Einfluss der Verhinderung der Kollagen-Degradation durch MMPs auf den Dentin-Klebeverbund

I型胶原在决定树脂-牙本质粘结耐久性中起着重要作用。最近，我们的研究结果以及体外和体内研究表明，牙本质胶原纤维在树脂-牙本质粘结界面上和界面下的水解性降解显著降低了粘结耐久性。人们普遍认为牙本质胶原基质的降解是由基质金属蛋白酶(MMPs)引起的，MMPs是一种锌依赖的宿主衍生的蛋白水解酶家族，存在于牙本质中，可以被现代的自酸蚀和酸蚀漂洗粘合剂激活。用合适的锌络合剂抑制MMPs，可能会减缓或阻止牙本质胶原的降解。因此，当务之急是将基质金属蛋白酶抑制功能引入牙本质粘结剂中，以抑制粘接过程中基质金属蛋白酶的激活。因此，在多学科的研究中，我们提出了一种新型的生物功能大分子单体，作为粘接剂中的生物相容性组分，具有持久的MMPs抑制特性，并能抑制牙本质树脂粘接过程中胶原的降解。它可能会促进脱钙牙本质的再矿化，从而使龋损自然愈合。这一新概念将大大有助于提高树脂-牙本质粘结的耐久性。在较大范围内，具有MMPs抑制特性的大分子单体可进一步应用于种植学和牙周病学，以抑制胶原降解引起的病理性组织破坏。

Type I collagen plays an important role in the determination of resin-dentin bonding durability. Recently, our results and in vitro and in vivo studies demonstrated that the hydrolytic degradation of dentin collagen fibrils in and under resin-dentin bonding interfaces significantly decreases the bonding durability. It is well accepted that the degradation of the dentinal collagen matrix is caused by Matrix Metalloproteinases (MMPs) - a family of zinc-dependent host-derived proteolytic enzymes, which are present in dentinal and can be activated by modern self-etch and etch-and-rinse adhesives. Inhibition of MMPs by a suitable complexing agent for zinc may slow down or prevent the degradation of dentinal collagen. And it is very urgent to incorporate MMP-inhibitory functionality into dentin adhesives to inhibite the activation of MMPs during bonding procedure. Therefore, in a multidisciplinary approach, we propose that a novel bio-functional macromonomer, as a biocompatible component in adhesives, possesses durable MMPs-inhibitory property and can inhibit collagen degradation in resin bonding to dentin. And it may promote the remineralization of decalcified dentin, allowing for natural healing of caries lesions. This new concept will significantly contribute to improving durability of resin-dentin bonds. At a lager scale, the macromonomer with MMPs-inhibitory property may be further applied to implantology and periodontology to inhibit pathological tissue destruction caused by collagen degradation.