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Biomedical subjects

G B Winter

Publications and source records attributed to G B Winter.

At least 19 recordsLinked to original sources
PubMed1996

Amelogenesis imperfecta with enamel opacities and taurodontism: an alternative diagnosis for 'idiopathic dental fluorosis'.

A retrospective study of 32 children (mean age 10.3 years) attending the Children's Department, Eastman Dental Hospital with enamel opacities resembling dental fluorosis in the majority showed that these changes were probably genetically determined and had a close association with taurodontism of permanent molar teeth. It seems likely that these enamel defects should be classified as hypomaturation types of amelogenesis imperfecta (AI) conveyed by mutant auto-somal genes. The clinical expression (phenotype) of these mutant genes has a greater heterogeneity than previously described.

Adolescent↗
PubMed1996

Fissure sealants: a 4-year clinical trial comparing an experimental glass polyalkenoate cement with a bis glycidyl methacrylate resin used as fissure sealants.

The 4-year results of a fissure sealant trial are reported. Glass polyalkenoate and bis GMA sealant were applied to 590 first permanent molar teeth using a half mouth study design in a group of 228 6-8-year-old children. Similar cariostasis was observed for the two materials at the end of 4 years despite marked differences in retention. Polyalkenoate cements probably should be regarded as 'fluoride depot' materials rather than fissure sealants when used in this context.

Bisphenol A-Glycidyl Methacrylate↗
PubMed1996

Splice site mutation causing deletion of exon 21 sequences from the pro alpha 2(I) chain of type I collagen in a patient with severe dentinogenesis imperfecta but very mild osteogenesis imperfecta.

An eight-year-old boy was referred for dental assessment of dentinogenesis imperfecta, a full clinical examination also revealed joint hypermobility and some features of mild osteogenesis imperfecta although he had suffered few fractures. Analysis of the collagens produced by both gingival and skin fibroblast cultures showed the synthesis and intracellular retention of an abnormal alpha 2(I) chain that migrated faster than normal on SDS-PAGE. Cyanogen bromide peptide mapping of this intracellular protein indicated a probable deletion in the N-terminal peptide alpha 2CB4. The denaturation temperature of the mutant protein was only 36 degrees C, some 6 degrees C below normal. At 37 degrees C secretion of abnormal protein was not detectable but a lower temperature (30 degrees C) some was secreted into the medium. RT-PCR amplification of mRNA coding for alpha 2CB4 revealed a heterozygous deletion of the 108 bp exon 21 of COL1A2. Sequencing of PCR amplified genomic DNA identified a G --> A transition in the moderately conserved + 5 position of the IVS 21 5' consensus splice site causing the skipping of exon 21. Hybridization with allele-specific oligonucleotides showed no other family member had this base change. Since the cDNA deletion was associated with the (-) allele of a Pvu II polymorphism in exon 25 of COL1A2 we could demonstrate that the mutant pre-mRNA was alternatively spliced yielding both full length and deleted transcripts. Family genotype analysis indicated the mutation had originated in the paternal alpha 2(I) gene.

Alternative Splicing↗
PubMed1995

Amelogenesis imperfecta in triplets: a unique family record.

A unique family is recorded in which triplets were observed with the hypomaturation type of amelogenesis imperfecta. A simple technique of DNA analysis showed that two of the more severely affected triplets were monozygotic and the third less severely affected triplet dizygotic.

Alleles↗
PubMed1995

Characterisation of molecular defects in X-linked amelogenesis imperfecta (AIH1).

Amelogenins are an heterogenous family of proteins produced by ameloblasts of the enamel organ during tooth development. Disturbances of enamel formation occur in amelogenesis imperfecta, a clinically heterogenous group of inherited disorders characterised by defective enamel biomineralisation. An amelogenin gene, AMGX, has been mapped to the short of the X chromosome (Xp22.1-p22.3) and has been implicated in the molecular pathology of X-linked amelogenesis imperfecta (AIH1). We have identified three families exhibiting AIH1 and screened the AMGX gene for mutations using single-strand conformational polymorphism analysis and DNA sequencing. Three novel mutations were identified: a C-T substitution in exon 5, and a G-T substitution and single cytosine deletion in exon 6, confirming the existence of extensive allelic heterogeneity in this condition. The identification of family-specific mutations will enable early identification of affected individuals and correlation of clinical phenotype with genotype will facilitate an objective system of disease classification.

Amelogenesis Imperfecta↗
PubMed1995

Absence of salivary glands in children with rampant dental caries: report of seven cases.

Seven cases of absence of two or more salivary glands in children are presented. In six of the cases the condition was congenital and in one it was the result of surgery to the submandibular ducts. The patients had been referred for treatment of rampant dental caries and were reviewed for periods ranging from 6 months to 15 years 9 months. The diagnosis of absence of salivary glands was based on careful inspection and palpation of the duct and duct orifice of each gland. One patient had dry lips and three had dry mouths, but none complained of excessive thirst or difficulty with mastication or swallowing. All the patients had very poor oral hygiene and rampant dental caries. The presence of carious lesions in mandibular incisors, particularly when their severity exceeds those present elsewhere in the mouth, should alert the clinician to the possibility that salivary glands may be absent.

Adolescent↗
PubMed1994

'Toothfriendly'.

Explore the source record for details and available documents.

Advertising↗
PubMed1994

Enamel opacities and dental caries in children who used a low fluoride toothpaste between 2 and 5 years of age.

A recent clinical trial investigated the cariostatic effectiveness of a low (550 ppm) fluoride toothpaste in comparison with a standard (1050 ppm) control paste in pre-school children who were 2-years-old at the start of the 3-year trial. The present study has investigated the prevalence of enamel opacities in permanent incisor teeth and of caries in children who had taken part. As well as children from test and control groups, a third group of non-trial children were included in the sample. A total of 1,523 children were examined in schools and had photographs taken of their upper permanent incisor teeth. The latter were scored using the Thylstrup and Fejerskov (TF) index for fluorosis and the modified Developmental Defects of Enamel (DDE) index. Differences between the groups were small in real terms but using the TF index the child and tooth prevalence of opacities were significantly lower in the children who had used the test paste with a lower fluoride content; the same trend was seen in diffuse defects scored using the modified DDE index. There was no significant difference in the prevalence of caries in either primary or permanent teeth although the trend in both cases was for slightly more disease in children who had used the test paste.

Cariostatic Agents↗
PubMed1990

Epidemiology of dental caries.

The most recent epidemiological data on the prevalence of dental caries in children indicate a halting of the increasing levels in many developing countries and a continuing decrease in many highly industrialized countries of the world. However, a further fall in caries levels predicted for 5-yr-old children in the U.K. has not occurred and the decline in caries may have begun to level out. 'Polarization' of caries to a minority of high-risk individuals is occurring in the developed world, with 20-25% of children accounting for more than 50% of the disease. Socio-economic factors are important in determining the proportion of high-risk children in these countries. The multifactorial aetiology of caries allows a number of different interpretations to account for changes in the prevalence of the disease with time, in both the developing and developed countries. These changes are variously ascribed to alterations in dietary habits, especially the consumption of sugar; variations in the patterns of oral hygiene; increased contact with trace elements, especially fluoride, in the environment; changes in the ecology and/or virulence of oral and dental plaque microflora and alterations in the oral protective mechanisms including the immune status. The epidemiological evidence available on the relationship of all these social, environmental and other factors to changes in the prevalence levels of caries does not, however, fully explain all the changes that have been observed. The claim that caries is no longer a public health problem is premature, as it ignores the still high proportion of individuals with tooth decay throughout the world.

Adolescent↗
PubMed1990

Enamel opacities in children whose mothers took part in a dental health education scheme.

One well recognised cause of enamel opacities is excessive fluoride ingestion during the period of tooth development. In the past, "fluorosis", or opacities arising from this cause, has been reported to occur in children given fluoride supplements. In a large experiment in dental health education, fluoride supplements were given regularly to many of the children in two out of three experimental groups. 126 children were dentally examined 10 yr after the scheme began, of whom 79 had regularly received fluoride drops and/or tablets for at least part of the period between birth and 5 yr of age. Labial surfaces of each child's erupted incisor teeth were examined for enamel opacities. 75% of the 126 children had at least one affected tooth. There was a statistically insignificant, but consistent, trend for the prevalence of opacities to increase with increasing duration of use of fluoride supplements.

Child, Preschool↗