或抗炎细胞因子释放)的分子机制。同样，NF-κB和NRF2调节的生物相容性通路的交联会调节由脂多糖和树脂单体相互作用引起的细胞死亡。意义通过独立但相互关联的NF-κB和NRF2调节的通路在龋病治疗的临床情况下被激活。不利或有利的后果严格取决于细菌产品和树脂单体的广泛组合和浓度。
ObjectiveResin monomers released from unpolymerized dental adhesives or composites and bacterial products like lipopolysaccharide (LPS) or lipoteichoic (LTA) are simultaneously present in specific applications following treatment of deep caries lesions. This review is focused on evidence concerning cell responses as a result of the interactions between adaptive mechanisms activated by resin monomers and signaling pathways of the immune response triggered by LPS or LTA originating from cariogenic microorganisms.MethodsCurrent understanding of dental caries progression and pathways in eukaryotic cells in response to LPS stimulation in a clinical situation as well as cell reactions to oxidative stress caused by resin monomers is analyzed based on publications available through online databases.ResultsLPS and LTA activate the redox-sensitive transcription factor NF-κB as a major regulator in immunocompetent dental pulp cells. Cell reactions to LPS/LTA associated with oxidative stress are downregulated by the redox-sensitive transcription factor Nrf2. Thus, activation of Nrf2 through resin monomer-induced oxidative stress due to the increased formation of reactive oxygen species (ROS) could be a molecular mechanism underlying the inhibition of LPS-stimulated responses such as the release of pro- or anti-inflammatory cytokines. Likewise, crosslinking of NF-κB and Nrf2-regulated biocompatibility pathways regulates cell death induced by the interaction of LPS and resin monomers.SignificanceA multidimensional scenario through independent but linked NF-κB- and Nrf2-regulated pathways is activated in the clinical situation of caries treatment. Unfavorable or beneficial consequences strictly depend on a wide range of combinations and concentrations of bacterial products and resin monomers.
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影响因子：
--
作者：
Kouros P;Koliniotou-Koumpia E;Koulaouzidou E;Helvatjoglu-Antoniades M;Tziafas D
通讯作者：
Tziafas D
DOI：
--
发表时间：
1995
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
K. Roebuck;A. Rahman;V. Lakshminarayanan;K. Janakidevi;A. B. Malik
通讯作者：
K. Roebuck;A. Rahman;V. Lakshminarayanan;K. Janakidevi;A. B. Malik
影响因子：
29.7
作者：
Brubaker SW;Bonham KS;Zanoni I;Kagan JC
通讯作者：
Kagan JC
影响因子：
4
作者：
Farges JC;Alliot-Licht B;Baudouin C;Msika P;Bleicher F;Carrouel F
通讯作者：
Carrouel F
影响因子：
3.5
作者：
Bolling, Anette Kocbach;Samuelsen, Jan Tore;Mathisen, Gro Haarklou
通讯作者：
Mathisen, Gro Haarklou