Measuring the Microscopic Structures of Human Dental Enamel Can Predict Caries Experience

Kelly, Ariana M.; Kallistová, Anna; Küchler, Érika Calvano; Romanos, Helena Freire; Lips, Andrea; Costa, Marcelo C.; Modesto, Adriana; Vieira, Alexandre R.

doi:10.3390/jpm10010005

Cited by 13 publications

(11 citation statements)

References 27 publications

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“…Before etching, the enamel is polished and cleaned. However, a large amount of protein remains on the enamel surface after polishing [ 25 ]. The degree of enamel demineralization after acid etching varies because of different degrees of mineralization on the enamel surface.…”

Section: Discussionmentioning

confidence: 99%

Effect of enamel-surface modifications on shear bond strength using different adhesive materials

et al. 2022

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Background This study aimed to investigate the effect of enamel-surface modifications on the shear bond strength between ceramic brackets bonded using different adhesive materials and the enamel surface and to identify the most suitable clinical adhesive and bonding method. Whether the non-acid-etching treatment met the clinical bond strength was also determined. Methods A total of 108 extracted premolars were divided into nine groups (n = 12) based on the different enamel-surface modification techniques (acid etching, deproteinization, and wetting). Group 1 was bonded with Transbond™ XT adhesive, whereas groups 2–9 were bonded with resin-modified glass ionomer cement (RMGIC). The treatment methods for each group were as follows: groups 1 and 2, acid etching; group 3, acid etching and wetting; group 4, acid etching and deproteinization; group 5, acid etching, deproteinization, and wetting; group 6, deproteinization; group 7, deproteinization and wetting; group 8, without treatment; and group 9, wetting. The samples' shear bond strength was measured using an universal testing machine. Adhesive remnant index (ARI) was examined using a stereomicroscope. The enamel-surface morphology was observed with a scanning electron microscope. One-way ANOVA with Tukey’s post-hoc test and chi-square test were used for statistical analysis, and p < 0.05 and α = 0.05 were considered statistically significant. Results The ARIs of groups 1–5 and 6–9 were statistically significant (p = 0.000). The enamel surface of groups 1–5 was demineralized, and only a tiny amount of protein remained in groups 7 and 8, whereas a thick layer of protein remained in groups 8 and 9. Conclusions RMGIC adhesive did not damage the enamel surface and achieved the required clinical bond strength. The enamel surface was better treated with 5.25% sodium hypochlorite preferably under non-acid-etching conditions.

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Section: Discussionmentioning

confidence: 99%

Effect of enamel-surface modifications on shear bond strength using different adhesive materials

et al. 2022

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“…Matrix metalloproteinase 2, also known as gelatinase A, is a membrane-bound protein with collagen-degrading ability [20,22] and has important roles in tooth formation and mineralization [23][24][25][26][27]. Genetic polymorphisms in enamel formation genes could contribute to structural alterations that could lead to enamel porosity, presence of enamel crystal inhibitory proteins and decreased mineral content [21,28,29]. Some studies have demonstrated the expression of MMP2 during enamel formation [23][24][25].…”

Section: Plos Onementioning

confidence: 99%

Maxillary incisor enamel defects in individuals born with cleft lip/palate

et al. 2020

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Cleft lip with or without cleft palate (CLP) is considered the most frequent congenital malformations of the head and neck, with cleft individuals exhibiting more chances of presenting abnormalities such as developmental defects of enamel (DDE). Matrix metallopeptidase 2 (MMP2) is a membrane-bound protein with collagen-degrading ability and has important roles in tooth formation and mineralization. The aim of this study was to evaluate the frequency, location, severity and extent of DDE found in the maxillary incisors for groups of individuals born with CLP, as well as understanding their relationship with the cleft side. Besides, this study addresses the hypothesis that DDE can be influenced by variation in the MMP2 genes (rs9923304). Individual samples, clinical history, intraoral photographs and panoramic radiographs were obtained from 233 patients under treatment at the Cleft Lip and Palate Service of the University Hospital Lauro Wanderley at the Federal University of Paraíba. Digital images were examined by the same evaluator using the Classification of Defects According to the Modified DDE Index, and then loaded into the Image Tool software, where two measurements were made: total area of the buccal surface (SA) and the area of the DDE (DA), obtaining the percentage of the surface area affected (%SAD) (ICC = 0.99). Genomic DNA was extracted from saliva samples from 124 participants. Genotyping was carried out using TaqMan chemistry for one marker in MMP2 (rs9923304). Statistical analyses were performed by The Jamovi Project software. The Shapiro-Wilk test was applied, followed by the Student’s t-test and the Mann-Whitney test. Chi-square and Fisher’s exact tests, and odds ratio (OR) with 95% confidence interval (CI) calculations were used to determine Hardy-Weinberg equilibrium and statistically significant differences with an alpha of 0.05. No significant differences in the prevalence and extent of enamel defects were found between male and female individuals born with CLP (p = 0.058256). The frequency of individuals presenting teeth with DDE, in relation to the cleft and non-cleft side, was statistically different (p <0.001; OR = 7.15, CI: 4.674> 7.151> 10.942). However, the averages of %SAD were similar (p = 0.18). The highest means of the %SAD were found in individuals with bilateral cleft lip with or without cleft palate (BCLP) when compared to individuals with unilateral cleft lip with or without cleft palate (UCLP), for the teeth inside (IA) and outside the cleft area (OA) (p <0.001). Regardless of the cleft side, individuals with BCLP were 7.85 times more likely to have more than one third of the tooth surface affected, showing more frequently defects in the three thirds (OA: p <0.001) (IA: p = 0.03), as well as a higher frequency of more than one type of defect (OA: p = 0.000358) (IA: p = 0.008016), whereas in UCLP, defects were isolated and restricted to only one third, more frequently, the incisal third (OA: p = 0.009) (IA: p = 0.001), with greater frequency of milder defects, such as demarcated (p = 0.02) and diffuse (p = 0.008) opacities. A higher frequency of the T allele, less common, was observed in the group of CLP individuals who had all the affected teeth or at least two teeth with %SAD greater than 20% (p = 0.019843). Our results suggest that MMP2 may have a role in the cases that presented DDE and genotyping rs9923304 could serve as the basis for a genomic approach to define risks for individuals born with CLP. Frequency and severity of DDE is strongly related to the CLP phenotype, since the highest values were found for BCLP. However, the extent of the DDE is independent of its relationship with the side of the cleft.

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“…We and others have hypothesized that variation in enamel formation genes could explain in part individual susceptibility to dental caries (1,3). Further, genetic variation in amelogenin was associated with caries experience (4-11), erosive tooth wear (12), variation in microscopic enamel structure (13), salivary calcium levels (14), and molar-incisor hypomineralization (MIH) (8) in a number of cohorts with distinct geographic origins, and with incisor enamel microhardness in amelogenin-impaired mouse models (15).…”

Section: Dental Caries Epidemiologymentioning

confidence: 99%

Amelogenesis Imperfecta Enamel Changes, Amelogenin, and Dental Caries Susceptibility

Vieira

Modesto

2020

Front. Dent. Med

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There is great interest in identifying the subset of individuals in the population that are more susceptible to dental caries. We proposed that a portion of these particular individuals are more susceptible to dental caries due to changes in dental enamel that are related to amelogenin genomic variation. However, apparently amelogenin function can be impacted by inflammation, and this can lead to small changes in the structure of the dental enamel that later in life increases the risk of dental caries.

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Measuring the Microscopic Structures of Human Dental Enamel Can Predict Caries Experience

Cited by 13 publications

References 27 publications

Effect of enamel-surface modifications on shear bond strength using different adhesive materials

Effect of enamel-surface modifications on shear bond strength using different adhesive materials

Maxillary incisor enamel defects in individuals born with cleft lip/palate

Amelogenesis Imperfecta Enamel Changes, Amelogenin, and Dental Caries Susceptibility

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