The multidisciplinary approach managing enamel defects.
Explore the source record for details and available documents.
Amelogenesis Imperfecta↗
SEARCH · Search PubMed
Results for “enamel defects”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A field survey of dental caries, periodontal disease and enamel defects in Tristan Da Cunha. 1. The background.
Explore the source record for details and available documents.
Atlantic Islands↗
[5 years' clinical follow-up of 2 composites in dental enamel defects].
Explore the source record for details and available documents.
Acid Etching, Dental↗
A photographic study of developmental defects of enamel in Brazilian school children.
The aims of this study were, to record developmental enamel in three areas of Brazil with a range of fluoride concentrations in their drinking water and to consider the association between clinical and photographic methods of recording enamel defects. A total of 457 subjects were examined from areas with less than 0.01, 0.7 and 2-3 ppm F in their drinking water. From the photographs, the prevalences of subjects with TF scores of one or more for the upper permanent central incisors were 7 per cent, 52 per cent and 92 per cent respectively for the three areas. The prevalence of demarcated opacities decreased with increasing fluoride levels in the drinking water (p < 0.008). There was substantial agreement between the Thylstrup Fejerskov (TF) scores using clinical and photographic methods (kappa = 0.63). However, prevalences of TF scores of one or more were higher using the photographic (44.9 percent) than clinical (41.4 percent) method (p < 0.01). The results of this study were compared with one undertaken in the United Kingdom and Ireland which also used the same photographic method. Although the prevalences of TF scores of one or more were similar in the areas with near 'optimal' levels of fluoride in the drinking water, in the groups with levels of fluoride less than 0.1 ppm the prevalence of subjects with TF scores of one or more was higher in the United Kingdom population than in Brazil. This study demonstrates the utility of photographic methods of collecting information on enamel opacities over a wide range of fluoride exposure. Results suggest that for the groups from areas with low levels of fluoride in the drinking water the overall fluoride exposure of the UK children was greater than the Brazilian.
Age Factors↗
Prevalence of developmental defects of enamel and dental caries in New Zealand children receiving differing fluoride supplementation.
A survey of the prevalence of dental caries and developmental enamel defects in 666 New Zealand children aged 9 years and with differing histories of fluoride supplementation was carried out in 1982. In the LF (low fluoride) group 22.8% of children had diffuse white opacities compared with the WF (water fluoridation) group, 36.7%, and the CT (continuous use of fluoride tablets) group 49.4% (P = 0.0018). When the tooth prevalence was determined, the differences were more marked with 4.9% of teeth affected in the LF group and 24.7% in the CT group. Dental caries prevalence in the fluoride history groups displayed an inverse relationship with fluoride supplementation, the LF group had a DMFT of 2.4, the WF group, 1.7 and the CT group, 1.2. The prevalence of both diffuse opacities and of dental caries in the PT group where tablets had been used to 5-6 yr of age was anomalous. The survey confirmed that diffuse opacities occur in children with a low fluoride intake but the prevalence increases in groups of children given fluoride supplements.
Child↗
Distribution of developmental defects of enamel on ten tooth surfaces in children aged 12 years living in areas receiving different water fluoride levels in Sri Lanka and England.
The prevalence of enamel defects on ten tooth surfaces per subject was recorded in 1990/91 in 12-year-old children living in areas which received drinking water containing either 0.1, 0.5 or 1.0 ppm F, in Sri Lanka and in England. In some communities, children of high and low socioeconomic groups were included. The teeth included were: 46, 14, 13, 12, 11, 21, 22, 23, 24 and 36; buccal surfaces only were examined. One examiner examined all the children under natural light using the modified DDE index (Clarkson and O'Mullane, 1989). Teeth were not especially cleaned or dried. A 10 per cent re-examination of subjects indicated that examiner reproducibility was good. Data were presented for 547 subjects (168 in Sri Lanka and 379 in England). While the maxillary central incisors were affected most often in England and in the 0.1 ppm F area in Sri Lanka, this was not the case in the 0.5 and 1.0 ppm F areas in Sri Lanka where prevalence was highest in premolar and canine teeth. Demarcated and diffuse opacities predominated in the 1.0 ppm F areas in both countries, while hypoplastic lesions were prevalent in Sri Lanka in the 0.1 and 0.5 ppm F areas, especially in maxillary incisor teeth. Nearly half the lesions extended to more than one-third of the tooth surface in the 1.0 ppm F areas. The findings indicate that maxillary canine and premolar teeth are affected much more in high fluoride areas in Sri Lanka and it is suggested that this may be due to their later development relative to incisors and first molars.
Child↗
The assessment of non-carious defects of enamel.
Developmental defects of dental enamel are very common with at least one in every three individuals having one or more teeth with obvious non-carious defect. The more common defects are opaque areas, hypoplasias (missing enamel) and discoloured enamel; the variety in form, severity and combination of defects is extensive. The lesions are sequelae of systemic, traumatic or genetic events during tooth development. A review of past and current terminologies, and classifications of developmental defects of enamel, reveals ambiguities, deficiencies and lack of uniformity in methods and criteria used in their study. The principal objective for collecting and recording observations on enamel defects is to determine their frequency, severity and distribution for the purpose of assessing the magnitude of the clinical problem they generate and their aetiology. Hence, an internationally recognized classification of developmental enamel defects and recording procedure would increase the value and comparability of future studies. An acceptable uniform terminology and a simple procedure for classifying the more commonly observed defects, defined by their visual characteristics, would achieve these aims. A classification is proposed which identifies and defines the type, number and location of developmental defects affecting tooth enamel on the buccal and lingual surfaces of all teeth. The procedure has been designed for easy interpretation and simple evaluation. It may be modified for use with much less extensive clinical examination.
Adolescent↗
Macroscopic and scanning electron microscopic appearance and hardness values of developmental defects in human permanent tooth enamel.
Defects present in 12 human permanent teeth were classified on the basis of their macroscopic appearance as hypoplasia (three teeth), diffuse opacities (three teeth), white demarcated opacities (one tooth but two defects), or yellow demarcated opacities (five teeth but six defects). The hardness values and SEM appearance of the defective enamel were determined after the teeth were sectioned through the lesion(s) and were distinctive for each type of defect. The thin enamel of the hypoplastic lesions was either opaque (with reduced hardness values) or translucent (with near-normal hardness values and sometimes a change in prism orientation external to an incremental line). The enamel of the diffuse and demarcated opacities was of normal thickness. The changes in the macroscopic and SEM appearance, and the reduced hardness values of the diffuse patchy opacities, were restricted to the outer 150 microns of the enamel. The demarcated opacities varied in position and depth, and in places had a clearly marked boundary with the adjacent normal enamel. Hardness values were related to color change, with yellow lesions being softer than white. Although prism direction was normal within demarcated opacities, prism outlines were less distinct. The findings suggest that temporary and permanent dysfunction of ameloblasts can occur in both secretory and maturation phases, influencing the final appearance of the lesion.
Dental Enamel↗
Development defects of enamel in humans with hereditary epidermolysis bullosa.
Developmental defects of enamel are often reported as a feature of the more severe forms of epidermolysis bullosa (EB). The purpose of this investigation was to determine the prevalence and character of enamel defects in each of the major hereditary EB types. Clinical evaluations were made on 237 individuals representing all of the major EB types and 58 unaffected individuals. All EB cases were categorized by phenotype, mode of inheritance and skin biopsy. The frequency of individuals having developmental enamel defects ranged from 8.6% in recessive dystrophic EB to 100% in junctional EB; 27.5% of the control population had these defects. Generalized hypoplasia characterized by either severe pitting and/or thin enamel was seen in all junctional EB cases but not in any other EB type. There was a tendency for the severe Herlitz form of junctional EB to have thin enamel while non-Herlitz junctional EB cases had less severe pitting and generally no reduction in enamel thickness. The prevalence of individuals with hypoplastic enamel bands was greater in the EB population (9.7%) than controls (1.9%). Thus individuals with simplex and dominant dystrophic EB typically have enamel defects that are similar in frequency and distribution to those of unaffected individuals. Developmental defects of enamel are a consistent feature of junctional EB, although the clinical expression is highly variable.
Adolescent↗
Kohlschütter-Tönz syndrome: epilepsy, dementia, and amelogenesis imperfecta.
Kohlschütter-Tönz syndrome is a central nervous system (CNS) degenerative disease with convulsions and mental regression in which the affected children present with yellow teeth due to defective enamel. We present a family in which 2 affected children (a boy and a girl) were born to consanguineous parents. This report confirms the autosomal recessive inheritance of the disorder. The combination of a CNS and an enamel defect may represent pleiotropy or a contiguous gene syndrome.
Abnormalities, Multiple↗
Enamel microabrasion for removal of superficial dysmineralization and decalcification defects.
Enamel surface "dysmineralization" can be defined as a disturbance in formation of the inorganic component of enamel during amelogenesis. Enamel microabrasion, a method of removing certain enamel dysmineralization and decalcification coloration defects, is described. In many cases, with insignificant and unrecognizable loss of enamel, superficial enamel discoloration defects can be permanently eliminated, improving the appearance of treated teeth.
Dental Enamel↗
Prevalence of enamel developmental defects in a group of 11- and 12-year-old children in South Wales.
The prevalence of enamel developmental defects was assessed in 579 children aged 11 and 12 yr using the DDE Index. The teeth were dried prior to the examination and a normal dental operating light was used for illumination. Teeth with some type of defective enamel were seen in 48.9% of children. White/single opacities were present in 26.4% of children and white/diffuse, patchy opacities in 9.9% of children. The enamel was abnormal in 5.74% of all teeth with white/single opacities and white/diffuse, patchy opacities occurring in 1.89% and 1.18% of teeth respectively. There was a significantly higher number of teeth affected by enamel defects in boys (P less than 0.01) and boys tended to have a higher prevalence of yellow opacities compared to girls.
Child↗
Dental health of aboriginal pre-school children in Brisbane, Australia.
This investigation studied the dental health status of a group of 184 Australian Aboriginal children with a mean age of 4.4 +/- 0.8 years, who were attending pre-schools in metropolitan Brisbane, a non-fluoridated state capital city. The DDE (Developmental Defects of Enamel) Index was used to chart enamel hypoplasia and enamel opacities. WHO criteria was used to diagnose dental caries. The results showed that 98% of children had at least one tooth showing developmental enamel defects. Each child had a mean of 3.8 +/- 1.7 teeth affected by enamel hypoplasia and another 1.1 +/- 0.8 teeth affected by enamel opacity. Seventy-eight percent of the children had dental caries. The mean number of decayed, missing, filled teeth (dmft) per child was 3.8 +/- 3.7. The decayed component constituted 3.5 (95%) of the mean dmft, indicating a high unmet restorative need in this group. The mean dmfs (decayed, missing, filled, surfaces) was 5.9 +/- 7.3. Maxillary anterior labial decay of at least one tooth affected 43 (23%) of the children. In this sub-group, the dmft and dmfs was 9.1 +/- 2.8 and 15.4 +/- 7.7 respectively. Oral debris was found in 98% of the children. It is hypothesized that the high levels of underlying developmental enamel defects, compounded by low fluoride exposure, poor oral hygiene and a diet high in refined sugars pose an important caries risk factor in this group of children.
Child, Preschool↗
Mutational analysis of candidate genes in 24 amelogenesis imperfecta families.
Amelogenesis imperfecta (AI) is a heterogeneous group of inherited defects in dental enamel formation. The malformed enamel can be unusually thin, soft, rough and stained. The strict definition of AI includes only those cases where enamel defects occur in the absence of other symptoms. Currently, there are seven candidate genes for AI: amelogenin, enamelin, ameloblastin, tuftelin, distal-less homeobox 3, enamelysin, and kallikrein 4. To identify sequence variations in AI candidate genes in patients with isolated enamel defects, and to deduce the likely effect of each sequence variation on protein expression and structure, families with isolated enamel defects were recruited. The coding exons and nearby intron sequences were amplified for each of the AI candidate genes by using genomic DNA from the proband as template. The amplification products for the proband were sequenced. Then, other family members were tested to determine their genotype with respect to each sequence variation. All subjects received an oral examination, and intraoral photographs and dental radiographs were obtained. Out of 24 families with isolated enamel defects, only six disease-causing mutations were identified in the AI candidate genes. This finding suggests that many additional genes potentially contribute to the etiology of AI.
Amelogenesis Imperfecta↗
Hypomineralized molars and incisors of unknown origin: treatment outcome at age 18 years.
OBJECTIVE: To assess the outcome of treatment of hypomineralized molars and incisors of unknown aetiology (MIH) in 18-year-olds. DESIGN: A follow-up study including clinical examination, panoramic radiography and intraoral photos. SAMPLE AND METHOD: Seventy-six individuals treated at the Eastman Dental Institute in Stockholm during 1978-2001 with the diagnosis MIH. Severity of enamel defects in molars and incisors, prevalence and distribution of extracted molars, type, quality and median duration of restorations, periradicular condition of affected molars, dental occlusion and space closure in cases of extraction, as well as the individual's satisfaction with the treatment, were assessed. RESULTS: Severe defects with enamel surface breakdown in all four molars occurred in 42% of the individuals and 29% had at least one incisor with yellow/brown opacity in the enamel. At follow up, 42% of the individuals had at least one molar extracted; 18% had all four molars extracted. The median duration of the molar restorations (n = 153) was 5 years. Of the individuals with restored molars, 48% had at least one unacceptable restoration. Periradicular pathology was observed in three molars. The sagittal relations did not differ between individuals with and without extraction of molars. Space closure was acceptable in 87% of the individuals with extracted molars. Eighty percent were satisfied with the treatment. CONCLUSIONS: Extraction of molars with severe enamel defects gave good or acceptable results in a majority of the patients while conservative restorative treatment resulted in a need for additional treatment in approximately half of the patients.
Adolescent↗
Baby-bottle tooth decay: are we on the right track?
The baby-bottle tooth decay (BBTD) risk factor literature was critically assessed for strength of evidence, and the prevention literature for the identification of which risk factors are being addressed. "Inappropriate" feeding practices (non-nutritive sucking, prolonged bottle/breast feeding, nap-time feeding) are believed to cause BBTD. The association of these practices with BBTD is inconsistent and the strength of association varies greatly. These practices increase exposure to lactose, a cariogenic carbohydrate, but the current causation model fails to explain why the majority of children with these risk factors do not develop BBTD. The association of BBTD with low socioeconomic status is stronger and more consistent. Prevention has focused almost exclusively on education directed at changing the postnatal feeding practices despite the fact that teeth begin formation in utero. Prenatal deficiencies of calcium and vitamin D can lead to enamel defects, and enamel defects in turn predispose teeth to caries. Baby-bottle tooth decay is especially prevalent in Aboriginal people, for whom studies have consistently reported diets deficient in vitamin D and calcium. BBTD may be a consequence of the poor socioeconomic conditions and malnutrition. Perhaps more attention should be given to primary prevention.
Arctic Regions↗
The aetiology of developmental defects of enamel: a prevalence and family study in East London, U.K.
The aim of this study was to investigate genetic and environmental factors associated with hypoplastic defects of enamel in a detailed family study combined with an overall prevalence study. 68 percent of 1,518 children with a "complete" permanent dentition had enamel defects, 14.6 percent having hypoplasia. The Family Study consisted of 101 Index Cases from the Prevalence Study having 2 or more teeth with hypoplasia and their first degree relatives: they were compared with 101 matched controls and their relatives. The clinical examinations were supplemented with structured interviews to obtain social, medical and dental histories. Three Index Cases had amelogenesis imperfecta and 18 had "chronological hypoplasia". Bilateral hypoplasia of lower central incisors had a multifactorial aetiology (heritability 70 percent +/- 38 percent), while hypoplasia of pre-molars was associated with familial occurrence of defects. There was evidence suggesting a predisposition in some families to developmental defects of enamel.
Adolescent↗
An in vitro investigation of developmental defects of enamel under wet and dry conditions.
Disagreement exists amongst investigators as to whether or not teeth should be dried before they are examined for developmental defects of enamel. To determine if results are affected by drying of the teeth, 91 extracted premolars and first permanent molars were examined first wet, and then again 1 week later after drying. Following removal of loose debris with an explorer, the enamel defects that were present were categorised according to a modified version of the FDI (DDE) Index. The drying of the surface of the tooth by compressed air allowed a more detailed and precise examination to be performed because the nature and extent of the defects were easier to see. This resulted in diffuse opacities being diagnosed in 144 (52.7 percent) of the tooth regions when the teeth were wet, and 161 (60.0 percent) after drying. The level of reproducibility of diagnosis was higher under dry conditions. It was easier to determine the colour of the teeth using a colour guide than without this assistance. These findings indicate that it is important that investigators performing clinical surveys on the prevalence of defects of enamel should clearly specify whether the teeth were examined wet or dry.
Adult↗