Effects of surface reaction-type pre-reacted glass ionomer on oral biofilm formation of Streptococcus gordonii
Effects of surface reaction-type pre-reacted glass ionomer on oral biofilm formation of Streptococcus gordonii
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DOI：
10.1007/s10266-015-0217-2
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发表时间：
2016-09-01
期刊：
影响因子：
2.5
通讯作者：
Karibe, Hiroyuki
中科院分区：
文献类型：
--
作者：
Shimazu, Kisaki;Oguchi, Riyo;Karibe, Hiroyuki
戈登链球菌是一种参与牙齿表面最初定植的细菌，它有助于牙齿生物膜的形成，是感染性心内膜炎的重要原因。本研究旨在研究表面反应型预反应玻璃离子(S-PRG)对口腔戈登葡萄球菌生长和聚集的影响。研究了不同浓度的S-PRG洗脱液对变形链球菌、口腔链球菌、嗜酸乳杆菌和白色念珠菌等口腔微生物的生长和生物膜形成的影响。此外，还考察了S-PRG洗脱液对戈尔登氏葡萄球菌与口腔葡萄球菌和核梭杆菌共聚集的影响。此外，还评价了S-PRG洗脱液对高登螺旋藻自聚集的影响。我们的结果表明，S-PRG洗脱液处理对所有生物的生长和生物膜都有抑制作用，且呈剂量依赖关系。S-PRG洗脱液可抑制戈登葡萄球菌与口腔沙门氏菌和有核沙门氏菌的共聚集，而一定浓度的S-PRG洗脱液可促进戈登沙门氏菌的自聚集。这些结果表明，S-PRG具有抗菌活性，其抗菌活性是通过抑制口腔微生物的生长和生物被膜，以及抑制戈登葡萄球菌的共聚来实现的。此外，这些发现表明戈登葡萄球菌与其他细菌的共聚集受到戈登葡萄球菌自身聚集增加的抑制。
Streptococcus gordonii, a bacterium involved in the initial colonization of tooth surfaces, contributes to dental biofilm formation and is an important cause of infective endocarditis. This study aimed to investigate the influence of surface reaction-type pre-reacted glass ionomer (S-PRG) filler on oral bacterial growth and aggregation of S. gordonii. The effect of various concentrations of S-PRG eluate on the growth and the biofilm formation of S. gordonii and other oral microorganisms (Streptococcus mutans, Streptococcus oralis, Lactobacillus acidophilus, and Candida albicans) was assessed. In addition, the effect of S-PRG eluate on coaggregation of S. gordonii with both S. oralis and Fusobacterium nucleatum was assessed. The effect of S-PRG eluate treatment on autoaggregation of S. gordonii was also evaluated. Our results indicate that S-PRG eluate treatment reduced both for the growth and for biofilm of all organisms in a dose-dependent manner. Coaggregation of S. gordonii with both S. oralis and F. nucleatum was inhibited by S-PRG eluate, whereas autoaggregation of S. gordonii increased at certain concentrations of S-PRG eluate. These results indicate that the S-PRG filler possesses antimicrobial activity that is mediated by inhibiting growth and biofilm of oral microorganisms, and by suppressing coaggregation of S. gordonii. In addition, these findings indicate that coaggregation of S. gordonii with other bacteria is inhibited by increased autoaggregation of S. gordonii.