Dataset Information

Shear bond strength of dentin and deproteinized enamel of amelogenesis imperfecta mouse incisors.

ABSTRACT: The purposes of this study were to: (1) investigate adhesion through shear bond strength (SBS) testing of a resin composite bonded with a self-etching bonding system (SEB) to amelogenesis imperfecta (AI)-affected deproteinized mouse enamel or dentin; and (2) compare wild-type (WT), amelogenin null (AmelxKO), and matrix metalloproteinase-20 null (Mmp20KO) enamel and dentin phenotypes using micro-CT and nanoindentation.Enamel incisor surfaces of WT, AmelxKO, and Mmp20KO mice were treated with SEB with and without sodium hypochlorite and tested for SBS. Incisor dentin was also treated with SEB and tested for SBS. These surfaces were further examined by scanning electron miscroscopy. Micro-CT and nanoindentation analyses were performed on mouse dentin and enamel. Data were analyzed for significance by analysis of variance.Deproteinization did not improve SBS of SEB to these AI-affected enamel surfaces. SBS of AmelxKO teeth was similar in dentin and enamel; however, it was higher in Mmp20KO dentin. The nanohardness of knockout enamel was significantly lower than WT, while knockout dentin nanohardness was not different from WT.Using animal amelogenesis imperfecta models, enamel sodium hypochlorite deproteinization of hypoplastic and hypoplastic-hypomaturation enamel did not increase shear bond strength, while removal of the defective enamel allowed optimal dentin bonding.

SUBMITTER: Pugach MK

PROVIDER: S-EPMC4196710 | biostudies-literature | 2014 Sep-Oct

REPOSITORIES: biostudies-literature

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Shear bond strength of dentin and deproteinized enamel of amelogenesis imperfecta mouse incisors.

Pugach Megan K MK Ozer Fusun F Mulmadgi Raj R Li Yong Y Suggs Cynthia C Wright J Timothy JT Bartlett John D JD Gibson Carolyn W CW Lindemeyer Rochelle G RG

Pediatric dentistry 20140901 5

<h4>Purpose</h4>The purposes of this study were to: (1) investigate adhesion through shear bond strength (SBS) testing of a resin composite bonded with a self-etching bonding system (SEB) to amelogenesis imperfecta (AI)-affected deproteinized mouse enamel or dentin; and (2) compare wild-type (WT), amelogenin null (AmelxKO), and matrix metalloproteinase-20 null (Mmp20KO) enamel and dentin phenotypes using micro-CT and nanoindentation.<h4>Methods</h4>Enamel incisor surfaces of WT, AmelxKO, and Mmp ...[more]

PMID: 25303500

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Project description:Amelogenesis imperfecta (AI) is the name given to a heterogeneous group of conditions characterized by inherited developmental enamel defects. AI enamel is abnormally thin, soft, fragile, pitted and/or badly discolored, with poor function and aesthetics, causing patients problems such as early tooth loss, severe embarrassment, eating difficulties, and pain. It was first described separately from diseases of dentine nearly 80 years ago, but the underlying genetic and mechanistic basis of the condition is only now coming to light. Mutations in the gene AMELX, encoding an extracellular matrix protein secreted by ameloblasts during enamel formation, were first identified as a cause of AI in 1991. Since then, mutations in at least eighteen genes have been shown to cause AI presenting in isolation of other health problems, with many more implicated in syndromic AI. Some of the encoded proteins have well documented roles in amelogenesis, acting as enamel matrix proteins or the proteases that degrade them, cell adhesion molecules or regulators of calcium homeostasis. However, for others, function is less clear and further research is needed to understand the pathways and processes essential for the development of healthy enamel. Here, we review the genes and mutations underlying AI presenting in isolation of other health problems, the proteins they encode and knowledge of their roles in amelogenesis, combining evidence from human phenotypes, inheritance patterns, mouse models, and in vitro studies. An LOVD resource (http://dna2.leeds.ac.uk/LOVD/) containing all published gene mutations for AI presenting in isolation of other health problems is described. We use this resource to identify trends in the genes and mutations reported to cause AI in the 270 families for which molecular diagnoses have been reported by 23rd May 2017. Finally we discuss the potential value of the translation of AI genetics to clinical care with improved patient pathways and speculate on the possibility of novel treatments and prevention strategies for AI.

Project description:Based on the frequent application of composite resins as tooth-colored fillings, this method is considered a viable alternative to dental amalgam. However, this method has the low bond strength of the composite to dentin. To solve this issue, various dental adhesive systems with different characteristics have been developed by dentistry experts.To assess the effect of an additional layer of unfilled resin in self-etch and total-etch dentin adhesives on the shear bond strength (SBS) of composite to dentin. Moreover, we assessed the effects of sample storage in artificial saliva on the SBS of composite to dentin.Methods: This experimental study was conducted on 160 freshly extracted human first or second premolar teeth, which were randomly divided into 16 groups. The teeth were prepared from Mashhad University of Medical Sciences, Mashhad, Iran (2008-2009). Scotchbond Multi-purpose (SBMP), single bond (SB), Clearfil SE Bond, and Clearfil S3 Bond were applied to dentin surface with or without the placement of hydrophobic resin (Margin Bond) in accordance with the instructions of the manufacturers. To expose the coronal dentin, the teeth were abraded with 600 grit SiC paper. Immediately after restoration, half of the samples were tested in terms of SBS, while the other samples were evaluated in terms of SBS after three months of storage in artificial saliva. SBS rates of dental composites evaluated by universal testing machine and samples were studied by optical stereomicroscopy to verify the failure type. Data analysis was performed in SPSS V.16 using Kolmogorov-Smirnov test, independent-samples t-test, ANOVA, and Duncan's logistic regression test.In this study, a significant reduction was observed in the SBS rates of SB and S3 bond adhesive systems after storage with and without hydrophobic resin (p>0.000). Without storage in normal saline, a significant increase was observed in the SBS rate of the SE bond (p=0.013). In addition, SBS rate of SBMP significantly increased after storage with hydrophobic resin (p=0.001). Finally, the highest and lowest rates of SBS were observed in the SE and S3 bonds in all the experimental groups, respectively.The effects of using a hydrophobic resin layer on shear bond strength values seem to be effective. The mild self-etch adhesive exhibited the best resin-dentine bond strength after aging.

Project description:Focal stacks are an alternative spatial arrangement of enamel rods within the inner enamel of mandibular mouse incisors where short rows comprised of 2-45 enamel rods are nestled at the side of much longer rows, both sharing the same rod tilt directed mesially or laterally. The significance of focal stacks to enamel function is unknown, but their high frequency in transverse sections (30% of all rows) suggests that they serve some purpose beyond representing an oddity of enamel development. In this study, we characterized the spatial distribution of focal stacks in random transverse sections relative to different regions of the inner enamel and to different locations across enamel thickness. The curving dentinoenamel junction (DEJ) in transverse sections complicated spatial distribution analyses, and a technique was developed to "unbend" the curving DEJ allowing for more linear quantitative analyses to be carried out. The data indicated that on average there were 36 ± 7 focal stacks located variably within the inner enamel in any given transverse section. Consistent with area distributions, focal stacks were four times more frequent in the lateral region (53%) and twice as frequent in the mesial region (33%) compared to the central region (14%). Focal stacks were equally split by tilt (52% mesial vs. 48% lateral, not significant), but those having a mesial tilt were more frequently encountered in the lateral and central regions (2:1) and those having a lateral tilt were more numerous in the mesial region (1:3). Focal stacks having a mesial tilt were longer on average compared to those having a lateral tilt (7.5 ± 5.6 vs. 5.9 ± 4.0 rods per row, p < 0.01). There was no relationship between the length of a focal stack and its location within the inner enamel. All results were consistent with the notion that focal stacks travel from the DEJ to the outer enamel the same as the longer and decussating companion rows to which they are paired. The spatial distribution of focal stacks within the inner enamel was not spatially random but best fit a null model based on a heterogenous Poisson point process dependent on regional location within the transverse plane of the enamel layer.

Dataset Information

Shear bond strength of dentin and deproteinized enamel of amelogenesis imperfecta mouse incisors.

Publications

Shear bond strength of dentin and deproteinized enamel of amelogenesis imperfecta mouse incisors.

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