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PubMed1992

Enamel defects in primary canines related to traditional treatment of teething problems in Sudan.

In parts of Sudan and some other countries, teething is thought to be the cause of severe health problems in infants, and a traditional treatment involves lancing the alveolar process over the unerupted canines with a heated needle, a procedure known as 'haifat'. Three hundred and ninety-eight children aged 4-8 years were examined for the presence of enamel defects on primary canines, and their parents or guardians were questioned regarding past teething problems and their treatment. Two hundred and fifty-eight (65%) of the children had experienced health problems that had been attributed to teething, and 89 (22%) had been subjected to 'haifat'. 'Haifat' had been practised by all socio-economic groups, but was most prevalent in the lower groups. Enamel defects on the buccal surface of the primary canines were found in 25 (28%) of the children in the 'haifat' group and in 25 (8%) of the other children.

Chi-Square Distribution↗
PubMed1986

Enamel defects in 11-12 year-old subjects in a fluoridated area.

Enamel defects were studied in a group of 11-12 year-old children in a fluoridated area using the DDE index. The mouth prevalence of this condition was 72.5 per cent with a tooth prevalence of 40.4 per cent. Enamel opacities accounted for 96.5 per cent of the total condition of which the diffuse patchy type predominates. The defects on the affected posterior teeth occurred most commonly on both the buccal and lingual/palatal surfaces, with most defects being located in the incisal one-half, gingival one-half and occlusal simultaneously. In the affected incisors, the highest proportion of defects affected the buccal surface only, with the most frequent location being the incisal one-half and gingival one-half simultaneously. In 20.9 per cent of the affected subjects, there was a 100 per cent tooth involvement.

Child↗
PubMed2004

Enamel defects and Lyonization in focal dermal hypoplasia.

We report a pattern of enamel hypoplasia in focal dermal hypoplasia similar to that found in females with X-linked amelogenesis imperfecta. Three cases of focal dermal hypoplasia are described, with specific focus on the oral and dental features. In these cases the teeth all had vertical grooving with notching of the incisal or cuspal tips. Also recorded were blunt roots of taurodont form with open apices and missing teeth in 1 case. Oral papillomas were present in 2 cases. The pattern of enamel defects is attributed to Lyonization, which is consistent with the pattern of skin and bone lesions typically seen in focal dermal hypoplasia. This supports the proposal that focal dermal hypoplasia is X-linked. The authors conclude that the pattern of dental defects in focal dermal hypoplasia is consistent with Lyonization.

Anodontia↗
PubMed1980

[Pit-shaped enamel defects in tuberous sclerosis].

In 6 patients affected with tuberous sclerosis, pit-shaped enamel defects were noted. Apparently, these defects are pathognomonic of this syndrome and may help to establish the diagnosis in oligosymptomatic cases.

Dental Enamel↗
PubMed1990

Enamel defects in a fluoridated south-east Asian community.

The prevalence and distribution patterns of enamel defects in maxillary incisors was assessed in 194 Singaporean children aged 11-15 years and belonging to three different ethnic groups. All were born and continuously resident in Singapore, which has a tropical climate. The water supply was fluoridated in 1957 at a level of 0.7 ppm. The mouth prevalence of defects was 71.5 per cent and the tooth prevalence was 55.9 per cent; 82 per cent of all affected teeth demonstrated white lesions of various forms. Although there was no sex difference in the prevalence and distribution pattern of defects, some racial differences were observed. The results were compared with data from other studies where the same classification of defects was used.

Adolescent↗
PubMed2001

[Factors associated with dental enamel defects in the first molar in a population of children].

OBJECTIVES: To assess factors related to defects in the tooth enamel of the first permanent molar. Factors studied include, pediatric assistance, hospital admittance, high and low respiratory illness, varicella, gastroenteritis, ear infections, urinary tract infections, and different pharmacological treatments. DESIGN: A retrospective case control study. PARTICIPANTS: Cases and controls were selected randomly from a pool of 1382 scholars born in years 1980, 1981 and 1982. MEASUREMENTS AND MAIN RESULTS: The study was conducted in march and may of year 2000. Finally 48 cases and 148 controls were selected. A dental examination was conducted at 8 years of age using the WHO criteria. Defects in the tooth enamel were defined according to the FDI criteria. We've measured and compared the study variables along the first five years of live. The epidemiological association was quantified by means of the odds ratio (OR) an its 95% confidence interval (CI). In the first year of live we estimated for pediatric assistance an OR of 2.26 (95% CI 1.05-4.92); in the second year for Urinary Tract Infections (UTI) we obtained an OR of 25.27 (95% CI 2.98-562.2); in the third year for UTI an OR of 6.68 (95% CI 1.01-54.52); in the fourth year the OR for pneumonia was 13.45 (95% CI 1.36-324.5) and finally in the fifth year the significant OR were: 2.56 (95% CI 1.23-5.34) for ear infections, 2.28 (95% CI 1.03-5.03) for macrolides and OR of 2.20 (95% CI 1.08-4.50) for anticongestive medications. CONCLUSIONS: UTI and pneumonia show a high association with the presence of defects in the tooth enamel. Other variables such as high frequency of pediatric assistance, hospital admittance, ear infections, varicella, and pharmacological treatments with macrolides, cefolosporines, anticongestive medications and lungs medications showed a weak association.

Case-Control Studies↗
PubMed1990

Deciduous enamel defects and caries susceptibility in a prehistoric Ohio population.

Clinical studies of the relationship between developmental enamel defects and caries susceptibility have often produced conflicting results. This has been due in part to a failure to distinguish between different types of defects. Studies of this association in prehistoric populations have been rare. The complete deciduous dentitions of 57 subadults from the Libben site, a large Late Woodland cemetery in Ottawa County, Ohio, were selected for analysis. Defects were classified as either hypoplasias (deficiencies in matrix apposition) or hypocalcifications (deficiencies in mineralization) and were graded for severity. The presence or absence of carious lesions was recorded for each tooth. Results indicate a strong positive relationship between hypocalcifications and caries susceptibility. The elevated caries susceptibility of hypocalcified teeth may be related to high levels of magnesium or altered enamel microcrystallite orientation within these teeth. Variations in the frequency of hypocalcifications may partially explain differences in caries rates that have been observed in different prehistoric populations.

Chi-Square Distribution↗
PubMed1985

Deciduous enamel defects in prehistoric Americans from Dickson Mounds: prenatal and postnatal stress.

The month of onset, duration, and incidence of dental enamel hypoplasia and hypocalcification was determined in sub-adults from the Dickson Mounds (Illinois) skeletal series (A.D. 950-1300). The onset of enamel defects occurred predominantly during the intrauterine period, suggesting maternal stress. There are marked differences in survivorship and the duration of enamel disruption in those affected prenatally and postnatally. The relationship between these data and studies of adult dentition is examined.

Dental Enamel Hypoplasia↗
PubMedDate not supplied

Factors associated with first molar dental enamel defects: a multivariate epidemiological approach.

PURPOSE: The purpose of this study was to ascertain factors linked to developmental defects of tooth enamel (DDE) in first permanent molars. METHODS: A retrospective epidemiological case-control study was conducted with 48 cases and 149 controls. Dental examinations were performed on 8-year-old children in accordance with World Health Organization (WHO) guidelines. DDE were defined according to FDI World Dental Federation criteria (DDE index). The various study variables were measured and compared during the first 3 years of life, using dental and health records. These variables included gender, pediatric care, hospital admission, certain specific diseases (urinary tract infections, upper and lower respiratory tract infections, varicella, gastroenteritis, otitis) and drug therapies. A multivariate analysis was performed using multiple logistic regression techniques. RESULTS: The multivariate analysis indicated that: girls had at least a two-fold risk of DDE; frequent pediatric care showed a strong association with DDE, which had an odds ratio (OR) of 3.40 to 4.16 according to year of life; urinary tract infection (UTI) registered a strong association in the second and third years of life with DDE, showing an OR of 32.4 in the second year of life and 6.33 in the third year of life; and mucolytics acted as a protective factor for DDE with an OR range of 0.53 to 0.23 according to year of life. CONCLUSIONS: Female gender, UTI, and high frequency of pediatric care registered a strong association with DDE. Treatment with mucolytics exerted a protective effect against DDE.

Age Factors↗
PubMed2006

Overexpression of transforming growth factor-beta1 in teeth results in detachment of ameloblasts and enamel defects.

Transforming growth factor-beta1 (TGF-beta1) is a key regulator of many cellular processes, including cell adhesion, the immune response and synthesis of extracellular matrix proteins. In the present study, we report the characterization of enamel defects in a transgenic mouse model overexpressing TGF-beta1 in odontoblasts and ameloblasts, its expression being driven by the promoter sequences of the dentin sialophosphoprotein gene. As reported earlier, these mice develop distinct dentin defects similar to those seen in human dentin dysplasia and dentinogenesis imperfecta. A further detailed examination of enamel in these mice revealed that from the early secretory stage, ameloblasts began to detach from dentin to form cyst-like structures. A soft X-ray analysis revealed that this cyst-like structure had a disorganized and partially mineralized matrix with an abnormal mineralization pattern and a globular appearance. In the molars, the enamel was not only pitted and hypoplastic, but enamel rods were completely lost. Thus, altered TGF-beta1 expression in the tooth seems to trigger detachment of ameloblasts and abnormal secretion and deposition of minerals in the cyst-like structures adjoining the dentin. We speculate that the altered expression of TGF-beta1 in teeth impacts the adhesion process of ameloblasts to dentin.

Ameloblasts↗
PubMed1999

Management of gingival overgrowth associated with generalized enamel defects in a child.

Gingival overgrowth is usually associated with systemic conditions or treatment (e.g. blood dyscrasias, anti-epileptic or immunosuppressive agents). A child is presented, who had enlarged gingiva associated with a generalized enamel defect (amelogenesis imperfecta (AI), hypoplastic type) and document the periodontal and restorative management of this case.

Amelogenesis Imperfecta↗
PubMed1991

Dental enamel defects in first-degree relatives of coeliac disease patients.

To find out whether dental changes can be used to screen for coeliac disease among apparently healthy relatives of patients with the disorder, 56 healthy first-degree relatives of such patients were subjected to dental examination and small bowel biopsy. 25 had coeliac-type general permanent-tooth enamel lesions. All 7 who had histological evidence of coeliac disease also had enamel lesions. The finding that enamel defects may occur without small bowel changes must be borne in mind in screening. The coeliac-type enamel changes were strongly associated with HLA-DR3, and most of the DR3 alleles belonged to the extended haplotype A1; B8; DR3 group.

Adolescent↗
PubMedDate not supplied

Polychlorinated biphenyls cause developmental enamel defects in children.

The aim of this study was to evaluate the effects of long-term exposure to polychlorinated biphenyls (PCBs) on developing dental enamel. 202 8- to 14-year-old children who were pre- and post-natally exposed to PCBs in the contaminated region of Bela Krajina, Slovenia, were studied. 202 controls from Brsljin were matched for age and sex. Risk assessment was based on the concentrations of toxic PCB congeners in the diet. Levels of PCBs in dentine were used to validate exposure. PCB levels were analysed by high-resolution gas chromatography. The prevalence of developmental defects of enamel was assessed using the FDI Index. Developmental defects of enamel in permanent teeth were found in 71.3% of exposed children, compared to 49.5% in the control group. The enamel was abnormal in 21.9% of the permanent index teeth of exposed children and in 12.7% of the control children. The difference was statistically significant (chi(2) = 84.18; p = 0.0019), mostly on account of demarcated opacities and hypoplasia. The extent of the defects was also greater in the exposed group (chi(2) = 61.3; p = 0.0001). No significant correlations were found between PCB exposure and developmental defects in deciduous teeth. In conclusion, our results showed that long-term exposure to PCBs may cause developmental defects of enamel.

Adolescent↗
PubMedDate not supplied

Antecedents and correlates of hypoplastic enamel defects of primary incisors.

Four hundred and fifty-five exfoliated primary incisors were obtained from children whose mothers provided information about a wide range of pre-, peri-, and postnatal characteristics of both the mother and child. These teeth then were examined for the presence of hypoplastic enamel defects (HED). The basic form of the null hypothesis tested was that children who had HED of a primary incisor did not differ from those who did not have such a defect. Of the primary incisors examined, 18.5% had HED (25.0% maxillary and 10.1% mandibular). The following items were found to be associated most strongly (P less than 0.003) with an increase in a child's risk of developing HED; 1) maternal antenatal history of smoking, higher prepregnancy weight, and failure to obtain prenatal care during the first trimester; 2) prematurity, low birth-weight and their associated correlates; and 3) postnatal measles infection. Left-handedness, maternal tea and Tylenol (McNeil Consumer Products Co., Fort Washington, PA) consumption, and failure to screen for undue lead burden were associated less prominently (P less than 0.05) with HED prevalence. Season of birth and serum and dentin lead levels were not related to the prevalence of HED. Many of these risk factors are also covariates of low socioeconomic status such as suboptimal nutrition and increased risk of infection. Additional investigation is needed to delineate the associations between specific pre- and perinatal nutritional and infectious factors, socioeconomic status, and HED development.

Child, Preschool↗
PubMed2007

Enamel defects and ectopic eruption in a child with Usher syndrome and a cochlear implant.

BACKGROUND: Usher syndrome is a genetic disorder consisting of progressive loss of vision and hearing. CASE REPORT: The paper describes an 8-year-old girl with Usher syndrome type I who presented with generalized defects of the permanent dentition and ectopic eruption of the right maxillary first permanent molar. A cochlear implant had been fitted for her hearing loss, and the report reviews the implications of this device for dental treatment. The impacted first permanent molar was encouraged to erupt into the correct position by shaving the distal surface of the second primary molar. CONCLUSION: This is the first report to describe in detail an association between Usher syndrome and enamel defects.

Child↗
PubMed2005

periostin null mice exhibit dwarfism, incisor enamel defects, and an early-onset periodontal disease-like phenotype.

Periostin was originally identified as an osteoblast-specific factor and is highly expressed in the embryonic periosteum, cardiac valves, placenta, and periodontal ligament as well as in many adult cancerous tissues. To investigate its role during development, we generated mice that lack the periostin gene and replaced the translation start site and first exon with a lacZ reporter gene. Surprisingly, although periostin is widely expressed in many developing organs, periostin-deficient (peri(lacZ)) embryos are grossly normal. Postnatally, however, approximately 14% of the nulls die before weaning and all of the remaining peri(lacZ) nulls are severely growth retarded. Skeletal analysis revealed that trabecular bone in adult homozygous skeletons was sparse, but overall bone growth was unaffected. Furthermore, by 3 months, the nulls develop an early-onset periodontal disease-like phenotype. Unexpectedly, these mice also show a severe incisor enamel defect, although there is no apparent change in ameloblast differentiation. Significantly, placing the peri(lacZ) nulls on a soft diet that alleviated mechanical strain on the periodontal ligament resulted in a partial rescue of both the enamel and periodontal disease-like phenotypes. Combined, these data suggest that a healthy periodontal ligament is required for normal amelogenesis and that periostin is critically required for maintenance of the integrity of the periodontal ligament in response to mechanical stresses.

Animals↗