研究树脂浸润技术对人工龋模型表面显微硬度（SMH）的影响及对变异链球菌生物膜的作用。

收集因正畸需要拔除的无龋坏前磨牙，制取釉质块共17个，其中5个用于研究树脂浸润治疗对人工龋模型SMH的影响，每个牙块分别于脱矿前（0 h）、脱矿24 h后、树脂浸润治疗后等不同时间点测量得到3组数据，自身前后对比。余下12个用于研究树脂浸润治疗对人工龋模型表面变异链球菌生物膜生长的影响，其中6个为空白对照组、6个为树脂浸润处理组，分别在4、24 h观测菌斑生物膜情况。以维氏表面微硬度仪检测人工龋模型SMH，以激光共聚焦扫描显微镜检测人工龋模型表面菌斑生物膜生物量、厚度、活菌百分比等。数据分别以配对t检验和独立样本t检验进行统计分析。

脱矿前釉质面SMH值为（316.07 ± 13.54）HV，脱矿24 h后为（22.44 ± 1.73）HV，树脂浸润治疗后为（139.45 ± 21.46）HV，两两比较差异有统计学意义（脱矿前-脱矿后t= 55.879，P<0.001；脱矿后-治疗后t=-14.400，P<0.001；脱矿前-治疗后t = 14.090，P<0.001）。变异链球菌生物膜检测中，4及24 h树脂浸润处理组生物量[（0.59 ± 0.24）、（9.53 ± 1.49）μm³/μm²]均低于空白对照组的生物量[（1.01 ± 0.30）、（15.47 ± 7.32）μm³/μm²]，差异有统计学意义（t_{4 h}= 3.232，P_{4 h}= 0.005；t_{24 h}= 2.384，P_{24 h}= 0.042）；4及24 h树脂浸润处理组活菌百分比[（48.73 ± 8.54）%、（60.49 ± 5.33）%]均高于空白对照组的活菌百分比[（31.84 ± 7.30）%、（34.87 ± 10.72）%]，差异有统计学意义（t_{4 h}=-4.508，P_{4 h}<0.001；t_{24 h}=-6.419，P_{24 h}<0.001）。树脂浸润处理组24 h生物膜厚度为（6.44 ± 1.51）μm，低于空白对照组的生物膜厚度（12.78 ± 7.17）μm，差异有统计学意义（t= 2.592，P= 0.030）。

树脂浸润治疗应用于早期人工龋模型上，能明显改善脱矿牙面的SMH，具有良好的机械性能；同时具有抑制变异链球菌生物膜形成的作用。

To study the effect of resin infiltration to the surface microhardness (SMH) and Streptococcus mutans (S.mutans) adhesion of artificial caries models.

After extraction for orthodontic treatment, caries-free human premolars were cut into 17 enamel blocks. Five enamel blocks were used to study the effect of resin infiltration on SMH. Microhardness of each enamel block was detected before and after demineralization and after resin infiltration. The remaining 12 enamel blocks were demineralized and used to study the effect of resin infiltration on S.mutans adhesion. Six samples treated with resin infiltration were detected S.mutans biofilm at 4 h and 24 h, and other six samples wer referred to the blank control group. Microhardness of enamel surfaces were detected by Vicker′s microhardness tester. Biomass, thickness and percentage of live bacteria of S.mutans biofilm were detected by confocal laser scanning microscope (CLSM) . The values were analyzed by paired t test and independent t test.

The mean microhardness value of enamel surfaces decreases from (316.07 ± 13.54) HV to (22.44 ± 1.73) HV after 24 hours′ demineralization, and increases to (139.45 ± 21.46) HV after resin infiltration significantly (Before demineralization-After demineralization t= 55.879, P<0.001; After demineralization-After treatment t=-14.400, P<0.001; Before demineralization-After treatment t= 14.090, P<0.001) . CLSM images showed reduced biofilm formation on resin-infiltrated specimens[ (0.59 ± 0.24) , (9.53 ± 1.49) μm³/μm²] compared to blank controls [ (1.01 ± 0.30) , (15.47 ± 7.32) μm³/μm²] both at 4 h and 24 h (t_{4 h}= 3.232, P_{4 h}= 0.005; t_{24 h}= 2.384, P_{24 h}= 0.042) , while the percentage of live bacteria in the biofilm of resin-infiltrated specimens [ (48.73 ± 8.54) %, (60.49 ± 5.33) %] was higher than that of the control [ (31.84 ± 7.30) %, (34.87 ± 10.72) %] (t_{4 h} = -4.508, P_{4 h}<0.001; t_{24 h} = -6.419, P_{24 h}<0.001) ; the thickness of biofilm of resin-infiltrated specimens at 24 h [ (6.44 ± 1.51) μm] was higher than that of the control [ (12.78 ± 7.17) μm] (t = 2.592, P = 0.030) .

Resin infiltration increased microhardness value of demineralized enamel lesions, which showed excellent mechanical characters, and resin infiltration can inhibit S.mutans biofilm formation.