Evaluation of the esthetic properties of developmental defects of enamel: a spectrophotometric clinical study.
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ABSTRACT:
SUBMITTER: Guerra F
PROVIDER: S-EPMC4385663 | biostudies-other | 2015
REPOSITORIES: biostudies-other
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Project description:Current studies on the aetiology of developmental defects of enamel (DDE) are subject to recall bias because of the retrospective collection of information. Our objective was to investigate potential risk factors associated with the occurrence of DDE through a prospective cohort study.Using a random community sample of Hong Kong children born in 1997, we performed a cohort study in which the subjects' background information, medical and dental records were prospectively collected. A clinical examination to identify DDE was conducted in 2010 when the subjects were 12 years old. The central incisor, lateral incisor and first molar in each quadrant were chosen as the index teeth and were examined 'wet' by two trained and calibrated examiners using the modified FDI (DDE) Index.With a response rate of 74.9%, the 514 examined subjects had matched data for background information. Diffuse opacites were the most common type of DDE. Of the various possible aetiological factors considered, only experience of severe diseases during the period 0-3 years was associated with the occurrence of 'any defect' (p = 0.017) and diffuse opacities (p = 0.044). The children with experience of severe diseases before 3 years of age were 7.89 times more likely to be affected by 'any defect' compared with those who did not have the experience (OR 7.89; 95% CI 1.07, 58.14; p = 0.043). However, after adjusting for confounding factors, the association no longer existed.No variables could be identified as risk factors of DDE in this Hong Kong birth cohort.
| S-EPMC4183707 | biostudies-other
Project description:BackgroundDevelopmental Defects of Enamel (DDE) is a pathology of the teeth that can greatly alter the quality of life of patients (hypersensitivity, esthetic issues, loss of function, etc.). The acquired DDE may occur as a result of a wide range of acquired etiological factors and his prevalence of this pathology may reach up to 89.9%. The main objective of this research was to identify and analyze, in current literature, the factors related to acquired DDE, in order to propose a general theory about the mechanisms involved.MethodsThe search of the primary literature was conducted until [December 31, 2021]. Our search strategy uses the Pubmed/MEDLINE database and was structured around 3 terms ["Development," "Defect," and "Enamel"]. To be included, references had to be primary studies, written in English. Exclusion criteria were reviews, in vitro, animal, genetic or archeology studies, and studies focused on clinical management of DDE. One hundred and twenty three articles were included in this scoping review: 4 Randomized clinical trials, 1 letter, 5 cases reports, 2 fundamentals studies, and 111 observational studies (33 Cross-sectional studies, 68 Cohort study and 10 Case-control study). The quality of evidence was assessed using the PEDro scale for clinical trials, the Newcastle-Ottawa scale for observational studies, and a published tool to assess the quality of case reports and case series.ResultsA scoping review of the literature identified 114 factors potentially involved in acquired DDE. The most frequently encountered pathologies are those causing a disorder of calcium homeostasis or a perturbation of the ARNT pathway in mother or child. The link between the ARNT pathway and metabolism deficiency in uncertain and needs to be defined. Also, the implication of this mechanism in tissue impairment is still unclear and needs to be explored.ConclusionsBy identifying and grouping the risk factors cited in the literature, this taxonomy and the hypotheses related to the mechanism allow health practitioners to adopt behaviors that limit the risk of developing aDDE and to set up a prevention of dental pathology. In addition, by reviewing the current literature, this work provides guidance for basic research, clinical studies, and literature searches.
| S-EPMC8907975 | biostudies-literature
Project description:OBJECTIVES:The aim of the study was to reveal the association between developmental defects of enamel (DDE) and single nucleotide polymorphisms (SNPs) in the ENAM, AMELX, AMBN, TUFT1, and TFIP11 genes. MATERIAL AND METHODS:The molecular analysis was carried out in 52 children, aged 10-42 months, from four nursery schools situated in the region of Poznan, Poland (26 individuals with hypomineralization and/or hypoplasia of enamel - "cases" and 26 unaffected children - "controls"), chosen from 262 individuals that had prior dental examination. Six selected SNP variants (rs17878486 in AMELX, rs4694075 in AMBN, rs3796704 in ENAM, rs134136 and rs5997096 in TFIP11, and rs3790506 in TUFT1) were genotyped by the TaqMan probes assay. Genotype and allele frequencies were calculated, and a standard chi-squared analysis was used to test for deviation from Hardy-Weinberg equilibrium. The association between genetic variations and developmental defects of enamel was assessed by the Fisher's exact test and p ? 0.05 was considered statistically significant. RESULTS:Statistically significant positive correlations were found between the rare T allele (p = 0.005) and the TT genotype (p = 0.0052) for rs17878486 in AMELX and occurrence of developmental enamel defects in primary dentition of children. For rs4694075 in AMBN, a higher incidence of the rare T allele (p = 0.0157) was observed in controls compared to DDE cases, whereas the wild-type CC homozygote was more frequent in DDE cases than in controls (p = 0.0062). CONCLUSIONS:The study showed that the single nucleotide polymorphisms in the AMELX and AMBN genes may be genetic variants that contribute to developmental defects of enamel in primary dentition of children. CLINICAL RELEVANCE:The single nucleotide polymorphisms of enamel formation genes may increase the risk for developmental defects of enamel (DDE) occurrence in primary dentition in children.
| S-EPMC5748405 | biostudies-literature
Project description:BACKGROUND AND OBJECTIVE:Gestational diabetes mellitus (GDM) is associated with short- and long-term maternal and perinatal repercussions. Our objective was to evaluate the long-term consequences of intrauterine exposure to hyperglycemia on Developmental Defects of Enamel (DDE) in offspring. RESULTS:Overall, 50 children of women with GDM and 250 children of normoglycemic women participated, the latter serving as controls. Children were examined at the age between 3 and 12 years. In addition to physical examination, two independent observers examined and rated photographs to identify specific types of DDE in a blinded fashion. Among offspring of mothers with GDM, rates of DDE (all types combined) and hypoplasia (specific type) were significantly higher (p<0.001, p = 0.04), in comparison to offspring of normoglycemic mothers. Considering only the affected teeth (1060 in GDM category; 5499 in controls), rates of DDE (all types combined) were significantly higher for total teeth (p <0.001) and deciduous teeth (p<0.001), but not permanent teeth. In specific types of DDE involving deciduous teeth, rates of demarcate opacity were significantly higher (p<0.001; canine and 2nd mandibular molars) and hypoplasia (p <0.001; 2nd maxillary molars and 2nd mandibular molars). In permanent teeth, the rate of diffuse opacity in association with GDM was significantly higher (p<0.001; maxillary central incisors and 1st maxillary molars). CONCLUSION:GDM was associated with the adverse effects of DDE on offspring. This study lays the foundation for future studies to determine the impact of GDM on long-term risk of DDE.
| S-EPMC6392233 | biostudies-literature
Project description:Digital photographs taken under controlled conditions were used to examine the incidence of linear enamel hypoplasia defects (LEHs) in burials from the Buckeye Knoll archaeological site (41VT98 Victoria county, Texas), which spans the Early to Late Archaic Period (ca. 2,500-6,500 BP uncorrected radiocarbon). The majority (68 of 74 burials) date to the Texas Early Archaic, including one extremely early burial dated to 8,500 BP. The photogrammetric data collection method also results in an archive for Buckeye Knoll, a significant rare Archaic period collection that has been repatriated and reinterred. We analyzed the incidence and developmental timing of LEHs in permanent canines. Fifty-nine percent of permanent canines (n = 54) had at least one defect. There were no significant differences in LEH frequency between the maxillary and mandibular canines (U = 640.5, n1 = 37, n2 = 43, p = .110). The sample studied (n = 92 permanent canines) had an overall mean of 0.93 LEH defect per tooth, with a median of one defect, and a mode of zero defects. Average age at first insult was 3.92 (median = 4.00, range = 2.5-5.4) and the mean age of all insults per individual was 4.18 years old (range = 2.5-5.67). Age at first insult is consistent with onset of weaning stress-the weaning age range for hunter-gatherer societies is 1-4.5. Having an earlier age of first insult was associated with having more LEHs (n = 54, rho = -0.381, p = 0.005).
| S-EPMC5815329 | biostudies-literature
Project description:This split-mouth, double-blind randomized controlled trial evaluated radiographic changes in infrabony defects treated with open flap debridement (OFD) or OFD associated with enamel matrix derivative (EMD) after a 24-month follow-up. The radiographic distance from the CEJ to the bottom of the defect (BD) was considered the primary outcome. CEJ-BC and defect angle were secondary outcomes.Ten patients presenting 2 or more defects were selected. An individualized film holder was used to take standardized radiographs of the 43 defects, at baseline and after 24 months. Images were digitized and used to measure the distances from the cemento-enamel junction (CEJ) to the alveolar crest (AC), CEJ to the bottom of the defect (BD) and infrabony defect angle. Statistical analysis was performed in SPSS for Windows (version 5.2). Paired samples t test was used to compare test and control groups and to evaluate changes within each group. The level of significance was set at ??=?0.05%.After 24 months, a significant crestal bone loss was observed for EMD (1.01 mm; p?=?0.049) but not for OFD (0.14 mm; p?=?0.622). However, no differences were detected between groups (p?=?0.37). Reduction of the bone defect depth was significant for OFD (0.70 mm; p?=?0.005) but not for EMD (0.04 mm; p?=?0.86), while no differences were detected between them (p?=?0.87). Both EMD (0.69°; p?=?0.82) and OFD (5.71°; p?=?0.24) showed an improvement in defect angle measurements but no significant differences were observed after 24 months or between the groups (p?=?0.35).Linear radiographic analysis was not able to demonstrate superiority of EMD treated infrabony defects when compared to ODF after 24 months.ClinicalTrials.gov: NCT02195765. Registered 17 July 2014.
| S-EPMC4266965 | biostudies-literature
Project description:Background. The inconsistent prevalence of fluorosis for a given level of fluoride in drinking water suggests developmental defects of enamel (DDEs) other than fluorosis were being misdiagnosed as fluorosis. The imprecise definition and subjective perception of fluorosis indices could result in misdiagnosis of dental fluorosis. This study was conducted to distinguish genuine fluorosis from fluorosis-resembling defects that could have adverse health-related events as a cause using Early Childhood Events Life-grid method (ECEL). Methods. A study was conducted on 400 9-year-old children from areas with high, optimal and low levels of fluoride in the drinking water of Fars province, Iran. Fluorosis cases were diagnosed on the standardized one view photographs of the anterior teeth using Dean's and TF (Thylstrup and Fejerskov) Indices by calibrated dentists. Agreements between examiners were tested. Early childhood health-related data collected retrospectively by ECEL method were matched with the position of enamel defects. Results. Using both Dean and TF indices three out of four dentists diagnosed that 31.3% (115) children had fluorosis, 58.0%, 29.1%, and 10.0% in high (2.12-2.85 ppm), optimal (0.62-1.22 ppm), and low (0.24-0.29 ppm) fluoride areas respectively (p < 0.001). After matching health-related events in the 115 (31.3%) of children diagnosed with fluorosis, 31 (8.4%) of children had fluorosis which could be matched with their adverse health-related events. This suggests that what was diagnosed as fluorosis were non-fluoride related DDEs that resemble fluorosis. Discussion. The frequently used measures of fluorosis appear to overscore fluorosis. Use of ECEL method to consider health related events relevant to DDEs could help to differentiate between genuine fluorosis and fluorosis-resembling defects.
| S-EPMC4782718 | biostudies-literature
Project description:Hypophosphatasia (HPP) is the inborn error of metabolism characterized by deficiency of alkaline phosphatase activity, leading to rickets or osteomalacia and to dental defects. HPP occurs from loss-of-function mutations within the gene that encodes the tissue-nonspecific isozyme of alkaline phosphatase (TNAP). TNAP knockout (Alpl(-/-), aka Akp2(-/-)) mice closely phenocopy infantile HPP, including the rickets, vitamin B6-responsive seizures, improper dentin mineralization, and lack of acellular cementum. Here, we report that lack of TNAP in Alpl(-/-) mice also causes severe enamel defects, which are preventable by enzyme replacement with mineral-targeted TNAP (ENB-0040). Immunohistochemistry was used to map the spatiotemporal expression of TNAP in the tissues of the developing enamel organ of healthy mouse molars and incisors. We found strong, stage-specific expression of TNAP in ameloblasts. In the Alpl(-/-) mice, histological, µCT, and scanning electron microscopy analysis showed reduced mineralization and disrupted organization of the rods and inter-rod structures in enamel of both the molars and incisors. All of these abnormalities were prevented in mice receiving from birth daily subcutaneous injections of mineral-targeting, human TNAP at 8.2?mg/kg/day for up to 44 days. These data reveal an important role for TNAP in enamel mineralization and demonstrate the efficacy of mineral-targeted TNAP to prevent enamel defects in HPP.
| S-EPMC3395779 | biostudies-literature
Project description:Abnormalities of enamel matrix proteins deposition, mineralization, or degradation during tooth development are responsible for a spectrum of either genetic diseases termed Amelogenesis imperfecta or acquired enamel defects. To assess if environmental/nutritional factors can exacerbate enamel defects, we investigated the role of the active form of vitamin A, retinoic acid (RA). Robust expression of RA-degrading enzymes Cyp26b1 and Cyp26c1 in developing murine teeth suggested RA excess would reduce tooth hard tissue mineralization, adversely affecting enamel. We employed a protocol where RA was supplied to pregnant mice as a food supplement, at a concentration estimated to result in moderate elevations in serum RA levels. This supplementation led to severe enamel defects in adult mice born from pregnant dams, with most severe alterations observed for treatments from embryonic day (E)12.5 to E16.5. We identified the enamel matrix proteins enamelin (Enam), ameloblastin (Ambn), and odontogenic ameloblast-associated protein (Odam) as target genes affected by excess RA, exhibiting mRNA reductions of over 20-fold in lower incisors at E16.5. RA treatments also affected bone formation, reducing mineralization. Accordingly, craniofacial ossification was drastically reduced after 2 days of treatment (E14.5). Massive RNA-sequencing (RNA-seq) was performed on E14.5 and E16.5 lower incisors. Reductions in Runx2 (a key transcriptional regulator of bone and enamel differentiation) and its targets were observed at E14.5 in RA-exposed embryos. RNA-seq analysis further indicated that bone growth factors, extracellular matrix, and calcium homeostasis were perturbed. Genes mutated in human AI (ENAM, AMBN, AMELX, AMTN, KLK4) were reduced in expression at E16.5. Our observations support a model in which elevated RA signaling at fetal stages affects dental cell lineages. Thereafter enamel protein production is impaired, leading to permanent enamel alterations.
| S-EPMC5217128 | biostudies-literature
Project description:Endocrine-disrupting chemicals (EDCs), including bisphenol A (BPA), are environmental ubiquitous pollutants and associated with a growing health concern. Anecdotally, molar incisor hypomineralization (MIH) is increasing concurrently with EDC-related conditions, which has led us to investigate the effect of BPA on amelogenesis. Rats were exposed daily to BPA from conception until day 30 or 100. At day 30, BPA-affected enamel exhibited hypomineralization similar to human MIH. Scanning electron microscopy and elemental analysis revealed an abnormal accumulation of organic material in erupted enamel. BPA-affected enamel had an abnormal accumulation of exogenous albumin in the maturation stage. Quantitative real-time PCR, Western blotting, and luciferase reporter assays revealed increased expression of enamelin but decreased expression of kallikrein 4 (protease essential for removing enamel proteins) via transcriptional regulation. Data suggest that BPA exerts its effects on amelogenesis by disrupting normal protein removal from the enamel matrix. Interestingly, in 100-day-old rats, erupting incisor enamel was normal, suggesting amelogenesis is only sensitive to MIH-causing agents during a specific time window during development (as reported for human MIH). The present work documents the first experimental model that replicates MIH and presents BPA as a potential causative agent of MIH. Because human enamel defects are irreversible, MIH may provide an easily accessible marker for reporting early EDC exposure in humans.
| S-EPMC3703547 | biostudies-literature