Fang Hui, Li Quan-Li, Han Min, Mei May Lei, Chu Chun Hung
College & Hospital of Stomatology, Key Lab of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei 230032, China.
College & Hospital of Stomatology, Key Lab of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei 230032, China.
Dent Mater. 2017 Oct;33(10):1075-1083. doi: 10.1016/j.dental.2017.07.008. Epub 2017 Jul 25.
To evaluate the effect of mussel adhesive protein (MAP) on collagenase activity, dentin collagen degradation and microtensile dentin bond strength (μTBS).
Three groups were designed: 1. experimental group: treated with MAP; 2. positive control: treated with GM6001 (collagenase-inhibitor); 3. negative control: treated with distilled water (DW). For collagenase activity, Clostridiopeptidase-A was added to each group (n=5), and collagenase activity was assessed by colorimetric assay. For dentin collagen degradation, thirty dentin slabs were allocated to the three above groups (n=10). Dentin collagen degradation was evaluated by measuring released hydroxyproline by colorimetric assay after being incubated in Clostridiopeptidase-A for 7 days. For microtensile bond strength, sixty human third molars with flat dentin surfaces were etched by phosphoric acid and then assigned to the three above groups (n=20). An etch-and-rinse adhesive system was applied to all three groups as stated in standard clinic protocol. The test of μTBS was performed before and after thermocycling and collagenase challenge.
The collagenase activities (nmol/min/mg) in the group of MAP was significantly less inactive compared to the group of GM6001 and DW (MAP<GM6000<DW, p<0.01). The hydroxyproline concentrations (μg/mL) was significantly less in the group of MAP compared to the group of GM6001 and DW (MAP<GM6000<DW, p<0.01). While there was no significant difference in the immediate μTBS (MPa) among three groups (p>0.06), the value of μTBSs after thermocycling and collagenase challenge was significantly greater in the group of MAP and GM6001 compared to the group of DW (MAP, GM6000>DW, p<0.001).
MAP inhibits collagenase activity, prevents dentin collagen degradation, and delays the deterioration of the dentin bonding of composite restoration over time.
评估贻贝黏附蛋白（MAP）对胶原酶活性、牙本质胶原降解及微拉伸牙本质黏结强度（μTBS）的影响。
设计三组：1. 实验组：用MAP处理；2. 阳性对照组：用GM6001（胶原酶抑制剂）处理；3. 阴性对照组：用蒸馏水（DW）处理。对于胶原酶活性，向每组（n = 5）中加入梭菌肽酶-A，通过比色法评估胶原酶活性。对于牙本质胶原降解，将30个牙本质片分配到上述三组（n = 10）。在梭菌肽酶-A中孵育7天后，通过比色法测量释放的羟脯氨酸来评估牙本质胶原降解。对于微拉伸黏结强度，将60颗牙本质表面平整的人类第三磨牙用磷酸酸蚀，然后分配到上述三组（n = 20）。按照标准临床方案，对所有三组应用酸蚀冲洗黏结系统。在热循环和胶原酶攻击前后进行μTBS测试。
与GM6001组和DW组相比，MAP组的胶原酶活性（nmol/min/mg）显著降低（MAP < GM6000 < DW，p < 0.01）。与GM6001组和DW组相比，MAP组的羟脯氨酸浓度（μg/mL）显著降低（MAP < GM6000 < DW，p < 0.01）。虽然三组之间即刻μTBS（MPa）无显著差异（p > 0.06），但与DW组相比，热循环和胶原酶攻击后MAP组和GM6001组的μTBS值显著更高（MAP，GM6000 > DW，p < 0.001）。
MAP抑制胶原酶活性，防止牙本质胶原降解，并随着时间推移延迟复合修复体牙本质黏结的恶化。
