Proanthocyanidins-Loaded Nanoparticles Enhance Dentin Degradation Resistance

Fawzy, A.; Priyadarshini, Balasankar Meera; Selvan, Subramanian Tamil; Lu, Thong Beng; Neo, Jaclyn L.

doi:10.1177/0022034517691757

Cited by 27 publications

(25 citation statements)

References 39 publications

(50 reference statements)

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“…3c). 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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“…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 ). Second, the level of in dentine of patients with DGI-I patient was shown to be lower compared with that in normal dentine, which may have influenced the dentine hardness and mineral content (Park et al, 2020 ).…”

Section: Discussionsupporting

confidence: 90%

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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“…radical scavenger, almost without side effects [28,29,32,33]. It was applied successfully in many dental treatments.…”

Section: Antioxidant Group Versus Non-antioxidant Groupmentioning

confidence: 99%

“…In order to prevent the delay of recovery treatment after bleaching, various antioxidant agents, including sodium ascorbate (SA) [16,21,27], proanthocyanidins (PC) [28,29], green tea extract [4,5,7,13,16], pine bark extract [30], aloe extract [5,16], and grape seed extract [16,31], have been attempted, among which, SA and PC have shown promising results [4,5,14,28,29]. Nevertheless, the results of antioxidants with different types and durations are quite different [4,5,[8][9][10]32,33]. Consequently, we conducted the present in vitro study to compare the effects of 10% SA and 5% PC on the immediate BS-RBE.…”

Section: Introductionmentioning

confidence: 99%

Comparative Evaluation of Two Antioxidants on Reversing the Immediate Bond Strength of Bleached Enamel: In Vitro Study

Zhang

Shao

et al. 2020

Med Sci Monit

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Departmental sources Background: Tooth bleaching causes a significant decrease in the bonding strength between the resin and human enamel. Nevertheless, the effects of different antioxidant types on the immediate bonding strength of resin and bleached enamel were significantly different. Therefore, the objective of this study was to compare the effects of 2 antioxidants for enhancing the bond strength of the resin to bleached enamel. Material/Methods: There were 48 enamel blocks performed from 48 recently extracted maxillary central incisors. There were 8 groups: NC (negative control, no bleached specimens restored without antioxidants); NA (no antioxidant, bleached specimens bonded immediately without any antioxidants); SA30, SA60, and SA120 (bleached specimens accepted the management of 10% sodium ascorbate (SA) for 30 minutes, 60 minutes, and 120 minutes, respectively, before restored); PC30, PC60, and PC120 (bleached specimens received treatment of 5% proanthocyanidins (PC) for 30 minutes, 60 minutes, and 120 minutes, respectively, before restored). We measured the micro-tensile bond strength of specimens and used 2-way ANOVA to analyze the data.

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Proanthocyanidins-Loaded Nanoparticles Enhance Dentin Degradation Resistance

Cited by 27 publications

References 39 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

Comparative Evaluation of Two Antioxidants on Reversing the Immediate Bond Strength of Bleached Enamel: In Vitro Study

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