Immunoblotting demonstration of antibodies to the organic matrix of developing bovine enamel

Antiserum was raised against an acetic acid extract of partly mineralized bovine enamel. By use of immunoblotting it was shown that rabbit antibodies react with both high and low molecular weight proteins. Most but not all of the enamel proteins isolated by different extraction solutions were antigenic identical. The blotting time was found to be important when immunoblotting of enamel proteins is carried out.     

Early childhood caries — a synopsis

All the papers presented at the conference are reviewed and comparisons are made with past beliefs on the topic. Early childhood caries (ECC) is a serious public health problem in disadvantaged communities in both developing and industrialized countries in which under-nutrition is common. ECC involves the maxillary primary incisors within months after their eruption and spreads rapidly to involve other primary teeth. The early implantation of mutans streptococci, the use of a feeding bottle containing sugary solutions and prolonged breast-feeding, especially at night, are important predisposing factors. Attention is drawn to the need for more research into the factors which determine the resistance of the enamel and particularly the elucidation of the relationship established in several countries between early enamel caries, enamel hypoplasia, and perinatal under- or malnutrition. Primary preventive measures should be applied during the ante- and immediate post-natal periods. Secondary preventive measures include the use of chemotherapeutic agents such as fluoride, and antimicrobials. The most appropriate tertiary preventive measure is the atraumatic restorative technique (ART). Broadly based committees should be established by governments to address the issues of caries risk in young children. Parents and all personnel involved in infant health and welfare should be shown how to recognize early signs of the condition, as well as to promote early intervention and referral.     

Primary Canine Hypoplasia in Head Start Children

Primary canine hypoplasia is an incomplete or defective development of the enamel matrix. The lesion is located on the labial surface and is seen more frequently on mandibular teeth. The purpose of this preliminary study was to determine the prevalence of this lesion among Head Start children. During a dental needs assessment of Mississippi Head Start children, 371 children from 11 centers were examined for this lesion. Of the centers, four were located in optimally fluoridated communities, and six were located in fluoride-deficient communities. Ages ranged from three to five years. There were 206 males and 165 females, 334 black and 37 white children. At ten centers all children were black, while all children at one center were white. Results indicated no significant differences in the black population between fluoridated (38.2%) and fluoride-deficient (36.3%) communities (P = .729) or between males (36.8%) and females (37.6%) (P = .877). When data were collapsed on sex and fluoridation status, the racial differences were highly significant (P = .001). The prevalence rate of dental caries associated with primary canine hypoplasia was 26.0 percent. These preliminary data indicate that the presence of primary canine hypoplasia may result in an increased potential for the tooth becoming carious.     

The ultrastructure of fluorosed human dental enamel

abstract — More than 80 specimens of enamel from 20 ground sections of eight teeth showing severe dental fluorosis have been examined in the transmission electron microscope. The study has shown that the prisms have normal size and form, but are surrounded by large periprismatic gaps. The individual crystals commonly appear in cross sections as regular, flattened hexagons with an average width of 91 nm and average thickness of 45 nm. Particularly in the tail regions and at prism peripheries, extensive intercrystalline spaces were found. The crystal lattice demonstrated a spacing of 0.82 nm. Demineralization of thin sections with PTA showed a preferential dissolution of the crystal centers. Based on the ultra-structural observations it is proposed that the hypomineralized regions of fluorosed enamel are produced by an arrest of enamel maturation, possibly due to toxic damage to the ameloblasts in the absorptive or maturative phase of their life cycle.     

Measurement of the severity of natural smooth surface (interproximal) caries lesions with polarization sensitive optical coherence tomography

BACKGROUND AND OBJECTIVES: Previous studies have demonstrated that polarization sensitive optical coherence tomography (PS-OCT) can be used to image early dental caries. The purpose of this study was to compare the measured reflectivity of natural caries lesions found on smooth surfaces (interproximal lesions) with the mineral loss measured using digital microradiography (DM) in order to determine if PS-OCT can be used as a non-destructive method to measure the severity of dental decay and resolve the internal structure of caries lesions. MATERIALS AND METHODS: A PS-OCT system operating at 1,310 nm was used to acquire polarization resolved images of natural white spot lesions and pigmented lesions on the smooth surfaces of extracted teeth. The integrated reflectivity from lesion areas was compared to polarized light microscopic images (PLM) and to the integrated mineral loss from the same lesion area measured using high resolution DM. RESULTS: The frequently complex internal structure of caries lesions could be resolved with PS-OCT. Such structural information is potentially useful for determining whether or not the lesion is active and progressing or whether it has become arrested and remineralized and does not require intervention. There was a strong correlation between the integrated mineral loss of the caries lesions measured using DM and the integrated reflectivity in the perpendicular polarization axis of the PS-OCT system. CONCLUSIONS: The integrated reflectivity in the perpendicular polarization channel can be used to represent the severity of demineralization in natural early caries lesions. Therefore, PS-OCT has considerable potential as a non-destructive clinical probe of early caries lesions to assess their severity, monitor their progression over-time and potentially assess lesion activity.     

Comparison of dental fluorosis and caries in primary teeth of preschool-children living in arid high and low fluoride villages

Abstract The aim of this study was to determine the degree of fluorosis in the primary dentition and the accompanying caries patterns in groups of preschool-children in high and low fluoride areas. Among 331 coloured children, aged 1 -5 years, living in an area with water F concentrations ranging from 2.2 to 4.1 parts/10⁶, 82% were caries free and the dmft values ranged from 0 to 15 with a mean dmft of 0.8 ± 2.1. Varying degrees of fluorosis in the primary teeth were present in 50.6% of the children. In 177 coloured children of similar ages from an adjacent area with 0.2 parts/10⁶ F in the drinking water the dmft values ranged from 0 to 20 with a mean dmft of 5.4 ± 5.8. Only 28% of the children were caries free. None of the children in this area had fluorosis. The caries prevalence was significantly higher in the low fluoride area than in the high fluoride area. The degree of fluorosis found in the primary dentition in the children from the high fluoride area was higher than had been anticipated and was accompanied by a very low caries prevalence.     

Ultrastructure of Dental Enamel afflicted with Hypoplasia: An Atomic Force Microscopic Study

The ultrastructure of the human tooth enamel from a patient diagnosed with hypoplasia (HYP) was investigated using atomic force microscopy (AFM) and compared with the surface of normal human tooth enamel. Hypoplasia is a hereditary defect of dental enamel in which the enamel is deficient in either quality or quantity. AFM results presented for the HYP tooth enamel clearly demonstrate that the apatite crystal morphology in hypoplasia tooth enamel is perturbed in the diseased state which could result from a defective synthesis of the extracellular matrix proteins, e.g., amelogenin, by the ameloblasts. HYP enamel consisting of loosely packed, very small grains does not present a tendency for association, as in the case of the normal healthy tooth. Indeed, the enamel surface affected by HYP is porous and is made of much smaller grains. In some samples, the HYP part of enamel surface appeared in the form of a point-defect, which we believe may be associated with the early stages of the HYP deformation.     

Anti-TGF-beta antibody blocks enamel matrix derivative-induced upregulation of p21WAF1/cip1 and prevents its inhibition of human oral epithelial cell proliferation

We have previously demonstrated that porcine enamel matrix derivative (EMD) contains TGF-beta 1 (or a TGF-beta-like substance), and that EMD rapidly translocates smad2, which is an effector of the TGF-beta signaling pathway, into the nucleus and modulates the proliferation of both human gingival fibroblastic and oral epithelial cells in a cell type-specific manner. To investigate the involvement of TGF-beta in the growth modulatory action of EMD, two approaches have been used in the present study: i) a neutralizing anti-TGF-beta antibody to block EMD action, and ii) authentic porcine TGF-beta 1 to compare with EMD. Both in epithelial and fibroblastic cells, TGF-beta 1 closely mimicked EMD in nuclear accumulation of smad2, phosphorylation of MAP kinase family members, and consequent cell type-specific growth modulation. Anti-TGF-beta antibody, at levels which completely blocked TGF-beta 1-induced smad2 translocation, strongly blocked EMD-induced smad2 translocation. This antibody also blocked other actions of EMD in epithelial cells, i.e. p38-MAP kinase (p38-K) phosphorylation, p21WAF1/cip1 expression, and inhibition of DNA synthesis. In support of our previous proposal, these data suggest that TGF-beta 1 (or a TGF-beta-like substance), which is delivered as a principal bioactive factor in EMD, inhibits epithelial cell proliferation probably by a smad2-mediated, p21WAF1/cip1-dependent mechanism. However, the same neutralizing antibody failed to convincingly block EMD-induced fibroblastic proliferation, which suggests that EMD may contain additional unidentified mitogenic factor(s), which act in combination with TGF-beta to fully stimulate fibroblastic proliferation.