Ozcan S, Seseogullari-Dirihan R, Uctasli M, Tay F R, Pashley D H, Tezvergil-Mutluay A
Department of Restorative Dentistry, Gazi University, Faculty of Dentistry, Ankara, Turkey.
Finnish Doctoral Program in Oral Sciences (FINDOS) University of Turku, Institute of Dentistry, Turku, Finland; Department of Restorative Dentistry and Cariology and Adhesive Dentistry Research Group, Institute of Dentistry, University of Turku, Turku, Finland.
Dent Mater. 2015 Aug;31(8):901-6. doi: 10.1016/j.dental.2015.04.018. Epub 2015 May 21.
This study tested whether treatment of demineralized dentin with polyacrylic acid (PAA) has any activatory or inhibitory activity on dentin matrix metalloproteinases (MMP)s or cathepsin K (CAT-K).
Dentin beams (1mm×2mm×6mm; n=10) were completely demineralized with EDTA. After initial dry mass assessment, the beams were dipped into 37% phosphoric acid (PA), PA+2% benzalkonium chloride (BAC), PA+2% chlorhexidine digluconate (CHX), 10% PAA, PAA+BAC or PAA+CHX for 20s. Demineralized beams without treatment served as control. All beams were incubated in simulated body fluid (SBF) for 1 week and the dry mass loss was evaluated. Aliquots of SBF were used to analyze solubilized telopeptide fragments using ICTP as indicator of MMP-mediated collagen degradation and CTX for CAT-K-mediated degradation. Additional demineralized beams (n=10) were used to measure the influence of different chemical treatments on total MMP activity of EDTA-demineralized dentin using generic MMP assay. Data were analyzed by ANOVA (α=0.05).
Dry mass loss ranged from 6% (PA) to 2% for (PA-BAC) or (PAA-BAC) (p<0.05). ICTP release of PAA-treated group was significantly higher (p<0.05) than the control, and not significantly different from the PA group (p>0.05). PA+CHX or PAA+CHX and PAA+BAC showed significantly lower ICTP than PA or PAA groups (p<0.05). CAT-K activity increased significantly after 10% PAA treatment compared to control (p<0.05) or to PA postreatment.
Demineralized dentin treated with 10% polyacrylic acid activated CAT-K more than 37% phosphoric acid; 2% chlorhexidine digluconate seems to be a better inhibitor of MMPs and CAT-K than 2% benzalkonium chloride.
本研究旨在测试用聚丙烯酸(PAA)处理脱矿牙本质对牙本质基质金属蛋白酶(MMP)或组织蛋白酶K(CAT-K)是否具有激活或抑制活性。
将牙本质梁(1mm×2mm×6mm;n = 10)用乙二胺四乙酸(EDTA)完全脱矿。在初始干质量评估后,将牙本质梁浸入37%磷酸(PA)、PA + 2%苯扎氯铵(BAC)、PA + 2%葡萄糖酸氯己定(CHX)、10% PAA、PAA + BAC或PAA + CHX中20秒。未处理的脱矿牙本质梁作为对照。所有牙本质梁在模拟体液(SBF)中孵育1周,并评估干质量损失。使用SBF的等分试样以I型胶原羧基末端肽(ICTP)作为MMP介导的胶原降解指标和I型胶原交联羧基末端肽(CTX)作为CAT-K介导的降解指标来分析溶解的端肽片段。另外使用脱矿牙本质梁(n = 10)通过通用MMP测定法测量不同化学处理对EDTA脱矿牙本质总MMP活性的影响。数据采用方差分析进行分析(α = 0.05)。
干质量损失范围从PA处理组的6%到PA - BAC组或PAA - BAC组的2%(p < 0.05)。PAA处理组的ICTP释放量显著高于对照组(p < 0.05),与PA组无显著差异(p > 0.05)。PA + CHX或PAA + CHX以及PAA + BAC组的ICTP显著低于PA或PAA组(p < 0.05)。与对照组(p < 0.05)或PA处理后相比,10% PAA处理后CAT-K活性显著增加。
用10%聚丙烯酸处理的脱矿牙本质比37%磷酸更能激活CAT-K;与2%苯扎氯铵相比,2%葡萄糖酸氯己定似乎是MMP和CAT-K更好的抑制剂。