Maske Tamires T, Isolan Cristina P, van de Sande Françoise H, Peixoto Aline C, Faria-E-Silva André L, Cenci Maximiliano S, Moraes Rafael R
Graduate Program in Dentistry, Federal University of Pelotas, Rua Gonçalves Chaves 457, room 505, Pelotas, RS, 96015-560, Brazil.
Clin Oral Investig. 2015 Jun;19(5):1047-53. doi: 10.1007/s00784-014-1331-1. Epub 2014 Oct 17.
This study was designed to adapt a previously developed in vitro microcosm biofilm model to create carries-affected dentin (CAD) and establish conditions for using the model in bonding studies.
Biofilms were originated from human saliva and grown on dentin discs for 0 (sound dentin), 3, 5, 7, 14, or 21 days under intermittent cariogenic condition (n = 10). At each time point, composite cylinders were bonded to the dentin using self-etch adhesive (Clearfil SE Bond). The response variables were integrated mineral loss (ΔS), lesion depth (LD), shear bond strength (SBS), and failure mode. Data were statistically analyzed (α = 0.05). Bonded interfaces were analyzed by scanning electron microscopy (SEM), and dentin surfaces characterized by infrared spectroscopy (Fourier transform infrared spectroscopy, FTIR).
Lower ΔS was found for sound dentin than for CAD in all experimental groups, except for the group under cariogenic challenge for 3 days. The SBS to CAD was significantly lower than control for all cariogenic challenge times. Adhesive failures were predominant in all groups. ΔS and LD had a significant negative correlation with SBS. A significant exponential decay in SBS was associated with increased ΔS values. CAD had lower mineral and amide I content and an irregular hybridization interface compared to sound dentin.
The microcosm biofilm model was able to artificially induce CAD, which imposed challenge to the bonding of the polymeric adhesive material.
Presence of CAD might interfere with the bonding of polymeric materials. The microcosm biofilm model proposed could be useful for preclinical dentin bonding studies.
本研究旨在对先前开发的体外微观生物膜模型进行改良，以制备患龋牙本质（CAD），并建立在粘结研究中使用该模型的条件。
生物膜源自人类唾液，在间歇性致龋条件下，于牙本质圆盘上培养0（正常牙本质）、3、5、7、14或21天（n = 10）。在每个时间点，使用自酸蚀粘结剂（Clearfil SE Bond）将复合树脂圆柱体粘结至牙本质。反应变量包括累计矿物质流失（ΔS）、病变深度（LD）、剪切粘结强度（SBS）和破坏模式。对数据进行统计学分析（α = 0.05）。通过扫描电子显微镜（SEM）分析粘结界面，并用红外光谱（傅里叶变换红外光谱，FTIR）对牙本质表面进行表征。
在所有实验组中，除致龋刺激3天的组外，正常牙本质的ΔS均低于CAD。在所有致龋刺激时间下，CAD的SBS均显著低于对照组。所有组中粘结剂破坏均占主导。ΔS和LD与SBS呈显著负相关。SBS随ΔS值增加呈显著指数衰减。与正常牙本质相比，CAD的矿物质和酰胺I含量较低，杂交界面不规则。
微观生物膜模型能够人工诱导CAD，这对聚合粘结材料的粘结构成了挑战。
CAD的存在可能会干扰聚合材料的粘结。所提出的微观生物膜模型可用于临床前牙本质粘结研究。
