Department of Preventive Dental Science, College of Dentistry, Jazan University, Jazan, Saudi Arabia; Department of Health Promotion, Maastricht University/CAPHRI, Maastricht, The Netherlands.
College of Dentistry, Jazan University, Jazan, Saudi Arabia.
J Contemp Dent Pract. 2022 Mar 1;23(3):371-377.
Esthetic satisfaction has been a prime concern for patients. This has led to a surge in the development of esthetic restorations and dental composites in the field of restorative dentistry over the past decade. Resins are the most preferred restorative material. However, their failure rate was observed to be high.
This review is aimed for clinician, discussing the influence of human and bacterial enzymes on resin restorations.
Composite restoration failure is multifactorial with an interplay of mechanical functions such as masticatory forces and abrasion with biological factors such as host modulated and bacterial enzymes. Salivary esterases and bacterial esterases act on the ester-link bond of resin restoration to form byproducts of methacrylic acid and Bis-hydroxy-propoxy-phenyl-propane. Salivary enzymes form microgaps between the resin-tooth interface and provide a suitable environment for bacterial growth. Bacteria colonize the resin-tooth interface to weaken the resin bond strength. The presence of bacteria draws neutrophils into the hybrid layer. The activation and degranulation of neutrophils leads to enzyme secretions that act on bacteria. However, this can also have adverse effects on resin restoration. Acids prompt the activation of matrix metalloproteinases (MMPs). Proteinases secreted by MMPs uncoil the collagen fibrils of the dentin matrix and degrade tooth structure. The salivary esterases, bacterial esterases, neutrophils, and MMPs work synergistically to degrade dental resin material, resin-tooth interface, and dentin. This causes failure of dental resin restorations and secondary caries formation.
Biological degradation of resin restorations is inevitable irrespective of the material and techniques used. Salivary esterases such as cholesterol esterase and pseudocholinesterase and cariogenic bacterial esterase can degrade dental resin, weakening the hybrid layer at the resin-tooth interface, affecting the bond strength, and causing failure. Ester-free resin and incorporation of antimicrobial materials, esterase, and MMP inhibitors are strategies that could ameliorate degradation of the restoration.
美观满意度一直是患者关注的首要问题。这导致在过去十年中,修复牙科领域的美学修复和牙科复合材料的发展迅速。树脂是最受欢迎的修复材料。然而,它们的失败率很高。
本综述旨在为临床医生讨论人类和细菌酶对树脂修复体的影响。
复合修复体的失败是多因素的,机械功能(如咀嚼力和磨损)与生物因素(如宿主调节和细菌酶)相互作用。唾液酯酶和细菌酯酶作用于树脂修复体的酯键,形成甲基丙烯酸和双羟丙氧基苯基丙烷的副产物。唾液酶在树脂-牙界面之间形成微小间隙,并为细菌生长提供合适的环境。细菌定植于树脂-牙界面,削弱树脂结合强度。细菌的存在将中性粒细胞吸引到混合层中。中性粒细胞的激活和脱颗粒导致酶的分泌,作用于细菌。然而,这也可能对树脂修复体产生不利影响。酸促使基质金属蛋白酶(MMPs)的激活。MMPs 分泌的蛋白酶解开牙本质基质中胶原纤维的螺旋结构并降解牙体结构。唾液酯酶、细菌酯酶、中性粒细胞和 MMPs 协同作用,降解牙用树脂材料、树脂-牙界面和牙本质,导致牙用树脂修复体的失败和继发龋的形成。
无论使用何种材料和技术,树脂修复体的生物降解都是不可避免的。唾液酯酶(如胆固醇酯酶和拟胆碱酯酶)和致龋细菌酯酶可以降解牙用树脂,削弱树脂-牙界面的混合层,影响结合强度,导致修复体失效。无酯树脂和添加抗菌材料、酯酶和 MMP 抑制剂是可以改善修复体降解的策略。