Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada; Institute of Biomedical Engineering, University of Toronto, Toronto, Ontario, Canada.
Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada.
Dent Mater. 2020 Dec;36(12):1666-1679. doi: 10.1016/j.dental.2020.10.017. Epub 2020 Nov 10.
Assess the ability of an antimicrobial drug-releasing resin adhesive, containing octenidine dihydrochloride (OCT)-silica co-assembled particles (DSPs), to enhance the biostability and preserve the interfacial fracture toughness (FT) of composite restorations bonded to dentin. Enzyme-catalyzed degradation compromises the dental restoration-tooth interface, increasing cariogenic bacterial infiltration. In addition to bacterial ingress inhibition, antimicrobial-releasing adhesives may exhibit direct interfacial biodegradation inhibition as an additional benefit.
Mini short-rod restoration bonding specimens with total-etch adhesive with/without 10% wt. DSPs were made. Interfacial fracture toughness (FT) was measured as-manufactured or post-incubation in simulated human salivary esterase (SHSE) for up to 6-months. Effect of OCT on SHSE and whole saliva/bacterial enzyme activity was assessed. Release of OCT outside the restoration interface was assessed.
No deleterious effect of DSPs on initial bonding capacity was observed. Aging specimens in SHSE reduced FT of control but not DSP-adhesive-bonded specimens. OCT inhibited SHSE degradation of adhesive monomer and may inhibit endogenous proteases. OCT inhibited bacterial esterase and collagenase. No endogenous collagen breakdown was detected in the present study. OCT increased human saliva degradative esterase activity below its minimum inhibitory concentration towards S. mutans (MIC), but inhibited degradation above MIC. OCT release outside restoration margins was below detection.
DSP-adhesive preserves the restoration bond through a secondary enzyme-inhibitory effect of released OCT, which is virtually confined to the restoration interface microgap. Enzyme activity modulation may produce a positive-to-negative feedback switch, by increasing OCT concentration via biodegradation-triggered release to an effective dose, then subsequently slowing degradation and degradation-triggered release.
评估一种含有盐酸奥替尼啶（OCT）-二氧化硅共组装颗粒（DSPs）的抗菌药物释放树脂胶粘剂，以增强复合修复体与牙本质粘结的生物稳定性并保持界面断裂韧性（FT）。酶催化降解会破坏牙修复体-牙界面，增加致龋细菌的渗透。除了抑制细菌进入外，抗菌释放型胶粘剂还可能表现出直接的界面生物降解抑制作用，作为额外的益处。
用全酸蚀胶粘剂制作带有/不带有 10%重量 DSPs 的迷你短棒修复体粘结试件。在制造时或在模拟人唾液酯酶（SHSE）中孵育长达 6 个月后测量界面断裂韧性（FT）。评估 OCT 对 SHSE 和全唾液/细菌酶活性的影响。评估 OCT 在修复体界面外的释放情况。
DSPs 对初始粘结能力没有有害影响。在 SHSE 中老化的试件降低了对照剂的 FT，但没有降低 DSP-胶粘剂粘结试件的 FT。OCT 抑制了胶粘剂单体的 SHSE 降解，可能抑制了内源性蛋白酶。OCT 抑制了细菌酯酶和胶原酶。本研究未检测到内源性胶原蛋白的降解。OCT 增加了人唾液降解性酯酶的活性，使其低于其对变形链球菌（MIC）的最小抑制浓度，但抑制了高于 MIC 的降解。在修复体边缘之外，OCT 的释放低于检测水平。
DSP 胶粘剂通过释放的 OCT 的二次酶抑制作用来保持修复体的粘结，而 OCT 释放的 OCT 几乎局限于修复体界面微间隙内。通过生物降解触发释放到有效剂量来增加 OCT 浓度，可以产生正向到负向的反馈开关，然后随后减缓降解和降解触发的释放。
