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Results for “enamel defects”

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At least 145 records · Page 8Linked to original sources
PubMed1984

Microscopic study of enamel defects in deciduous teeth of infants of diabetic mothers.

Ground sections of deciduous teeth from infants of diabetic mothers were examined in polarized light and by microradiography. Widened neonatal lines and subsurface lesions were the main findings in the enamel. Three teeth showed enamel hypoplasia in connection with the neonatal line. The widening of the neonatal line and the hypoplasias are related to the more frequent and more pronounced neonatal hypocalcemia occurring among infants of diabetic mothers.

Dental Enamel↗
PubMed1989

[Volume estimation of non-caries related enamel defects].

The volume of wedge shaped defects can be estimated by means of massa suppositoriorum on a plaster cast. The substance are pressed in a graduated pipette. The average relative error is six percent. The absolute error of defects of 2.0, 10.0 respectively 20.0 mm3 ranges from 0.12, 0.6 to 1.2 mm3.

Calcium Sulfate↗
PubMed1989

Fluoride and enamel defects.

The concentration of fluoride in drinking water is the major determinant of the prevalence and severity of dental fluorosis in a community. Fluorosis is more prevalent and discernible in permanent teeth than in primary teeth; the intensity can range from barely perceptible, whitish striations in enamel to confluent pitting and dark staining. The traditional belief is that fluorosis is produced only during the secretory stages of ameloblastic activity. Some recent reports suggest that the maturation stages of enamel development are as important as or even more important than the secretory stages as the time when fluorosis can be produced. The question of timing remains unresolved. Many questions also remain about general and individual physiologic variations in relation to susceptibility to dental fluorosis. Good criteria for differential diagnosis exist to distinguish dental fluorosis from non-fluoride enamel opacities. An increasing number of reports indicates that the prevalence of fluorosis may be increasing among children in fluoridated and non-fluoridated communities. Reasons for the increases may relate to misuse of dietary fluoride supplements, ingestion of fluoride toothpastes, or increasing amounts of fluoride in foods or the atmosphere. The intensity of the increased fluorosis is in the milder categories and is not generally unsightly. It should be recognized that a small amount of fluorosis may be an alternative to a greater prevalence of dental caries, a disease that may produce cosmetic problems and sequelae worse than those produced by fluorosis.

Animals↗
PubMed1986

Developmental defects of enamel: a study of 12-year-olds in Hong Kong.

The prevalence of enamel defects in Hong Kong was determined using a randomly selected group of 12-year-olds (N = 1,069). The most common defects were enamel opacities, which occurred in 99.6% of the Chinese children, with 63.4% of them having more than 20 teeth affected. Almost 17% of the Chinese children had disfiguring enamel discoloration, but only one of the non-Chinese children had this defect. The high prevalence of enamel defects may be related to the high frequency of use of tetracycline, metabolic disturbances, and a greater-than-optimal intake of dietary fluoride.

Child↗
PubMed1989

A photographic study of enamel defects among South Australian school children.

Colour photographs were taken of the anterior teeth of 1757 consenting 8-9 year old primary school children in fluoridated and non-fluoridated areas of South Australia. Children with a lifelong exposure to fluoridated water were significantly more likely to have blemished permanent incisor teeth than the children who had never resided in a fluoridated area. Children who resided in a non-fluoridated area but had taken fluoride supplements at some stage in their first five years had a prevalence of enamel blemishes equivalent to those of children in fluoridated areas of the State.

Bias↗
PubMed1997

Inherited enamel defects.

This paper describes the clinical, histological and genetic findings in individuals with amelogenesis imperfecta diagnosed in more than 50 families in the county of Västerbotten, northern Sweden. Using pedigree analysis, families with autosomal and X-linked inheritance as well as sporadic cases of amelogenesis imperfecta have been recognized. A clinical subclassification in eight different variants of amelogenesis imperfecta has been made. The gene defects have been identified for two of these variants and the chromosomal location has been established for a third variant.

Amelogenesis Imperfecta↗
PubMed2004

Defective enamel ultrastructure in diabetic rodents.

We investigated six different types of diabetic rodents. Four expressed a genetic obesity resulting in diabetes. One developed diabetes induced by a diet-dependent obesity, and one with genetic diabetes received anti-diabetic medication. The tooth samples were examined under a scanning electron microscope and with an energy dispersive microanalysis (EDX). The electron micrographs showed severe, varying degrees of damage within the six different diabetic animal types, such as irregular crystallite deposition and prism perforations in genetically obese animals compared to less-disordered prism structures in diet-dependent obesity. Anti-diabetic medication resulted in normal enamel ultrastructure. The EDX analysis revealed a reduction in the amount of calcium and phosphorus in all regions affected by diabetes. Based on these animal studies, we suggest that both juvenile diabetes type I (in infants) and adult diabetes type II (in pregnant mothers, affecting the developing foetus) may affect the normal development of teeth in humans.

Animals↗