Reasons for poor durability of resin-dentin bonds

描述：树脂-牙本质粘结剂缺乏耐久性导致巨大的医疗成本，因为由于树脂复合材料与牙本质的界面耦合恶化，牙色修复体需要频繁更换。我们的总体假设是，缺乏耐久性涉及混合层的树脂和胶原相的降解，这产生了界面耦合。由于采用了湿法粘接技术，胶粘剂配方比过去更亲水。粘合剂中的亲水树脂促进不均匀的吸水，从而产生充满水的空隙和通道，加速聚合物中酯键的水解。我们建议通过测量树脂的电阻抗变化来非破坏性地跟踪这些过程的速率。体外和体内的长期结合研究表明，杂化层中的胶原蛋白丢失。即使在没有细菌的情况下，牙本质基质中的胶原纤维似乎在体外也会被基质金属蛋白酶(MMPs)降解，基质金属蛋白酶(MMPs)在形成过程中被困在基质中，并缓慢地攻击渗透到树脂中的脱矿胶原纤维。这一总体假设将通过旨在对比亲水和疏水树脂稳定性的实验来验证；我们还将测试胶原基质在完全脱矿时的稳定性，以及当它们与矿化的牙本质10微米以内可缓慢暴露更多MMPs的脱矿基质结合时，或者当牙本质中的MMPs被加热或酶抑制剂灭活时的稳定性。将测试各种MMPs的抑制剂，以确定它们是否可以防止导致低结合强度和耦合故障的基质的机械性能损失。希望一种非特异性的基质金属蛋白酶抑制剂(如洗必泰或双膦酸类)可以在粘接过程中作为粘结的前处理或结合到粘结树脂中，从而极大地提高树脂-牙本质粘结的耐久性。将对使用含氟树脂等替代方法进行评估，以防止基质脱矿，我们认为基质脱矿是导致金属基质从底层矿化基质中暴露出来的原因。这种提高树脂-牙本质粘结耐久性的综合方法最终应该会在医疗保健方面节省数十亿美元，并为人类带来更多痛苦。

DESCRIPTION: The lack of durability of resin-dentin bonds results in enormous health care costs as tooth-colored restorations require frequent replacement due to deteriorating interfacial coupling of resin composites to dentin. Our overall hypothesis is that the lack of durability involves degradation of both the resin and collagen phases of the hybrid layer that creates the interracial coupling. Due to the wet bonding technique, adhesive formulations are more hydrophilic than in the past. Hydrophilic resins in the adhesive promote nonuniform water absorption that creates water-filled voids and channels that accelerate hydrolysis of ester bonds in the polymers. We propose to follow the rate of these processes nondestructively by measuring changes in the electrical impedance of resins. Long-term bonding studies in vitro and in vivo show the loss of collagen from the hybrid layer. Collagen fibrils in the dentin matrix appear to be hydrolyzed in vitro, even in the absence of bacteria, by matrix metalloproteinases (MMPs) that were trapped in the matrix during its formation, and that slowly attack the demineralized collagen fibrils infiltrated with resin. This overall hypothesis will be tested by experiments designed to contrast the stability of hydrophilic versus hydrophobic resins; we will also test the stability of collagen matrices when they are fully demineralized versus when they are bonded to demineralized matrices that are within 10 um of mineralized dentin that can slowly expose more MMPs, or when MMPs in dentin are inactivated by heat or enzyme inhibitors. A variety of inhibitors of MMPs will be tested to determine if they can prevent the loss of the mechanical properties of the matrix that leads to low bond strengths and coupling failures. Hopefully, a nonspecific inhibitor of MMP (e.g. chlorhexidine or bisphosphonates) can be applied as a pretreatment during bonding or incorporated into bonding resins to greatly improve the durability of resin-dentin bonds. Alternative approaches such as the use of fluoride-containing resins will be evaluated in an attempt prevent matrix demineralization that we believe is responsible for the exposure of MMPs from the underlying mineralized matrix. This comprehensive approach to improving the durability of resin-dentin bonds should ultimately save billions of dollars in health care and much human suffering.