几种粘结树脂在粘结失败后的不同牙本质界面进行再粘结的微拉伸粘结强度和形态学观察

目的:研究3种不同树脂在粘结失败后的不同牙本质表面粘结的微拉伸粘结强度及形态学的观察.方法:磨除因正畸拔除的前磨(牙合)面牙釉质暴露中层牙本质,用Single Bond 2进行粘结建立再粘结模型.在打磨机上打磨再粘结模型样本,产生含有混合层的牙本质表面和去除混合层的牙本质表面.用3种粘结树脂分别在正常牙本质表面,含有混合层的牙本质表面和去除混合层的牙本质表面进行粘结.Z250树脂充填.在低速锯下切割样本进行微拉伸测试(μTBS)和扫描电镜观察粘结界面及断裂类型.结果:每种树脂在含有混合层的牙本质表面粘结的μTBS数值及所产生的混合曾的厚度显著低于在正常牙本质表面粘结的数值.而且较正常牙本质产生较多的玷污颗粒.结论:本实验表明混合层及树脂玷污层的存在降低了在牙本质表面进行再粘结的粘结强度.     

Er,Cr:YSGG激光照射后硬化牙本质表面超微结构观察

目的 通过比较Er,Cr:YSGG激光照射、磷酸酸蚀等方法处理后硬化牙本质表面的超微结构特点,寻找适合硬化牙本质粘接的表面处理方法.方法 选择16颗有硬化牙本质的离体牙,使用随机数字表随机分为4组,每组4颗,分别进行磷酸酸蚀(A组)、激光照射(B组)、磷酸酸蚀+激光照射(C组)、激光照射+磷酸酸蚀(D组)处理,扫描电镜观察硬化牙本质表而的超微结构.结果 A组硬化牙本质表而可见大部分牙本质小管被硬化柱堵塞;B组硬化牙本质表面为均匀一致的蜂窝状改变;C组硬化牙本质表面形态特点与B组类似;D组硬化牙本质表面形态类似于A组,无激光照射后形成的蜂窝状改变.结论 Er,Cr:YSGG激光照射硬化牙本质后增加了表面粗糙度,形成的粗糙面可能有利于粘接.     

2种类型牙本质对粘接界面影响的激光扫描共聚焦显微镜研究

目的:应用激光共聚焦显微镜(LSCM)研究正常和龋病影响牙本质粘接界面的超微结构和粘接机制.方法:选择临床常见2 种牙本质:正常牙本质(ND) 、龋病影响牙本质(CAD),以Rhodamine B 为荧光剂,用激光扫描共聚焦显微镜分别观察正常和龋病影响牙本质粘接后形成的牙本质粘接界面微观形态的异同.结果:龋病影响牙本质的混合层厚度为正常牙本质的2 倍,两者有明显差异.对正常牙本质2 种粘接系统之间没有差异,但对龋病影响牙本质,牙本质小管中树脂突较细,数量减少,且有中断现象,尤其Xeno组更为明显.结论:2 种牙本质粘接系统在正常牙本质表面较龋病影响牙本质渗透更加的充分.     

马尾松树皮和葡萄籽提取物对牙本质耐酸脱矿作用影响的比较研究

目的:评价马尾松树皮提取物(PMBE)和葡萄籽提取物(GSE)对根面牙本质耐酸蚀脱矿作用的影响.方法:表面一半被覆盖的根面牙本质块40个,被随机分为4组(n=10),分别用去离子蒸馏水(DDW)溶液、0.1％NaF溶液、12％ PMBE溶液和12％ GSE溶液作为实验溶液,进行为期8d的pH循环(实验溶液,酸性缓冲液和中性缓冲液).显微CT测定各组未脱矿侧和脱矿侧牙本质的矿物密度(dentin mineral density,DMD),场发射扫描电镜观察各组pH循环后牙本质表面显微形貌.结果:牙本质的矿物密度显示DDW组脱矿侧和未脱矿侧牙本质矿物密度差(△DMD) 198.64±59.97,NaF组为45.94±24.21,PMBE组为90.23±28.77,GSE组为105.07±29.53.PMBE组和GSE组△DMD均高于NaF组(P＜0.05),低于DDW组(P＜0.05),两者相互之间无显著差异(P＞0.05).扫描电镜见DDW组牙本质表面牙本质小管完全开放,NaF组牙本质小管基本封闭,PMBE组和GSE组牙本质小管口成梭形或狭长微裂隙开口.结论:PMBE和GSE均能提高牙本质的耐酸蚀脱矿作用.     

柔性陶瓷涂层与牙本质的结合强度及耐磨性研究

目的:将柔性陶瓷涂于经不同方法处理的牙本质表面,研究其结合强度、耐磨性,以寻求预防和治疗牙齿磨损的新方法.方法:结合强度实验中将牙本质试件随机分为A(表面不处理)、B(37％正磷酸处理)、C(超级粘接剂处理)3组,每组14个试件,A、B两组表面刷涂柔性陶瓷为实验组,C组表面刷超级粘接剂作为对照组.扫描电镜观察涂层表面及...     

Nd:YAG激光对水门汀与牙本质剪切强度的影响

目的:评价脉冲Nd:YAG激光对水门汀与牙本质间剪切强度的影响,并观察激光照射前后的牙本质表面结构变化。方法:取人前磨牙30个,暴露牙本质粘接面形成60个测试样本,随机分为激光组和对照组。激光组以0.8W、10Hz脉冲Nd:YAG激光照射牙本质表面25sec,联合3种水门汀充填;对照组直接使用3种水门汀充填于牙本质表面,置于37℃生理盐水24h后,测试剪切强度,并进行统计学分析,在根管显微镜下观察断裂模式并分类。扫描电镜观察激光照射前后的牙本质表面形态。结果:聚羧酸锌组、玻璃离子组和树脂加强玻璃离子组在Nd:YAG激光照射前(后)的剪切强度分别为4.63±1.39(4.77±0.97)MPa、5.15±0.67(5.26±1.21)MPa和0.92±0.46(0.99±0.35)MPa,激光照射前后的差别均无统计学意义(P>0.05)。扫描电镜观察,0.8W、10Hz的Nd:YAG激光照射会使牙本质表面熔融,玷污层基本去除,大部分牙本质小管封闭,且在局部会出现裂纹。结论:Nd:YAG激光(0.8W、10Hz)处理牙本质,对聚羧酸锌和玻璃离子水门汀与牙本质间的粘接强度无影响。     

中药五倍子提取物对牙本质表面性能的强化作用

目的:评价中药五倍子对牙本质抗酸作用及表面强化的影响。方法:45个牛牙本质标本随机分为3组,以4 g/L五倍子提取液为实验药物,1 g/L NaF为阳性对照组,去离子水为阴性对照组,同时进行体外pH循环致龋实验。采用显微硬度仪测定各样本pH循环前后表面显微硬度,观察牙本质显微硬度的变化,并用扫描电镜和X线能谱仪分析pH循环后各组牙本质表面形貌和元素含量。数据采用SPSS17.0软件包进行统计学分析。结果:与去离子水相比,4 g/L五倍子可以显著减少牙本质表面显微硬度的降低(P<0.05),效果与1 g/L NaF无显著差异(P>0.05)。五倍子组和NaF组牙本质小管大部分呈闭合和堵塞状,而去离子水组牙本质小管呈开放状。五倍子组和NaF组的Ca和P成分显著高于去离子水组(P<0.05)。结论:五倍子可增强牙本质表面的抗酸能力,强化牙本质的表面性能,有抑制牙本质龋进展、保护牙本质免受酸腐蚀的作用。     

粘接处理剂对自粘接树脂水门汀和RMGIC的牙本质粘接强度的影响

目的:实验评价牙本质粘接处理剂对自粘接树脂水门汀和树脂加强型玻璃离子水门汀(RMGIC)的牙本质微拉伸粘接强度的影响.方法:选用离体人无龋第三恒磨牙24颗,用低速切片机垂直于牙体长轴方向将磨牙冠(牙合)中1/3交界线处切开待用.实验组牙本质表面涂布牙本质粘接处理剂,对照组不涂粘接处理剂.后将试样分别用自粘接树脂水门汀(Unicem,3M ESPE;seT PP,SDI)或树脂加强型玻璃离子水门汀(Fuji CEM,GC)原位对位粘接.水浴中储存24h后,用低速切片机把样本切割成约1mm×1mm×8mm条状,随后进行微拉伸测试.用扫描电镜观察粘接界面形貌.结果:无论是否使用粘接处理剂,Unicem的牙本质粘接强度显著高于seT PP 和Fuji CEM(P <0.01).与对照组相比,实验组的粘接强度显著提高(P <0.05).结论:粘接处理剂表面处理增强自粘接树脂水门汀及树脂加强型玻璃离子水门汀的牙本质粘接强度.     

乙醇湿黏结对髓室牙本质树脂黏结界面影响的扫描电镜观察

目的 比较乙醇湿黏结与传统水湿黏结条件下髓室牙本质树脂黏结界面的微观结构,以评价乙醇湿黏结对髓室牙本质树脂黏结界面的影响.方法 12颗人阻生第三磨牙沿水平方向去除髓室顶暴露髓腔,去除牙髓组织,封闭根管口.4颗牙髓室壁表面37%磷酸溶液处理,扫描电镜(SEM)下观察处理前后表面形貌;8颗牙随机分为4组(n=2),分别采用传统水湿黏结和乙醇湿黏结技术.用乙醇/水基Single Bond 2(SB)和丙酮基One Step(OS)两种"单瓶"全酸蚀黏结剂进行髓室牙本质与树脂黏结,SEM观察黏结界面结构.结果 髓室牙本质与两种黏结剂所形成的黏结界面均无典型的混合层结构;乙醇湿黏结条件下.两种黏结剂与髓室牙本质黏结界面树脂突的长度[SB:(72.26±4.5)μm和OS:(74.75±3.42)μm]均比水湿黏结条件下[SB:(37.14±4.36)μm和OS:(40.40±3.19)μm]增加(P＜0.05),差异有统计学意义,且长度较均匀.结论 乙醇湿黏结技术较水湿黏结技术能更有利于树脂黏结剂渗入,从而形成良好的髓室牙本质黏结界面.提高髓室牙本质黏结效果.     

EDTA预处理硬化牙本质前后的电镜观察

目的:通过扫描电镜观察硬化牙本质经乙二胺四乙酸(ethylene diamine tetraacetic acid,EDTA)预处理前后的差异,在超微结构下分析硬化牙本质的结构改变,为临床应用EDTA预处理法提供理论依据。方法:选择10颗具有硬化牙本质(视觉分类Ⅲ级及以上)的离体牙,经扫描电镜观察比较EDTA预处理前后硬化牙本质表面超微结构的变化。结果:扫描电镜所拍摄的图片显示,经EDTA预处理后硬化牙本质表面的超矿层以及接近牙本质小管开口5 μm内的钙盐沉积物全部或大部分溶解,且不破坏管口处的管周牙本质,而在牙本质小管深部,可见到较小的散在晶体。结论:EDTA能有效清除溶解牙本质小管内的矿盐沉积晶体,改善硬化牙本质的不良粘结表面,提高粘结修复的成功率。     

含精氨酸的抗敏抛光膏对暴露牙本质表面变异链球菌黏附的影响

目的 研究含精氨酸抗敏抛光膏对暴露牙本质表面变异链球菌黏附的影响。方法 暴露牙本质小管,使用浮石粉和抗敏抛光膏处理表面,观察其粗糙度的变化。体外培养变异链球菌,观察其在牙本质片表面黏附及葡糖基转移酶（GTFs）基因表达情况。结果 使用浮石粉及抗敏抛光膏均能有效降低表面粗糙度,抗敏抛光膏处理后的牙本质能明显抑制gtfB和gtfC基因的表达。结论 含精氨酸抗敏抛光膏能抑制变异链球菌黏附及gtfB和gtfC基因的表达,对敏感牙本质区域龋病发生具有一定防治作用。     

The effects of orthodontic bonding steps on biofilm formation of Streptococcus mutans in the presence of saliva

Abstract Objective. To investigate the effects of various orthodontic bonding steps on biofilm formation of Streptococcus mutans in the presence of saliva. Materials and methods: Hydroxyapatite (HA) and orthodontic adhesive (AD) disks were prepared to a uniform size. HA disks were etched with 37% phosphoric acid gel in the etched group (HE). In the primed group (HP), Transbond XT primer was applied to the etched HA surface and light-cured. For biofilm formation, Streptococcus mutans was grown on each specimen in a biofilm medium with either glucose or sucrose in the presence of fluid-phase UWS (F-UWS) or surface adsorbed saliva (S-UWS). The adherent bacteria were quantified by enumeration of the total viable counts of bacteria. Biofilms formed on each surface were examined by scanning electron microscopy. Results. When glucose was used, both F-UWS and S-UWS suppressed biofilm formation of S. mutans. Compared to HA and HE, biofilm formation was significantly inhibited on HP and AD in the presence of glucose. Biofilm-forming patterns that were inhibited by saliva were restored in a sucrose-containing medium. F-UWS promoted biofilm formation on HA and HE, while S-UWS significantly promoted biofilm formation on HP. S. mutans developed biofilm better on HA and HE than on AD when sucrose was used as the sole carbohydrate source. Conclusions. This study suggests that the biofilm development by S. mutans is significantly influenced by the orthodontic bonding procedure. Biofilm formation of S. mutans was inhibited on AD more than other surfaces, irrespective of the presence of saliva or a carbohydrate source.     

Effects of human milk on adhesion of Streptococcus mutans to saliva-coated hydroxyapatite in vitro

Adhesion of bacteria to pellicle-coated tooth surfaces is the first step in biofilm formation on teeth. The aim of this study was to explore whether human milk prevents or promotes adhesion of cariogenic Streptococcus mutans to saliva-coated hydroxyapatite (HA) using an in vitro model system. S. mutans binding to HA coated with human parotid saliva (s-HA) or human milk was studied, in addition to binding inhibition to s-HA by human milk. S. mutans did not bind to HA coated with milk. S. mutans binding to s-HA was inhibited by milk from 15 (71 %) of 21 women, whereas milk from the remaining 6 mothers enhanced binding of S. mutans to s-HA. Inhibition of S. mutans binding correlated with bacterial binding to s-HA (r = 0.76). Human milk does not mediate adhesion of S. mutans to HA in vitro, but affects adhesion in an individually varying fashion. Phenotypic variations in milk and saliva glycosylation may explain the inhibitory capacity and possibly affect susceptibility to colonization by S. mutans in childhood.     

In vitro study of bacterial invasion in radicular dentin

The purpose of this study was to investigate whether plaque bacteria invade exposed radicular dentin after root planing or chemical root treatment in vitro. Pieces of dentin were cut out from impacted third molars. The surface of all dentin pieces was treated with sandpaper (#240) so as to make the surface roughness of dentin pieces equal to that of the root surface after root planing (RP surface). Half of the dentin pieces were treated with citric acid (pH 1.0) for 3 minutes (CA surface). After sterilization, each dentin piece was incubated at 37 degrees C in a culture medium inoculated with either S. mutans or S. sanguis. After 1, 3, 7 and 28 days of incubation, the invasion of microorganisms into the dentinal tubules was histologically examined using a light microscope. The following results were obtained. 1. The invasion of S. mutans and S. sanguis into the dentinal tubules was observed at 1, 3, 7 and 28 days. The depth and number of bacterial invasion into the dentinal tubules were positively correlated with incubation time on CA surfaces but not with RP surfaces. 2. The depth and the number of bacterial invasion into the dentinal tubules were higher on the CA surfaces than the RP surfaces. 3. Since the citric acid treatment of scaled and root planed root surfaces may accelerate bacterial invasion from treated root surfaces, the use of citric acid might be harmful in patients with inadequate plaque control.     

Effects of root dentin surface coating with all-in-one adhesive materials on biofilm adherence

OBJECTIVES: Sealing of exposed root dentinal surfaces with adhesive materials is expected to be a promising approach for preventing root dentin caries. The aim of this study was to evaluate the effects of surface coating with all-in-one adhesives on inhibiting Streptococcus mutans biofilm attachment. MATERIALS AND METHODS: Bovine root dentin was cut and ground with #600-grit SiC paper. Each of the three all-in-one adhesives, Hybrid Bond (HB), Reactmer Bond (RB) or Shake One (SO) was single-coated on the dentin surfaces according to the manufacturers' instructions. The dentin surface without coating served as the control. The surface roughness of the coated and non-coated dentin surfaces was recorded by means of laser microscope measurements. S. mutans artificial biofilms were then grown on the surface of each specimen in a microcosm for 20h. The amounts of bacteria and water insoluble glucan in the retained biofilm on the surface of the specimens were measured. All numerical data were statistically analyzed using one-way ANOVA & Tukey's HSD (p<0.05). RESULTS: All of the coated groups showed significantly lower susceptibility to biofilm attachment compared with the non-coated root dentin (p<0.05). Among the coated groups, SO showed the lowest susceptibility for biofilm formation. CONCLUSIONS: Three all-in-one adhesive materials could be effective for root surface coating. A fluoride-releasing adhesive, SO demonstrated the strongest potentiality in resisting biofilm formation.     

Statherin and histatin 1 reduce parotid saliva-promoted Streptococcus mutans strain MT8148 adhesion to hydroxyapatite surfaces

Small salivary phosphoproteins--statherin (ST) and histatin 1 (HT1) - are found in the acquired enamel pellicle which modulates Streptococcus mutans adhesion onto dental enamel. However, their roles in S. mutans adhesion onto enamel surfaces are still undefined. The aim of this study was to investigate whether and how ST and HT1 affect (i) S. mutans adhesion and (ii) the adsorption of S. mutans adhesion-promoting salivary proteins onto hydroxyapatite (HA) in vitro. We fractionated human parotid saliva by adsorption to HA and further by gel filtration chromatography. Adhesion of [3H]-labeled S. mutans strain MT8148 onto sintered HA plates was promoted significantly (>10-fold) by high-molecular weight glycoprotein fraction (HMWGP), but not by purified ST or HT1. More interestingly, promotion of S. mutans adhesion onto HA by HMWGP was significantly reduced by adding purified ST or HT1 to HMWGP. [3H]-labeled S. mutans adhesion on HA was positively correlated to the [14C]-labeled HMWGP adsorption onto HA, which was also reduced by the addition of purified ST and HT1. Synthetic peptides corresponding to ST and HT1 reduced the parotid saliva-promoted S. mutans adhesion. However, removal of the negative charges in the N-terminal domains of ST and HT1 diminished their inhibitory effects on S. mutans adhesion promoted by parotid saliva. We conclude that ST and HT1 competitively inhibit the adsorption of salivary HMWGP, and thereby reduce S. mutans adhesion onto HA surfaces.     

Saliva-promoted adhesion of Streptococcus mutans MT8148 associates with dental plaque and caries experience

Colonization of enamel surfaces by Streptococcus mutans is thought to be initiated by the attachment of bacteria to a saliva-derived conditioning film (acquired pellicle). However, the clinical relevance of the contribution of saliva-promoted S. mutans adhesion in biofilm formation has not yet been fully elucidated. The aim of this study was to correlate saliva-promoted S. mutans adhesion with biofilm formation in humans. We correlated all measurements of salivary factors and dental plaque formation in 70 healthy subjects. Dental plaque development after thorough professional teeth cleaning correlated positively with S. mutans adhesion onto saliva-coated hydroxyapatite pellets and the glycoprotein content of either parotid or whole saliva. Saliva-promoted S. mutans adhesion and glycoprotein content were also positively correlated with each other in parotid and whole saliva. By contrast, neither salivary mutans streptococci, Lactobacillus nor Candida correlated with biofilm formation. Parotid saliva-mediated S. mutans adhesion was significantly higher in 12 caries-experienced (CE) subjects than in 9 caries-inexperienced (CI) subjects. Salivary S. mutans adhesion was significantly less (p < 0.01) in the CI group than in the CE group. In conclusion, the present findings suggest the initial S. mutans adhesion, modulated by salivary protein adsorption onto the enamel surface, as a possible correlate of susceptibility to dental plaque and caries.     

Demineralization of dentin by Streptococcus mutans biofilms grown in the constant depth film fermentor

To develop a bacterial demineralization model, we grew Streptococcus mutans biofilms in a constant depth film fermentor (CDFF) and studied the effects of sucrose pulsing frequency (SPF) in time on dentin demineralization. S. mutans biofilms were grown in dentin specimens with grooves and on dentin surface specimens for 20 days. During the experiments, 2% sucrose was pulsed either 4 or 8 times per day for periods of 30 min. Diluted brain-heart infusion medium containing 25 mM PIPES buffer and 1.5 mM CaCl2 was pulsed as the alternative growth medium. Specimens with intact biofilms were taken out on days 5, 12 and 20. The model was assessed by viable counts of the biofilm, mineral loss and lesion depth in the dentin specimens (by transversal microradiography) and pH measurements in the groove (by pH microelectrode). The results showed that biofilms formed on the dentin surface specimens were constant in viable counts for the low SPF, while this parameter tended to increase with time under the high SPF. Lesions with intact surfaces were formed and the lesion size increased significantly over time and increased significantly with increasing SPF. Typical Stephan curves were found after sucrose pulsing. The pH inside the groove returned to neutral under low SPF, but remained below 6.5 under high SPF. With the CDFF S. mutans biofilm model, lesions can be created in dentin within reasonable experimental time periods, as a result of the presence of a biofilm and in response to carbohydrate challenges.     

变形链球菌牙面粘附唾液受体的筛选和纯化

目的：筛选和纯化变形链球菌血清型ｃ（简称变链）的牙面粘附唾液受体。方法：用全唾液包被羟基磷灰石形成实验性获得性膜（ＳＡＰ）,后用１ｍｏｌ／Ｌ ＮａＣｌ和０．５ｍｏｌ／Ｌ磷酸盐缓冲液分步洗脱,再用Ｓｅｐｈａｄｅｘ Ｇ７５分子筛层析和ＤＥＡＥ－Ｓｅｐｈａｄｅｘ Ａ２５离子交换层析对ＳＡＰ组分进行分离纯化,用细菌粘附实验和细菌粘附竞争抑制实验筛选受体,经聚丙烯酰胺凝胶电泳,等电聚焦电泳,淀粉酶活性测定等     

Fibrin clot adhesion to dentin conditioned with protein constructs: an in vitro proof-of-principle study

OBJECTIVES: Periodontal regeneration is contingent on the adsorption, uninterrupted adhesion, and maturation of a fibrin clot to a periodontally compromised root surface. Clot adhesion appears vitally dependent on the formation of a resilient union between the clot and the root surface. Root surface demineralization will remove a root surface smear layer exposing dentin tubules and collagen matrix for enhanced clot adhesion. Recently, protein constructs have been introduced to condition the root during periodontal surgery. The effect of such root conditioning on clot adhesion has not been clarified. The objective of this study was to evaluate clot adhesion to protein conditioned dentin surfaces. METHODS: Human dentin blocks (4 x 6 x 1 mm) were exposed to a saturated citric acid solution (CA) or a commercial ethylenediaminetetraacetic acid (EDTA) preparation using standardized protocols. Some dentin blocks were additionally conditioned with proteins, either bovine serum albumin (BSA) or an enamel matrix protein preparation (EMP). Fresh human whole blood was applied to the blocks. The blood was allowed to clot for 20 min. in a humidified chamber. The dentin blocks were rinsed 3 x 5 min. in phosphate-buffered saline under standardized conditions to test clot adhesion. They were then processed for scanning electron microscopy (SEM). Two masked examiners independently evaluated the SEM images. RESULTS: CA removed the dentin smear layer, exposing dentin tubules and collagen. EDTA appeared less efficacious leaving smear layer residues. The BSA or EMP application resulted in a surface morphology similar to that of a smear layer. Fibrin clot adhesion was best supported by the CA-treated dentin surface. Forces produced by the rinse protocol partially removed the fibrin clot from EDTA-treated surfaces. BSA- or EMP-treated surfaces poorly retained the fibrin clot. CONCLUSIONS: CA surface demineralization removes a dentin surface smear layer to promote adhesion of a fibrin clot. The EDTA gel appears less effective. Further conditioning of the dentin surface with protein constructs produces a surface morphology similar to that of the smear layer with poor fibrin clot retention.