The interrelationship of microstructure and hardness of human coronal dentin using reference point indentation technique and micro-Raman spectroscopy

Seyedmahmoud, Rasoul; McGuire, Jacob D.; Wang, Yong; Thiagarajan, Ganesh; Walker, Mary P.

doi:10.1016/j.dental.2017.07.005

Cited by 17 publications

(15 citation statements)

References 30 publications

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“…In this study the hardness values of normal dentin were in good agreement with the previous studies of dentin [32,33]. And in our studies, the element P in DGI-dentine shown a lower level compared with normal dentine, which verify the positive association between dentin hardness and mineral content [34,35].…”

Section: Discussionsupporting

confidence: 91%

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

Zeng¹,

Pan²,

Mo³

et al. 2021

Preprint

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Background：Osteogenesis imperfecta (OI) is a genetic disorder characterized by bone fragility, blue sclerae and dentinogenesis imperfecta (DGI), which are mainly caused by a mutation of the COL1A1 or COL1A2 genes that encode type I procollagen.Methods: The ultrastructure of dentin was analyzed by micro-CT, scanning electron microscopy, energy-dispersive spectroscopy analysis, nanoindentation test and Toluidine Blue Staining. Whole-exome sequencing (WES) was performed to identify the pathogenic gene. The function of the mutant COL1A1 was studied by real-time PCR, western blotting, subcellular localization. Functional analysis in dental pulp stem cells (DPSCs) was also performed to explore the impact of the identified mutation on this phenotype. Results: WES identified a missense mutation (c.1463G > C) in exon 22 of the COL1A1 gene. However, the cases reported herein only exhibited DGI-I in the clinical phenotype, there is no bone disease and any other common abnormal symptom caused by COL1A1 mutation. In addition, ultrastructural analysis of the tooth affected with non-syndromic DGI-I showed that the abnormal dentin was accompanied by disruption of odontoblast polarization, reduced numbers of odontoblasts, loss of dentinal tubules, and reduction in hardness and elasticity, suggesting severe developmental disturbance. What’s more, the odontoblast differentiation ability based on DPSCs that were isolated and cultured from the DGI-I patient was enhanced compared with those from an age-matched, healthy control.Conclusion: This study helped the family members to understand the disease progression and provided new insights into the phenotype-genotype association in collagen-associated diseases and improve clinical diagnosis of OI/DGI-I.

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Section: Discussionsupporting

confidence: 91%

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

Zeng¹,

Pan²,

Mo³

et al. 2021

Preprint

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show abstract

“…Accordingly, we have also observed that the quality of mineralization in DGI-I dentine was far from satisfactory. First, the dentine hardness and collagen elasticity in the proband were significantly lower than in the control samples (p < 0.05), which was consistent with the clinical high brittleness phenomenon (Seyedmahmoud et al, 2017). Meanwhile, the hardness values of the control dentine were in good agreement with the results of previous studies on dentine (Fawzy et al, 2017;Yi et al, 2020).…”

Section: Discussionsupporting

confidence: 88%

Case Report: A Novel COL1A1 Missense Mutation Associated With Dentineogenesis Imperfecta Type I

Zeng

Pan

et al. 2021

Front. Genet.

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Background: Osteogenesis imperfecta (OI) is a clinical and genetic disorder that results in bone fragility, blue sclerae and dentineogenesis imperfecta (DGI), which is mainly caused by a mutation in the COL1A1 or COL1A2 genes, which encode type I procollagen.Case Report: A missense mutation (c.1463G > C) in exon 22 of the COL1A1 gene was found using whole-exome sequencing. However, the cases reported herein only exhibited a clinical DGI-I phenotype. There were no cases of bone disease or any other common abnormal symptom caused by a COL1A1 mutation. In addition, the ultrastructural analysis of the tooth affected with non-syndromic DGI-I showed that the abnormal dentine was accompanied by the disruption of odontoblast polarization, a reduced number of odontoblasts, a reduction in hardness and elasticity, and the loss of dentinal tubules, suggesting a severe developmental disorder. We also investigated the odontoblast differentiation ability using dental pulp stem cells (DPSCs) that were isolated from a patient with DGI-I and cultured. Stem cells isolated from patients with DGI-I are important to elucidate their pathogenesis and underlying mechanisms to develop regenerative therapies.Conclusion: This study can provide new insights into the phenotype-genotype association in collagen-associated diseases and improve the clinical diagnosis of OI/DGI-I.

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“…The determined

ν_{1} ((), normalP O_{4}^{3 -})

peak FWHM values were different between superficial and deep dentine, located near the enamel‐dentine junction and at the border of the coronal pulp chamber, respectively. The results showed a significant increase in FWHM in dentine near the pulp region, which was attributed to structural disorder …”

Section: Resultsmentioning

confidence: 99%

Application of low‐wavenumber Raman spectroscopy to the analysis of human teeth

Bērziņš

Sutton

Loch

et al. 2019

J Raman Spectroscopy

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Low‐wavenumber Raman spectroscopy is demonstrated for its potential to analyse mineralization abnormalities in human teeth. Four different dental samples were analysed in this study, denoted as healthy control, mild hypomineralization, enamel caries, and AI (severely degraded due to Amelogenesis imperfecta). All specimens were imaged using principal component analysis. The spectra from low‐ wavenumber and midwavenumber regions were simultaneously collected allowing for direct comparison between the two regions. This approach provided a method to characterize structural and chemical variation within samples. Structurally different hydroxyapatite was found to be present in the surface and bulk of the enamel. The thin outer layer of the enamel contained the most structurally ordered mineral. The obtained Raman images enabled characterization and comparison of lesion domains as well as relative hydroxyapatite abundances across all dental samples.

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The interrelationship of microstructure and hardness of human coronal dentin using reference point indentation technique and micro-Raman spectroscopy

Cited by 17 publications

References 30 publications

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

Whole Exome Sequencing Identifies a Novel COL1A1 Missense Mutation Causing Dentinogenesis Imperfecta Type I Without Skeletal Abnormalities

Case Report: A Novel COL1A1 Missense Mutation Associated With Dentineogenesis Imperfecta Type I

Application of low‐wavenumber Raman spectroscopy to the analysis of human teeth

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