Lack of association between celiac disease and dental enamel hypoplasia in a case-control study from an Italian central region.

Head Face Med. 2007;3:25

Authors: Procaccini M, Campisi G, Bufo P, Compilato D, Massaccesi C, Catassi C, Lo Muzio L

BACKGROUND: A close correlation between celiac disease (CD) and oral lesions has been reported. The aim of this case-control study was to assess prevalence of enamel hypoplasia, recurrent aphthous stomatitis (RAS), dermatitis herpetiformis and atrophic glossitis in an Italian cohort of patients with CD. METHODS: Fifty patients with CD and fifty healthy subjects (age range: 3-25 years), matched for age, gender and geographical area, were evaluated by a single trained examiner. Diagnosis of oral diseases was based on typical medical history and clinical features. Histopathological analysis was performed when needed. Adequate univariate statistical analysis was performed. RESULTS: Enamel hypoplasia was observed in 26% cases vs 16% in controls (p > 0.2; OR = 1.8446; 95% CI = 0.6886: 4.9414). Frequency of RAS in the CD group was significantly higher (36% vs 12%; p = 0.0091; OR = 4.125; 95% CI = 1.4725: 11.552) in CD group than that in controls (36% vs 12%). Four cases of atrophic glossitis and 1 of dermatitis herpetiformis were found in CD patients vs 1 and none, respectively, among controls. CONCLUSION: The prevalence of enamel hypoplasia was not higher in the study population than in the control group. RAS was significantly more frequent in patients with CD.

PMID: 17537244 [PubMed]

[Prevalence of enamel defects and the relationship to dental caries in deciduous and permanent dentition in Indaiatuba, São Paulo, Brazil]

Cad Saude Publica. 2007 Feb;23(2):435-44

Authors: Hoffmann RH, de Sousa Mda L, Cypriano S

The aim of this study was to determine the prevalence of hypoplasia, demarcated opacity and dental fluorosis among schoolchildren with deciduous and permanent dentition. The association between enamel defects and dental caries was also verified. The sample consisted of 624 schoolchildren aged 5 and 309 aged 12. The dmft and DMFT indexes were used to assess dental caries prevalence, DDE to assess enamel defects, and Dean to assess fluorosis. Chi-squared test was used to test significance (p < 0.05) and odds ratio to analyze prevalence of dental caries and enamel defects. A positive association between dental caries and enamel defects (hypoplasia, demarcated opacity and dental fluorosis) was observed for schoolchildren aged 5. However, only hypoplasia and demarcated opacity were associated with caries experience in permanent dentition. The results of this study indicated that children had increased odds of dental caries when enamel defect was present, both in deciduous and permanent dentition; further studies are needed to give evidence to this association.

PMID: 17221093 [PubMed - indexed for MEDLINE]

[Genetic, clinical and molecular analysis of a family affected by amelogenesis imperfecta]

Rev Med Chil. 2005 Nov;133(11):1331-40

Authors: Urzúa O B, Ortega P A, Rodríguez M L, Morales B I

BACKGROUND: Amelogenesis Imperfecta (AI) is a group of conditions where there is an abnormal formation of enamel in terms of quantity, structure and composition. AI is clinically and genetically heterogeneous, there are sex linked and autosomal versions, dominant and/or recessive, with phenotypes of hypoplastic, hypocalcified or hypomature enamel. Only recently, through clinical, genetic and molecular studies of affected families, phenotypic-genotypic correlations are being established in this group of anomalies. AIM: To carry out a genetic, clinical and molecular analysis of a Chilean family affected with an enamel malformation, which probably would correspond to Amelogenesis Imperfecta Dominant Autosomal (AIDA), of hypoplastic type, resulting from g.6395G>A mutation in the enamelin gene. PATIENTS AND METHODS: A genealogical pattern was created for five generations. Five members of this family group were clinically examined, and four of them had a molecular analysis that consisted of the detection of a mutation in the enamelin gene using PCR. RESULTS: In this family, the enamel malformation presents a dominant autosomal pattern of inheritance. The clinical examination of the group allowed a diagnosis of Amelogenesis Imperfecta, of the hypoplastic local type. However, the molecular analysis revealed that the members analyzed did not exhibit the g.6395G>A mutation reported for the enamelin gene (ENAM). CONCLUSIONS: The enamel phenotype in this family could be explained by the presence of one of four other mutations recently described in this or another gene, thereby supporting the findings of allelic heterogeneity reported in the literature.

PMID: 16446857 [PubMed - indexed for MEDLINE]

Acid-etching effects in hypomineralized amelogenesis imperfecta. A microscopic and microanalytical study.

Med Oral Patol Oral Cir Bucal. 2006 Jan;11(1):E40-3

Authors: Sánchez-Quevedo C, Ceballos G, Rodríguez IA, García JM, Alaminos M

OBJECTIVES: The purpose of this study was to use quantitative x-ray microprobe analysis with scanning electron microscopy to define the morphostructural and calcification patterns in the enamel of teeth with the hypomineralized variant of amelogenesis imperfecta. STUDY DESIGN: We compared 5 fragments of permanent human canines from patients with clinically diagnosed hypomineralized amelogenesis imperfecta and 5 normal permanent canines from subjects without amelogenesis imperfecta. All specimens were etched with phosphoric acid for morphological and microanalytical examination. RESULTS: Two types of etching patterns were found; in addition, islets of pattern I were seen within areas of pattern II. Microanalysis detected no significant differences in calcium concentration between specimens with amelogenesis imperfecta and normal control specimens after acid etching. Pattern III was not observed. CONCLUSIONS: The changes and their distribution in the enamel structure after 30 s of acid etching are described in teeth with this rare disorder. Although these data seem to coincide with alterations in prism development, no alterations in calcium concentration were found.

PMID: 16388292 [PubMed - indexed for MEDLINE]

Assessment of DMFT and enamel hypoplasia among junior high school children in Iran.

J Contemp Dent Pract. 2005 Nov 15;6(4):85-92

Authors: Daneshkazemi AR, Davari A

AIM: The main purpose of this study was to assess the prevalence and distribution of decayed, missing, and filled teeth (DMFT) and enamel hypoplasia in 12-year old students in junior high school in Iran. MATERIALS AND METHODS: This descriptive study was carried out in 2001 on 1,223 12-year old students, which were randomly selected in Yazd and Hadi-Shahr, Iran. A questionnaire was designed to record the status of the teeth along with the occupational and educational levels of parents. Data was analyzed using SPSS software, the Chi-square test, and analysis of variance (ANOVA). RESULTS: The mean DMFT score was 1.8 +/- 1.75 and 28.6% of the students were caries-free. There was no significant relationship between DMFT and the rate of dental caries with parents' education and occupation. The percentage of enamel hypoplasia was 32.7%. No statistically significant relationships were found between hypoplasia and DMFT with regard to gender. The relationship between enamel hypoplasia with DMFT score and dental caries was statistically significant. CONCLUSION: In the present study findings for DMFT scores in 12-year old junior high school children are higher than global standards according to the World Health Organization (WHO) references for the year 2000. There was a strong association between enamel hypoplasia and dental caries, and this subject suggests early diagnosis of enamel defects, health education programs, and suitable treatments should be emphasized in junior high school-aged children.

PMID: 16299610 [PubMed - indexed for MEDLINE]

Relationship between dental fluorosis and quality of life: a population based study.

Braz Oral Res. 2005 Apr-Jun;19(2):150-5

Authors: Michel-Crosato E, Biazevic MG, Crosato E

The aim of this study was to verify the prevalence of dental fluorosis in schoolchildren aged 6 to 15 and its possible association with the impacts on their daily activities. This study is observational, cross-sectional and analytical. A total of 513 schoolchildren from the city of Pinheiro Preto, SC, took part in this study. The children were examined by three calibrated dentists, after obtaining a kappa > 0.80. To assess the prevalence of fluorosis, clinical examinations were performed according to the methodology set forth by the 4th edition of the WHO. To assess the impact of fluorosis on their daily activities, a modified OIDP (Oral Impacts on Daily Performance) was adopted. The statistical analysis used was the Chi-squared test with a 5% significance level. Of the total number of children examined, 262 (51.1%) were of the female gender and 251 (48.9%) were of the male gender. In regard to the prevalence of fluorosis, 94 (18.3%) of the children presented this condition, while 419 children (81.7%) presented a normal condition. In regard to the severity of fluorosis, few children presented severe alterations. No association was found between dental fluorosis and gender (p = 0.646), between fluorosis and socioeconomic status (p = 0.848) or between fluorosis and access to public water supply system (p = 0.198). The activities that most affected children's daily performance were: oral hygiene (40.9%) and food intake or enjoying food (40.4%). None of the daily activities could be associated with the occurrence of dental fluorosis. The prevalence of dental fluorosis was consonant with the standards found for locations with optimum fluoride content in the water supply. The questionable and very slight levels of fluorosis were the most frequently found, without influence in the quality of life of the schoolchildren participating in the study.

PMID: 16292450 [PubMed - indexed for MEDLINE]

Prevalence and distribution of developmental enamel defects in the primary dentition of pre-school children.

Braz Oral Res. 2005 Apr-Jun;19(2):144-9

Authors: Lunardelli SE, Peres MA

Developmental defects of the enamel (D.D.E.) are changes in the deciduous dentition that have been little studied in Brazil, although they lead to aesthetic problems, dental sensitivity and may be predictors of dental caries. The objective of this study was to estimate the prevalence and distribution of D.D.E. in the deciduous dentition of pre-school children in the municipality of Itaja&#xED;, Santa Catarina, in 2003. A cross-sectional study was carried out with a sample of 431 children aged 3 to 5 enrolled in public day care centres. All of the teeth were examined and the enamel defects were assessed according to the Modified DDE Index (FDI, 1992). The prevalence of D.D.E. was 24.4% (CI 95% 20.3-28.5). Diffuse opacities were the most common defects found (17.9%), followed by hypoplasia (11.1%) and demarcated opacities (6.1%). The most affected teeth were the second molars (44.4%), followed by the first molars (23.5%). Defects were observed more frequently in the upper arch (58.2%). Assessing enamel hypoplasia separately, a prevalence of 15.1% (CI 95% 11.7-18.5) was observed, with the most affected teeth being the canines (33.6%) and second molars (33.6%). One quarter of the pre-school children presented enamel defects, with diffuse opacities being the most prevalent ones.

PMID: 16292449 [PubMed - indexed for MEDLINE]

Malnutrition and dental caries: a review of the literature.

Caries Res. 2005 Nov-Dec;39(6):441-7

Authors: Psoter WJ, Reid BC, Katz RV

Protein-energy malnutrition occurs when there are deficiencies in protein, energy foods or both, relative to a body's needs. This paper reviews the association of early childhood malnutrition with: (1) dental caries, (2) enamel hypoplasia, (3) salivary gland hypofunction, and (4) delayed eruption. Studies suggest that caries of the primary dentition is associated with early childhood malnutrition, though the effect on caries of the permanent dentition has essentially not been studied. Enamel hypoplasia, salivary glandular hypofunction and saliva compositional changes may be mechanisms through which malnutrition is associated with caries, while altered eruption timing may create a challenge in the analysis of age-specific caries rates.

PMID: 16251787 [PubMed - indexed for MEDLINE]

A Gja1 missense mutation in a mouse model of oculodentodigital dysplasia.

Development. 2005 Oct;132(19):4375-86

Authors: Flenniken AM, Osborne LR, Anderson N, Ciliberti N, Fleming C, Gittens JE, Gong XQ, Kelsey LB, Lounsbury C, Moreno L, Nieman BJ, Peterson K, Qu D, Roscoe W, Shao Q, Tong D, Veitch GI, Voronina I, Vukobradovic I, Wood GA, Zhu Y, Zirngibl RA, Aubin JE, Bai D, Bruneau BG, Grynpas M, Henderson JE, Henkelman RM, McKerlie C, Sled JG, Stanford WL, Laird DW, Kidder GM, Adamson SL, Rossant J

Oculodentodigital dysplasia (ODDD) is an autosomal dominant disorder characterized by pleiotropic developmental anomalies of the limbs, teeth, face and eyes that was shown recently to be caused by mutations in the gap junction protein alpha 1 gene (GJA1), encoding connexin 43 (Cx43). In the course of performing an N-ethyl-N-nitrosourea mutagenesis screen, we identified a dominant mouse mutation that exhibits many classic symptoms of ODDD, including syndactyly, enamel hypoplasia, craniofacial anomalies and cardiac dysfunction. Positional cloning revealed that these mice carry a point mutation in Gja1 leading to the substitution of a highly conserved amino acid (G60S) in Cx43. In vivo and in vitro studies revealed that the mutant Cx43 protein acts in a dominant-negative fashion to disrupt gap junction assembly and function. In addition to the classic features of ODDD, these mutant mice also showed decreased bone mass and mechanical strength, as well as altered hematopoietic stem cell and progenitor populations. Thus, these mice represent an experimental model with which to explore the clinical manifestations of ODDD and to evaluate potential intervention strategies.

PMID: 16155213 [PubMed - indexed for MEDLINE]

[Evaluation of the dental eruption pattern and of enamel defects in the premature child]

Rev Assoc Med Bras. 2005 Jul-Aug;51(4):195-9

Authors: Caixeta FF, Corr&#xEA;a MS

BACKGROUND: The purpose of this study was to analyze the relation between enamel defects and delay of dental eruption with prematurity. METHODS: the sample consisted of 100 premature children ranging from six months to six years of age, observed in the Children Institute of the Medical School of the USP. An anamnesis of the oral cavity was carried out by just one observer who analyzed the chronology of teeth eruption as well as the occurrence of enamel defects. A medical evaluation was also conducted in order to detect potential problems during the prenatal, neonatal and postnatal periods. The statistical assessment included descriptive analysis, average frequency and a confidence interval of 95%. RESULTS: Defects appeared in 35% of the premature children; 51.43% of those affected had been born with a low weight (< 2500g), compared to 14.29% born with normal weight (> 2500g). No relationship was found between the occurrence of defects with a low Apgar score during the first minute, second minute and five minutes (p=0.628; p=0.308;p=0.,193). The most common defects were white opacities, in the deciduous (19.0%) as well as in the permanent dentition (100%). The incisor and cervical halves of the vestibular faces were the most affected reaching values of 88.04% for the deciduous dentition and of 100% for the permanent one. In about 42% of children eruption of teeth took place between 6 to 10 months of age. CONCLUSIONS: Premature children may have enamel defects caused by different factors that appear during pregnancy with a possible association between low weight and enamel defects. Furthermore, premature children had teeth eruption in a normal period, nevertheless, until 36 months of age with less teeth total than children born at normal term.

PMID: 16127578 [PubMed - indexed for MEDLINE]

Esthetic perception and psychosocial impact of developmental enamel defects among Malaysian adolescents.

J Oral Sci. 2004 Dec;46(4):221-6

Authors: Sujak SL, Abdul Kadir R, Dom TN

The aim of this study was to investigate the prevalence and psychosocial impact of enamel defects among 16-year-old school children on the island of Penang. The data were collected through a self-administered questionnaire survey and an oral examination, using the Modified Developmental Defects of Enamel Index (FDI, 1992). In all, 1024 subjects were selected using a multistage random sampling technique. About two-thirds of the sample (67.1%) had at least one tooth affected by enamel defects. Enamel opacities accounted for 85.6% of the total condition. Diffuse-type opacity predominated (63.5%). Among subjects who expressed dissatisfaction, 18.8% reported covering their mouths when smiling, 8.7% avoided going out with friends and 39.1% had consulted their dentists. About 17% of the subjects reported that their parents had complained about the color of their front teeth but only 5.7% had experienced being teased by their friends about the problem. Two-thirds of the subjects were affected by enamel defects involving at least one tooth; however, the esthetic perception and psychosocial impact of those affected were minor.

PMID: 15901066 [PubMed - indexed for MEDLINE]

ENAM mutations in autosomal-dominant amelogenesis imperfecta.

J Dent Res. 2005 Mar;84(3):278-82

Authors: Kim JW, Seymen F, Lin BP, Kiziltan B, Gencay K, Simmer JP, Hu JC

To date, 4 unique enamelin gene (ENAM) defects have been identified in kindreds with amelogenesis imperfecta. To improve our understanding of the roles of enamelin in normal enamel formation, and to gain information related to possible genotype/phenotype correlations, we have identified 2 ENAM mutations in kindreds with hypoplastic ADAI, 1 novel (g.4806A>C, IVS6-2A>C) and 1 previously identified (g.8344delG), and have characterized the resulting enamel phenotypes. The IVS6-2A>C mutation caused a severe enamel phenotype in the proband, exhibiting horizontal grooves of severely hypoplastic enamel. The affected mother had several shallow hypoplastic horizontal grooves in the lower anterior teeth. In the case of the g.8344delG mutation, the phenotype was generalized hypoplastic enamel with shallow horizontal grooves in the middle 1/3 of the anterior teeth. In general, mutations in the human enamelin gene cause hypoplastic enamel, often with horizontal grooves, but the severity of the enamel defects is variable, even among individuals with the same mutation.

PMID: 15723871 [PubMed - indexed for MEDLINE]

Does caries in primary teeth predict enamel defects in permanent teeth? A longitudinal study.

J Dent Res. 2005 Mar;84(3):260-4

Authors: Broadbent JM, Thomson WM, Williams SM

The notion that caries in primary teeth causes developmental defects of enamel in permanent teeth has been recently revived. The research objective was to test this hypothesis through analysis of data from the Dunedin Multidisciplinary Health and Development Study, a longstanding prospective cohort study. The maxillary incisors of 663 children were assessed for existing restorations and dental caries at age five and for developmental defects of enamel at age nine. Where a primary tooth had been carious, the permanent successor was more likely to have a demarcated opacity after adjustment for gender, family socio-economic status, years of exposure to water fluoridation, trauma to primary teeth, and early loss of primary teeth (unadjusted OR = 2.3, 95% CI 1.3, 4.1; adjusted OR = 2.2, 95% CI 1.1, 4.3). These findings support a time-ordered association between dental caries in primary maxillary incisors and demarcated opacities in their permanent successors.

PMID: 15723867 [PubMed - indexed for MEDLINE]

Agenesis and microdontia of permanent teeth as late adverse effects after stem cell transplantation in young children.

Cancer. 2005 Jan 1;103(1):181-90

Authors: H&#xF6;lttä P, Alaluusua S, Saarinen-Pihkala UM, Peltola J, Hovi L

BACKGROUND: The objective of the current study was to examine the occurrence of tooth agenesis and microdontia in pediatric stem cell transplantation (SCT) recipients. METHODS: The impact of total body irradiation (TBI) and age at SCT on agenesis and microdontia of permanent teeth was examined in 55 patients from panoramic radiographs. Assessment A1 (for tooth agenesis and microdontia) excluded the third molars, and assessment A2 (for tooth agenesis) included the third molars. Patients were grouped according to TBI status (the TBI group vs. the non-TBI group) and age at SCT (patients age < or = 3.0 years [Group Y], patients ages 3.1-5.0 years [Group M], and patients age > or = 5.1 years [Group O]). RESULTS: From 1 to 12 teeth were missing in 77%, 40%, and 0% of patients (assessment A1) in Groups Y, M, and O, respectively (Group Y vs. Group M, P=0.055; Group Y vs. Group O, P < 0.001; and Group M vs. Group O, P=0.002), increasing to 83%, 78%, and 43%, respectively, when the third molars were included (assessment A2; P values were not significant). Correspondingly, 75%, 60%, and 13%, respectively, of patients had 1-12 microdontic teeth (assessment A1: Group Y vs. Group M, P=0.306; Group Y vs. Group O, P <0.001; and Group M vs. Group O, P=0.003). Recipient age at the time of SCT was found to have a negative correlation with the number of missing teeth (P=0.001) and microdontic teeth (P=0.005). TBI appeared to have little effect on the prevalence of tooth agenesis (assessment A1: TBI group, 32%; non-TBI group, 29%; assessment A2: TBI group, 72%; non-TBI group, 46%; P values were not significant) or on the prevalence of microdontia (assessment A1: TBI, 41%; non-TBI, 50%; P value was not significant). A tendency toward an increased number of affected teeth was noticed in the group of patients who received TBI. CONCLUSIONS: Depending on their age at SCT, 50-100% of pediatric SCT recipients will later present with agenesis and/or microdontia of permanent teeth that may jeopardize occlusal development. Young age (< or = 5.0 years) at SCT was found to be a stronger risk factor than TBI, although TBI caused additive impairment.

PMID: 15540242 [PubMed - indexed for MEDLINE]

Plasminogen mediates the pathological effects of urokinase-type plasminogen activator overexpression.

Am J Pathol. 2004 Jun;164(6):2299-304

Authors: Bolon I, Zhou HM, Charron Y, Wohlwend A, Vassalli JD

Increased expression of urokinase-type plasminogen activator (uPA) and its receptor (uPAR) is associated with different pathological conditions. Both uPAR-mediated signaling and plasmin-catalyzed extracellular proteolysis may contribute to pathogenesis. To evaluate the involvement of plasminogen in such circumstances, we have taken advantage of transgenic mouse models in which overexpression of uPA and/or uPAR in enamel epithelium, basal epidermis, and hair follicles leads to a pathological phenotype; uPA transgenic mice have chalky-white incisors and, when uPAR is co-expressed, develop extensive alopecia, epidermal thickening, and subepidermal blisters. We report here that when these transgenic mice were backcrossed into a plasminogen-deficient (Plg-/-) background, the dental and skin phenotypes appeared completely normal. Heterozygous Plg+/- transgenic mice exhibited a haplo-insufficiency, with an intermediate or normal phenotype. These results do not argue in favor of a role for uPAR-mediated signaling in our experimental model; rather, they demonstrate an essential, dose-dependent, requirement for plasminogen in uPA-mediated tissue alterations. They also support the hypothesis that plasminogen could play a part in certain skin diseases.

PMID: 15161662 [PubMed - indexed for MEDLINE]

Amelogenin p.M1T and p.W4S mutations underlying hypoplastic X-linked amelogenesis imperfecta.

J Dent Res. 2004 May;83(5):378-83

Authors: Kim JW, Simmer JP, Hu YY, Lin BP, Boyd C, Wright JT, Yamada CJ, Rayes SK, Feigal RJ, Hu JC

Mutations in the human amelogenin gene (AMELX, Xp22.3) cause a phenotypically diverse set of inherited enamel malformations. We hypothesize that the effects of specific mutations on amelogenin protein structure and expression will correlate with the enamel phenotype, clarify amelogenin structure/function relationships, and improve the clinical diagnosis of X-linked amelogenesis imperfecta (AI). We have identified two kindreds with X-linked AI and characterized the AMELX mutations underlying their AI phenotypes. The two missense mutations are both in exon 2 and affect the translation initiation codon and/or the secretion of amelogenin (p.M1T and p.W4S), resulting in hypoplastic enamel. Primary anterior teeth from affected females with the p.M1T mutation were characterized by light and scanning electron microscopy. The thin enamel had defective prism organization, and the surface was rough and pitted. Dentin was normal. The severity of the enamel phenotype correlated with the predicted effects of the mutations on amelogenin expression and secretion.

PMID: 15111628 [PubMed - indexed for MEDLINE]

Novel ENAM mutation responsible for autosomal recessive amelogenesis imperfecta and localised enamel defects.

J Med Genet. 2003 Dec;40(12):900-6

Authors: Hart TC, Hart PS, Gorry MC, Michalec MD, Ryu OH, Uygur C, Ozdemir D, Firatli S, Aren G, Firatli E

The genetic basis of non-syndromic autosomal recessive forms of amelogenesis imperfecta (AI) is unknown. To evaluate five candidate genes for an aetiological role in AI. In this study 20 consanguineous families with AI were identified in whom probands suggested autosomal recessive transmission. Family members were genotyped for genetic markers spanning five candidate genes: AMBN and ENAM (4q13.3), TUFT1 (1q21), MMP20 (11q22.3-q23), and KLK4 (19q13). Genotype data were evaluated to identify homozygosity in affected individuals. Mutational analysis was by genomic sequencing. Homozygosity linkage studies were consistent for localisation of an AI locus in three families to the chromosome 4q region containing the ENAM gene. ENAM sequence analysis in families identified a 2 bp insertion mutation that introduced a premature stop codon in exon 10. All three probands were homozygous for the same g.13185_13186insAG mutation. These probands presented with a generalised hypoplastic AI phenotype and a class II openbite malocclusion. All heterozygous carriers of the g.13185_13186insAG mutation had localised hypoplastic enamel pitting defects, but none had AI or openbite. The phenotype associated with the g.13185_13186insAG ENAM mutation is dose dependent such that ARAI with openbite malocclusion segregates as a recessive trait, and enamel pitting as a dominant trait.

PMID: 14684688 [PubMed - indexed for MEDLINE]

Enamel hypoplasia in a litter of rats with alloxan-induced diabetes mellitus.

Braz Dent J. 2003;14(2):87-93

Authors: Silva-Sousa YT, Peres LC, Foss MC

Enamel hypoplasia is an important clinical problem commonly seen in children born to diabetic women. We aimed to characterize the enamel hypoplasia in Wistar rats born to alloxan-induced diabetes mellitus rats. Groups consisted of pregnant rats supplemented (ISDR) or not (NISDR) with insulin and controls, in which sterile saline solution was administered instead of alloxan or insulin. The mandibular incisors of one-month-old rats born to these mothers were analyzed. Whitish defective enamel was found macroscopically in both experimental groups (ISDR = 37.5%, NISDR = 33.3%) but not in the control group. Mild to severe enamel hypoplasia was observed by scanning electron microscopy (ISDR = 93.8%; NISDR = 100%, control = 4.2%). The severity of hypoplasia correlated positively with the maternal level of blood glucose. In conclusion, the intensity of enamel hypoplasia in the teeth of the litter born to alloxan-induced diabetic rats was variable and was dependent on the glycemic level of the pregnant rat.

PMID: 12964650 [PubMed - indexed for MEDLINE]

Oral health and related factors in cystic fibrosis and other chronic respiratory disorders.

Arch Dis Child. 2003 Aug;88(8):702-7

Authors: Narang A, Maguire A, Nunn JH, Bush A

AIM: To compare the prevalence of dental caries, dental calculus, and enamel defects in children with cystic fibrosis (CF) and children with other chronic respiratory disorders. METHODS: A cross sectional observational survey. One examiner (AN) undertook oral examinations to assess dental caries, periodontal health, and enamel defects in children attending respiratory outpatient clinics. RESULTS: A total of 74 patients with CF (35 male; mean age 10.7 years, range 2.5-16.5) were compared with a control group of 106 patients with other chronic respiratory disorders (52 male; mean age 9.1 years, range 3.0-16.5). There were significantly more defects of enamel in the permanent teeth of CF patients, compared with the teeth of those children with other chronic respiratory disorders. In addition, non-significant trends towards a lower caries prevalence in both dentitions, increased numbers of sextants with calculus deposits, and a reduced number of healthy gingival sextants were observed in the patients with cystic fibrosis. CONCLUSIONS: Enamel defects, particularly enamel opacities, which can be disfiguring, are more common in CF patients. Early, regular dental visits may prevent such defects becoming dentally disabling and would also permit the removal of dental calculus deposits. The use of long term antibiotics and pancreatic enzymes may confer some protection against the development and progression of dental caries in patients with cystic fibrosis. The inclusion of a specialist paediatric dentist, as part of the multiprofessional team managing the care of these children, would be an advantage.

PMID: 12876168 [PubMed - indexed for MEDLINE]

Temporal trends in demographic profiles and stress levels in medieval (6th-13th century) population samples from continental Croatia.

Croat Med J. 2002 Oct;43(5):598-605

Authors: Slaus M, Kollmann D, Novak SA, Novak M

AIM: To analyze and compare the demographic profiles and disease frequencies of early (6th-9th century) and late (10th-13th century) medieval skeletal series from continental Croatia. METHODS: Age and sex distributions in three early (n=277) and six late (n=175) medieval skeletal series were compared. All skeletons were analyzed for the presence of dental enamel hypoplasia, periostitis, trauma, and presence of Schmorl s depressions in vertebral bodies. RESULTS: Data collected from the skeletal series suggested significantly higher stress in the late medieval period. This stress may have affected mortality, as evidenced by significantly higher subadult mortality and shorter adult average life span. Men in the late medieval series, in particular, seem to have been under greater stress. They exhibited significantly higher mortality in the 21-25 years age category, and significantly higher frequencies of periosteal lesions, cranial and postcranial trauma, and Schmorl s depressions. CONCLUSION: The frequencies of all skeletal indicators of stress increased significantly during the late medieval period. This was accompanied by a significant increase in subadult mortality and shortening of the average life span of adult men and women.

PMID: 12402404 [PubMed - indexed for MEDLINE]

A case of amelogenesis imperfecta of deciduous and all permanent teeth.

Bull Tokyo Dent Coll. 2001 Feb;42(1):45-50

Authors: Sekiguchi H, Tanakamaru H, Minaguchi K, Machida Y, Yakushiji M

We experienced a case with severe enamel defects of both the deciduous teeth and all the permanent teeth. In order to clarify the etiology of enamel defects in this patient, we performed a DNA analysis in addition to conventional examinations. Although we suspected a variety of systemic factors causing enamel defects, there was no evidence suggesting disturbances of amelogenesis. In the present case, we suspected a mutation in the amelogenin gene and performed nucleotide sequencing of the exons of the amelogenin gene, but we could not find any evidence of mutation. We suggest that a mutation of some other gene related to enamel formation or the adventitious factors contributed to the amelogenesis imperfecta in this case.

PMID: 11484794 [PubMed - indexed for MEDLINE]

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

Aten Primaria. 2001 Feb 28;27(3):166-71

Authors: Tapias MA, Gil A, Jim&#xE9;nez R, Lamas F

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.

PMID: 11262321 [PubMed - indexed for MEDLINE]

Discolouration of permanent teeth and enamel hypoplasia due to tetracycline.

Postgrad Med J. 1999 Dec;75(890):772

Authors: Kashyap AS, Sharma HS

PMID: 10755912 [PubMed - indexed for MEDLINE]

Unusual indelible enamel staining following fixed appliance treatment.

J Orthod. 2000 Dec;27(4):303-6

Authors: Hodges SJ, Spencer RJ, Watkins SJ

Two cases are described of indelible enamel staining following fixed appliance therapy. The acquired pigmentation occurred in patients with an identifiable enamel defect prior to treatment. The interaction of factors to cause the staining is discussed and it's prevention in future cases highlighted. Subsequent restoration of the affected teeth is shown.

PMID: 11099567 [PubMed - indexed for MEDLINE]

Picture of the month. Autoimmune polyglandular syndrome type 1.

Arch Pediatr Adolesc Med. 2000 Jul;154(7):745-6

Authors: Winer KK, Merke DP

PMID: 10891030 [PubMed - indexed for MEDLINE]

Root development in mice lacking functional tissue non-specific alkaline phosphatase gene: inhibition of acellular cementum formation.

J Dent Res. 1999 Jun;78(6):1221-9

Authors: Beertsen W, VandenBos T, Everts V

Tissue non-specific alkaline phosphatase (TNAP) is richly present in developing teeth including the cells of the periodontal ligament. Here, we investigated tooth and root development in mice lacking the TNAP gene. Heterozygous mutants were obtained from The Jackson Laboratory, Animal Resources (Bar Harbor, ME, USA) and bred. TNAP-deficient mice and their littermates were killed from 6 to 25 days after birth and their molar blocks processed for light and electron microscopy. It was observed that the eruption of the incisors into the oral cavity was delayed for 2 to 3 days. Also, the onset of mineralization of the mantle dentin in the roots of the developing molars was delayed for 2 to 3 days. Yet, dentin and enamel formation in the homozygous mutants showed a more or less normal pattern, with the exception of localized enamel hypoplasias. The most conspicuous finding was the defective formation of acellular cementum along the molar roots. Instead of a continuous layer, the cementum was deposited as very thin and irregularly shaped patches around the bases of the periodontal ligament fibers. Sharpey's fibers were short and poorly developed. In contrast, the development of the alveolar bone, the periodontal ligament, and the cellular cementum was seemingly unaffected. It is concluded that TNAP represents an essential factor in mantle dentin mineralization and in the formation of acellular cementum.

PMID: 10371245 [PubMed - indexed for MEDLINE]

Laminin gamma2 expression is developmentally regulated during murine tooth morphogenesis and is intense in ameloblasts.

J Dent Res. 1998 Aug;77(8):1589-96

Authors: Sahlberg C, Hormia M, Airenne T, Thesleff I

Mutations in the laminin gamma2 gene cause junctional epidermolysis bullosa, and enamel hypoplasias are frequently seen in these patients. Laminin gamma2 is one of the three polypeptide chains forming the basement membrane glycoprotein laminin-5. We have localized the expression of the laminin gamma2 gene by in situ hybridization during mouse tooth development from early morphogenesis to completion of crown development. The expression was restricted to epithelial cells. During the early morphogenesis of the tooth germ, laminin gamma2 was expressed by the outer dental epithelium and by the stellate reticulum cells. No expression was detected in the cells of the inner dental epithelium giving rise to ameloblasts. The pre-ameloblasts remained negative during the early bell stage, but, interestingly, expression was very prominently upregulated as the cells differentiated into ameloblasts. This upregulation appeared to coincide with the start of enamel matrix secretion. The ameloblasts expressed laminin gamma2 intensely throughout the period of active enamel deposition. The expression continued at a lower level in the maturation-stage ameloblasts covering the enamel surface. Immunolocalization of laminin-5 with polyclonal antibodies indicated that the protein formed a continuous lining at the basal surfaces of the cells expressing the laminin gamma2 transcripts. We suggest that the role of laminin-5 during enamel formation may be to strengthen the anchorage of the ameloblasts to the enamel matrix, and that the pathogenesis of enamel hypoplasias in cases of laminin-5 mutations could be associated with detachment of the ameloblast cell layer from the enamel surface.

PMID: 9719032 [PubMed - indexed for MEDLINE]

Compound heterozygosity for a dominant glycine substitution and a recessive internal duplication mutation in the type XVII collagen gene results in junctional epidermolysis bullosa and abnormal dentition.

Am J Pathol. 1996 Jun;148(6):1787-96

Authors: McGrath JA, Gatalica B, Li K, Dunnill MG, McMillan JR, Christiano AM, Eady RA, Uitto J

Junctional epidermolysis bullosa is a heterogeneous autosomal recessively inherited blistering skin disorder associated with fragility at the dermal-epidermal junction. Previously, mutations in this condition have been described in the three genes for the anchoring filament protein laminin 5 (LAMA3, LAMB3, and LAMC2), in the gene encoding the hemidesmosome-associated beta4 integrin (ITGB4), and in the gene for the hemidesmosomal protein type XVII collagen (COL17A1/BPAG2). In this study, we report a patient with a form of junctional epidermolysis bullosa with skin fragility and dental anomalies who is a compound heterozygote for a novel combination of mutations, ie, a glycine substitution mutation in one allele and an internal duplication in the other allele of COL17A1. The patient also has two offspring, both of whom have inherited the glycine substitution mutation, whereas the other COL17A1 allele is normal. The latter individuals show no evidence of skin fragility but have marked dental abnormalities with enamel hypoplasia and pitting. The clinical phenotype of junctional epidermolysis bullosa in the proband in this family probably arises due to a combination of the glycine substitution and the internal duplication in COL17A1, whereas the dental abnormalities of her offspring may be the result of the glycine substitution in COL17A1 alone, resulting in this dominantly inherited clinical phenotype.

PMID: 8669466 [PubMed - indexed for MEDLINE]

Structural changes in fluorosed dental enamel of red deer (Cervus elaphus L.) from a region with severe environmental pollution by fluorides.

J Anat. 1996 Feb;188 ( Pt 1):183-95

Authors: Kierdorf U, Kierdorf H, Sedlacek F, Fejerskov O

A macroscopic, microradiographic and scanning electron microscope study was performed on the structure of fluorosed dental enamel in red deer from a fluoride polluted region (North Bohemia, Czech Republic). As was revealed by analysis of mandibular bone fluoride content, the rate of skeletal fluoride accumulation in the fluorotic deer was about 6 times that in controls taken from a region not exposed to excessive fluoride deposition. In all fluorosed mandibles, the 1st molar was consistently less fluorotic than the other permanent teeth. This was related to the fact that crown formation in the M1 takes place prenatally and during the lactation period. Fluorosed teeth exhibited opaque and posteruptively stained enamel, reduction or loss of enamel ridges, moderately to grossly increased wear and, in more severe cases, also enamel surface lesions of partly posteruptive, partly developmental origin. Microradiographically, fluorosed enamel was characterised by subsurface hypomineralisation, interpreted as a result of fluoride interference with the process of enamel maturation. In addition, an accentuation of the incremental pattern due to the occurrence of alternating bands with highly varying mineral content was observed in severely fluorosed teeth, denoting fluoride disturbance during the secretory stage of amelogenesis. A corresponding enhancement of the incremental pattern was also seen in the dentine. The enamel along the more pronounced hypoplasias consisted of stacked, thin layers of crystals arranged in parallel, indicating that the ameloblasts in these locations had lost the distal (prism-forming) portions of their Tomes processes. The findings of the present study indicate that red deer are highly sensitive bioindicators of environmental pollution by fluorides.

PMID: 8655406 [PubMed - indexed for MEDLINE]

Dental enamel growth, perikymata and hypoplasia in ancient tooth crowns.

J R Soc Med. 1992 Aug;85(8):460-6

Authors: Hillson SW

This paper describes the hypoplastic defects commonly seen on the surface of ancient human tooth crowns, excavated from archaeological sites, and presents a new method for estimating the ages at which these defects were initiated during life. The method is based upon examination of microscopic incremental structures on the enamel surface and it is possible also to apply it to reconstruction of the sequence and timing of dental crown development. The method of examination is non-destructive and allows full use to be made of the large numbers of complete, unworn dentitions which are found amongst archaeological remains.

PMID: 1404194 [PubMed - indexed for MEDLINE]

The role of albumin in developing rodent dental enamel: a possible explanation for white spot hypoplasia.

J Dent Res. 1992 Jun;71(6):1270-4

Authors: Robinson C, Kirkham J, Brookes SJ, Shore RC

The uptake of serum albumin by maturation-stage rodent enamel and the resulting effects on the growth of enamel crystallites were investigated in vitro. Albumin uptake was demonstrated by means of gel electrophoresis and confirmed by Western blotting with use of monoclonal antibodies. Measurement of crystal size was carried out by direct TEM measurement of enamel crystallite outlines after incubations in metastable solutions of calcium phosphate. The ability of endogenous enamel enzymes to degrade albumin was investigated by substrate-specific zymography. The results showed that albumin could be taken up by maturation-stage enamel and produce inhibition of crystallite growth. There was no detectable proteolytic activity in the enamel against albumin substrate, which suggests that albumin entering enamel by extravasation in vivo may produce incomplete tissue maturation, resulting in a white, opaque appearance on eruption.

PMID: 1319435 [PubMed - indexed for MEDLINE]

Dental enamel hypoplasias in prehistoric populations.

Adv Dent Res. 1989 Sep;3(2):265-71

Authors: Goodman AH

Recent years have witnessed an impressive increase in research on enamel hypoplasias in archaeological populations. By reviewing a series of studies of enamel hypoplasias at Dickson Mounds, Illinois, North America (950-1300 A.D.), a prehistoric site involved in the transition from gathering-hunting to agriculture, this paper provides an illustration of this type of research. The location of linear hypoplasias on labial tooth surfaces of 111 adults was studied with a thin-tipped caliper, and this location was converted to an age at development. Most defects developed between two and four years of developmental age. Hypoplasias increased in prevalence from 45% in the pre-agriculture group to 80% in the agricultural group (p less than 0.01). The transition to agriculture occurred at a cost to infant and childhood health. Defects are associated with decreased longevity. Individuals with defects have a life expectancy of nearly ten years fewer than those without defects, suggesting that the development of a defect marks a significant and lasting health event. Enamel hypoplasias occur most frequently on anterior teeth, polar teeth in developmental fields, and the middle developmental thirds of teeth. Analysis of these data suggests that enamel may be differentially susceptible to growth disruption and that susceptibility varies both within and among teeth. The study of enamel defects at Dickson provides insights into the health and nutritional consequences of the economic change from hunting and gathering to agriculture. More generally, with the availability of teeth from genetically homogeneous populations, studies of enamel hypoplasias in prehistory should provide a useful complement to research on this condition in contemporary peoples.

PMID: 2701160 [PubMed - indexed for MEDLINE]

Developmental enamel defects in primary teeth in children with cerebral palsy, mental retardation, or hearing defects: a review.

Adv Dent Res. 1989 Sep;3(2):132-42

Authors: Bhat M, Nelson KB

Developmental enamel defects in primary teeth have been found at least twice as frequently in children with cerebral palsy or mental retardation as in control children, and frequently also in children with sensori-neural hearing deficits. The developing tooth germ is sensitive to a range of systemic disturbances, some of which may also affect neurologic development. Because the enamel cannot recover once it is damaged, it may provide a repository of information on the timing and nature of insults potentially affecting other ectodermally derived structures, including the brain. This paper reviews the literature on developmental defects of enamel in primary teeth, asking whether these might be useful as biological markers of the timing and in some cases the nature of insults. Among systemic factors related to development of enamel that might also have implications for neurologic development are certain genetic disorders including tuberous sclerosis, premature birth, neonatal nutritional disturbances (especially hypocalcemia), viral infections (such as rubella and cytomegalovirus during gestation), thyroid disorders, and maternal diabetes. It is concluded that further research is warranted concerning whether developmental defects of dental enamel can be useful markers for the timing of intra-uterine or perinatal events associated with certain neurologic and sensory disorders of children.

PMID: 2701156 [PubMed - indexed for MEDLINE]

Review of terminology, classifications, and indices of developmental defects of enamel.

Adv Dent Res. 1989 Sep;3(2):104-9

Authors: Clarkson J

A wide variety of terms and definitions are used to describe various developmental defects of enamel. Some are simple descriptive clinical terms, and others are linked with the causative agent or the histopathology of the defect. Some confusion exists as to the most appropriate type of index to use to measure defects of enamel due to fluoride ingestion (dental fluorosis). This is primarily due to difficulties some researchers have in distinguishing between defects of fluoride and non-fluoride origin. This problem has resulted in the development of specific fluorosis indices and purely descriptive indices. The main fluorosis indices are those of Dean, Thylstrup and Fejerskov, and the TSIF Index. Dean's Index does not provide adequate information on the distribution of fluorosis within the dentition and is not sensitive at high fluorosis levels. The Thylstrup and Fejerskov Index is related to the histology of florosis; however, the initial minute changes observed on dry enamel surfaces are of little esthetic importance. The TSIF Index does overcome some of the limitations of Dean's Index. The DDE Index has replaced the Al-Alousi Index as the main descriptive index. The DDE Index is time-consuming, and the analyses of data are complicated. Modifications have now been proposed to make it simpler to use and the data more meaningful. Further research needs to be carried out into both the validity of the fluorosis indices and making the DDE Index more universally acceptable.

PMID: 2701155 [PubMed - indexed for MEDLINE]

Macroscopic and scanning electron microscopic appearance and hardness values of developmental defects in human permanent tooth enamel.

Adv Dent Res. 1989 Sep;3(2):219-33

Authors: Suckling GW, Nelson DG, Patel MJ

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.

PMID: 2640433 [PubMed - indexed for MEDLINE]

Enamel hypomineralization viewed from the pattern of progressive mineralization of human and monkey developing enamel.

Adv Dent Res. 1989 Sep;3(2):188-98

Authors: Suga S

Microradiograms and their computer-aided image analysis of ground sections of the developing enamel of human permanent third molars and monkey permanent teeth (Macaca fuscata) indicate that the mode of progressive mineralization of enamel is completely different between the matrix formation and maturation stages. During the former stage, the enamel matrix is slightly mineralized. During the latter stage, which takes a much longer period than the previous stage, the increase in the secondary mineralization takes place first slightly, from the surface toward the inner layer, and then heavily, from the inner layer toward the surface. The narrow outer layer mineralizes very slowly during the middle and late stages of maturation, but finally achieves the highest mineralization of the entire enamel layer. The very narrow innermost layer mineralizes slowly without expanding its width. The former three processes seem to be under the direct control of the ameloblasts. Hypoplastic areas which appear during the matrix formation stages are not necessarily accompanied by hypomineralization. Dysfunction of the cells immediately after the completion of matrix formation appears to cause hypomineralization throughout the entire width of matrix except for the innermost layer. Disorders of the cells occurring during the middle and/or the late stage of maturation--due to chronic metabolic disturbances, such as fluorosis--induced hypomineralization localized mainly at the outer layer. The hypomineralized enamel is not necessarily accompanied by hypoplasia. The process of enamel mineralization is not necessarily fully synchronized with that of tooth eruption. Therefore, the narrow outer layer, especially in the fissure and cervical regions, is sometimes hypomineralized even after the teeth have erupted normally.

PMID: 2640430 [PubMed - indexed for MEDLINE]

Hypocalcification and hypoplasia in permanent teeth of children from different ethnic groups in South Africa assessed with a new index.

Adv Dent Res. 1989 Sep;3(2):126-31

Authors: Hargreaves JA, Cleaton-Jones PE, Williams SD

A new descriptive index, the HHI (hypocalcification-hypoplasia index), is described for comparing enamel defects in groups of people. The index was used in a study completed in 1986, in which 1251 11-year-old children from different ethnic groups resident in South Africa were examined: 210 rural black, 203 urban black, 206 urban colored, 426 urban Indian, and 206 urban white. The index can be used as a screening examination, and the results from these different ethnic groups are presented.

PMID: 2640424 [PubMed - indexed for MEDLINE]

Developmental defects of enamel in Chinese girls and boys in Hong Kong.

Adv Dent Res. 1989 Sep;3(2):120-5

Authors: King NM

The FDI (DDE) Index--with some modifications and a re-designed recording sheet--was used to determine the prevalence of the different types of developmental defects of enamel. The public water supply contained 1.0 ppm when the children were bron and 0.7 ppm at the time of the examinations. All surfaces of the teeth of 460 female and 484 male, 12-year-old, Chinese children were examined after the teeth had been cleaned and dried. Mouth prevalences for all types of opacities, hypoplasia, and discoloration were 99.6%, 82.8%, and 16.6%, respectively. There was no apparent statistically significant difference between girls and boys. However, a statistically significant difference was seen between the sexes for white patches (p less than 0.05), missing enamel (p less than 0.05), and horizontal grooves (p less than 0.01). There were 811 (85.7%) children with more than 13 teeth affected by opacities, and 417 (44.2%) children had more than four teeth affected by hypoplasia. The most common defect was the diffuse white patch, and the least common was the vertical groove. There were 189 (39.0%) boys with between four and 12 teeth affected by more than two types of defect per tooth. White lines were the most difficult defect to diagnose reproducibly. Intra-examiner reproducibility for all other defects achieved levels of "almost perfect" and "substantial" by calculation of the Kappa coefficient.

PMID: 2640423 [PubMed - indexed for MEDLINE]

Prevalence of developmental defects of tooth enamel (DDE) in a pediatric hospital department of dentistry population (1).

Adv Dent Res. 1989 Sep;3(2):114-9

Authors: Hall RK

This paper reports the first part of a three-part study of developmental defects of tooth enamel in a pediatric hospital population. The dental records of 8411 children who were discharged from the Department of Dentistry at the Royal Children's Hospital, Melbourne, Australia, between 1960 and 1987 were divided into an experimental group of 7518 patients comprising 25 groups of medical conditions, and a control group of 893 children who had dental disorders only. The aim of the study was to investigate the prevalence of hypoplastic and severe-opacity developmental defects of tooth enamel (DDE), in children and adolescents with major medical disorders, and to compare the prevalence with that in the control group of normal children. The prevalence figures obtained for the different medical conditions in this study agreed generally with those of other recent investigators. The high prevalence of defects found in Rubella Embryopathy children (81.8%) and in children with Prematurity alone (56.5%) is surprising, whereas the prevalence of 27.9% defects in Clefts of Lip and Palate and 26.4% defects in Clefts of Lip and Alveolus are probably well below the true prevalence. The control group prevalence was 9.3%, which is higher than in some other studies of 'normal' children. A pediatric hospital is a most useful source of fully documented medical and dental histories for the investigation of possible relationships between medical disorders and developmental defects of tooth enamel. The control group prevalence was 9.3%, which is higher than in some other studies of normal children. A pediatric hospital is a most useful source of fully documented medical and dental histories for the investigation of possible relationships between medical disorders and developmental defects of tooth enamel.

PMID: 2640422 [PubMed - indexed for MEDLINE]

Hypocalcification and hypoplasia in primary teeth of pre-school children from different ethnic groups in South Africa.

Adv Dent Res. 1989 Sep;3(2):110-3

Authors: Hargreaves JA, Cleaton-Jones PE, Roberts GJ, Williams SD

A study was completed in 1985/86 which examined the dental health of pre-school children from different ethnic groups and communities in South Africa: rural black, urban black, urban colored, urban Indian, and urban white. Enamel defects were recorded in primary teeth by use of the HHI, an index developed to measure hypocalcification and hypoplasia of enamel. The findings showed that colored children had the greatest number of enamel defects. The teeth most commonly affected were the maxillary anterior teeth and mandibular molar teeth. It is suggested that further epidemiological studies utilizing the HHI should be undertaken in pre-school children, especially from developing countries, to gain more information on the causes of enamel defects in the primary dentition and the possible use of such findings to predict nutritional health of individuals.

PMID: 2640421 [PubMed - indexed for MEDLINE]

A modified DDE Index for use in epidemiological studies of enamel defects.

J Dent Res. 1989 Mar;68(3):445-50

Authors: Clarkson J, O'Mullane D

The aim of this study was to investigate possible modifications to the DDE Index to make it simpler to use and to make the data collected more meaningful and amenable to analyses and interpretation. After the use of the DDE Index in a National Study in Ireland, initial alterations to the Index were tested on a group of children with enamel defects, in Ireland and New Zealand. The DDE Index was then modified to allow for the measurement of demarcated, diffuse, and hypoplastic defects and their severity. With the Modified Index, the prevalence of defects both on index teeth and all permanent tooth surfaces of 8- and 15-year-old children in fluoridated Cork City and non-fluoridated areas of Cork County and Manchester, U.K., was measured. The prevalence of enamel defects on one or more index teeth of children in the three areas ranged from 30 to 42% in 8-year-olds and from 31 to 38% in 15-year-olds. The percentage of children affected as seen by full-mouth examination was somewhat higher, ranging from 38 to 51% for 8-year-olds and 58 to 63% for 15-year-olds. The percentage of index teeth affected (7 to 14%) was generally higher than for all teeth (5 to 9%). Demarcated opacities were the most common defect seen. Diffuse opacities were found to be the discriminating factor between the fluoridated and non-fluoridated areas. In all areas, the vast majority of diffuse opacities extended over less than 1/3 of the surface area of the teeth affected.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2921385 [PubMed - indexed for MEDLINE]

Etiological factors influencing the prevalence of developmental defects of dental enamel in nine-year-old New Zealand children participating in a health and development study.

J Dent Res. 1987 Sep;66(9):1466-9

Authors: Suckling GW, Herbison GP, Brown RH

Over 1000 children, participating in a longitudinal study of health and development, possess documented medical histories based on birth records and regular assessments starting at age 3. A dental examination at age 5 of 923 participants recorded their exposure to fluoride and evidence of trauma to the deciduous teeth. The prevalence of developmental defects of dental enamel in 696 of the children when aged 9 was reported as 56% (Suckling et al., 1985). For the present study, a number of illnesses, accidents, and other experiences were selected from the recorded information as possible etiological factors for any defect, demarcated and diffuse opacities, and hypoplasia. Despite extensive statistical testing, positive and strong associations were few. The prevalence of hypoplasia, seen in 15% of the sample, was higher in those children who had chicken pox before age 3 and, as reported previously, in those children with a history of trauma to their deciduous incisors. This study illustrates the difficulty of establishing the etiology of enamel defects, even when medical and dental histories are available.

PMID: 3476618 [PubMed - indexed for MEDLINE]

Distribution of enamel defects and the association with respiratory distress in very low birthweight infants.

J Dent Res. 1984 Jan;63(1):59-64

Authors: Johnsen D, Krejci C, Hack M, Fanaroff A

Although dental defects have long been observed among surviving pre-term infants, only few systematic studies address this problem. In a clinic limited to recall of infants of very low birthweight (less than 1.5 kg), enamel hypoplasia of primary incisors was found in 14/67 (21%) children, and enamel opacities were found in an additional 31% of the children. In contrast, enamel hypoplasia and opacities were found in 4% and 22%, respectively, of a control group of 46 normal birthweight children. The difference was significant (p less than 0.05) for the hypoplasia but not for the opacities. Primary incisor enamel hypoplasia was more commonly noted in maxillary central incisors than in lateral incisors (X2 = 28.0, p less than 0.01). Furthermore, hypoplasia was more common in maxillary incisors than in mandibular incisors (X2 = 48.4, p less than 0.01). In infants with dental defects, there was no significant correlation with pregnancy risk factors, gestational age, birthweight, septicemia, first-week caloric intake, serum bilirubin, or calcium. Infants with enamel hypoplasia were more likely, however, to have severe respiratory distress syndrome (X2 = 7.2, p less than 0.01), than infants with unaltered enamel. Central incisor edge involvement may indicate post-natal processes and/or a systemic disturbance extending back to the middle trimester of pregnancy.

PMID: 6582082 [PubMed - indexed for MEDLINE]

Hereditary enamel hypoplasia in a prehistoric Indian child.

J Dent Res. 1980 Sep;59(9):1522

Authors: Cook DC

PMID: 6995509 [PubMed - indexed for MEDLINE]

Enamel hypoplasia in relation to caries in Guatemalan children.

J Dent Res. 1977 May;56(5):493-8

Authors: Infante PF, Gillespie GM

Guatemalan children with anterior linear enamel hypoplasia (LEH) had a significantly greater caries experience in posterior dentition than their peers who did not have anterior LEH. The findings suggest that the synergistic mechanism of undernutrition and infection, which may underlie the occurrence of anterior LEH, may also predispose clinically normal appearing deciduous molars to an excessive caries attack equal to that observed in the grossly hypoplastic anterior teeth. The nutritional implications merit further investigation.

PMID: 267103 [PubMed - indexed for MEDLINE]

Age distribution of enamel hypoplasia in prehistoric California Indians.

J Dent Res. 1975 Jul-Aug;54(4):913

Authors: Schulz PD, McHenry HM

PMID: 1099140 [PubMed - indexed for MEDLINE]

The tricho-dento-osseous (TDO) syndrome.

Am J Hum Genet. 1972 Sep;24(5):569-82

Authors: Lichtenstein J, Warson R, Jorgenson R, Dorst JP, McKusick VA

PMID: 5054226 [PubMed - indexed for MEDLINE]

Hypoplastic enamel defects in the guinea pig: effects of -streptococcal infections, fever, abscess formation, and ether anesthesia.

J Dent Res. 1971 Nov-Dec;50(6):1635-41

Authors: Elwood WK

PMID: 5288904 [PubMed - indexed for MEDLINE]

Dull in tooth and mind.

Br Med J. 1971 Feb 20;1(5746):419-20

Authors:

PMID: 5101342 [PubMed - indexed for MEDLINE]

Male hypogonadotrophic hypogonadism treated with human chorionic gonadotrophin.

Proc R Soc Med. 1970 Jun;63(6):575-6

Authors: Anderson DC, Fraser TR

PMID: 5453449 [PubMed - indexed for MEDLINE]