Cloning, characterization and immunolocalization of human ameloblastin

Amelogenesis imperfecta is a broad classification of hereditary enamel defects, exhibiting both genetic and clinical diversity. Most amelogenesis imperfecta cases are autosomal dominant disorders, yet only the local hypoplastic form has been mapped to human chromosome 4q between D4S242 1 and the albumin gene. An enamel protein cDNA, termed ameloblastin (also known as amelin and sheathlin), has been isolated from rat, mouse and pig. Its human homolog has been mapped to chromosome 4q21 between markers D4S409 and D4S400, flanking the local hypoplastic amelogenesis imperfecta critical region. Therefore, ameloblastin is a strong candidate gene for this form of amelogenesis imperfecta. To facilitate genetic studies related to this dental disease, we isolated and characterized a human ameloblastin cDNA. A human third molar cDNA library was screened and two ameloblastin clones identified. Nucleotide sequencing of these cDNAs indicated alternative splicing of the putative open reading frame, use of different polyadenylation signals, and a high degree of similarity to reported rat, mouse and porcine cDNAs. Immunohistochemistry studies on embryonic human teeth using an antibody to recombinant ameloblastin indicated ameloblastin expression by ameloblasts with localization in the enamel matrix associated with the sheath structures.     

Influence of firing times and temperature on color stability of low-fusing porcelains for high-functional gold alloys

The purpose of this study was to investigate the effect of firing conditions on color stability. Three commercially available porcelains for high functional gold alloys, Carrara (CA), Deguceram Gold (DE) and Duceragold (DU) were used. In this study color stability was investigated under fire treatment of 1st, 3rd, 5th times and firing temperatures of 0, 20, and 40 degrees C higher than the manufactures standard temperature (CA: 845 degrees C, DE: 780 degrees C, DU: 780 degrees C). L* was degreased in CA 5 times, DE 3 times, DU by repeated firing. No difference was observed among L* of firing temperatures DE and DU, but L* was degreased in CA with firing temperatures of 40 degrees C higher. a* was degreased in CA, DU, DE with repeated firing, a* was degreased 5 times at firing temperatures of higher. b* was degreased in DU, but b* was increased in CA and DE with 5 firings. b* was increased with 5 findings at firing temperatures of 40 degrees C higher.     

Acid profile in carious dentin

Organic acids in carious dentin from 69 permanent teeth were analyzed by gas chromatography. Lactate, acetate, propionate, and butyrate were detected in most samples, and limited amounts of isobutyrate, valerate, isovalerate, caproate, and isocaproate were occasionally detected. Lactate, acetate, and propionate were major acids and altogether accounted for about 90% of total acid in most samples of carious dentin. However, the proportion of these three acids varied among the samples. Some samples contained over 85% lactate, while others contained mainly acetate and propionate. A high percentage of acetate was usually accompanied by an appreciable amount of propionate. All seven samples in carious dentin under fillings or restorations had little lactate, but a high percentage of acetate plus propionate. The differences in acid profiles of carious dentin may reflect differences in the microbial ecology of carious dentin, and a stage of progress of dentin caries or a type of dentin caries.     

Artificial plaque removal with Carisolv system: a clinical approach

In the present study, removal of artifcial plaque in pits and fissures with the Carisolv system was compared with that of conventional bristle brush methoda in vitro. The results indicate that in the dental clinic, complete plaque removal with the Carisolv is possible, and in addition to acid etching, treated cavity was almost free of debris which might increase sealant retention.     

Regulation of PLAP-1 expression in periodontal ligament cells

Periodontal-ligament-associated protein-1 (PLAP-1) is preferentially expressed in the periodontal ligament (PDL) and encodes a novel small leucine-rich repeat proteoglycan protein. PLAP-1 expression was induced during the course of cytodifferentiation of PDL cells into mineralized-tissue-forming cells in vitro, suggesting the possible involvement of PLAP-1 in the mineralization process of PDL cells. In this study, we hypothesized that PLAP-1 expression is regulated by mineralization-related cytokines in PDL cells. PLAP-1 expression was clearly down-regulated when the cytodifferentiation of PDL cells was reversibly inhibited by fibroblast growth factor-2 (FGF-2). In contrast, bone morphogenetic protein-2 (BMP-2) enhanced PLAP-1 expression. Up-regulation of PLAP-1 expression by BMP-2 was confirmed at the protein level when PDL cells were immunostained with anti-PLAP-1 polyclonal antibody. These results revealed the cytokine-mediated regulatory mechanisms of PLAP-1 expression and suggested that PLAP-1 expression may be associated with the process of cytodifferentiation of PDL cells.     

Relationship between bilateral condylar bone change and mandibular morphology: a study using morphometry

This study was undertaken to evaluate the relationship between bilateral condylar bone change (BCBC) and mandibular morphology. Thirty Japanese women with BCBC as diagnosed from computed tomographic scans were compared to 2 control groups: 26 Class I and 25 Class II Japanese women. All cephalograms were traced and scanned, and 14 homologous landmarks were digitized. Coordinates were used for cephalometric analysis, Procrustes analysis, Euclidean distance matrix analysis (EDMA), and thin-plate spline (TPS) analysis. Comparison of the cephalometric data for the BCBC and Class I groups revealed significant shrinkage in the condylar process and ramus height, in addition to a shorter body length. The centroid size showed that BCBC mean geometric forms were smaller than those of Class I and Class II. The landmark morphology of the BCBC group differed from both Class I and Class II, as shown by the residuals (P < .001). EDMA showed expansion of infradentale-pogonion (9.9%) and along the anterior slope height of the condyle (28.6%), while the posterior slope height decreased (21.6%). The vertical ramus height (gonioncondylion) also decreased by 11.8% in comparison to Class I. Compared to Class II, BCBC ramus height was shorter by 8.9%, condylar width decreased 13.7%, and the posterior condylar slope was 22% shorter. TPS analysis showed increased antegonial notching, a vertically expanded symphysis, and a collapsed and more horizontal condyle in the BCBC group. The combination of the above methods was very helpful in assessing mandibular morphology and showed that BCBC might be related not only to changes in the condyle, but may dictate changes in the rest of the mandible as well.     

Gene expression and immunolocalization of amelogenin in enamel hypoplasia induced by successive injections of bisphosphonate in rat incisors

Successive injections of 1-hydroxyethylidene-1, 1-bisphosphonate (HEBP) in rats induce enamel hypoplasia. To elucidate the pathogenesis of this hypoplasia, male Wistar rats were daily injected with HEBP or physiological saline for 7 days. After the last injection, they were killed under anaesthesia and their maxillary incisors were examined using an in situ hybridization technique and immunohistochemical staining to detect the gene expression and localization of amelogenin protein, respectively. In the HEBP-injected rats, several islets of partially mineralized enamel were present along crown-analogous surface of the incisor in the secretory stage of amelogenesis and enamel-free zones existed between these islets. In situ hybridization demonstrated amelogenin gene expression over the ameloblasts facing the islets of the matrix enamel as well as over those of the enamel-free zones. Immunohistochemical studies using rabbit antiamelogenin antibody revealed positive reaction both in the enamel matrix of the control group and in the islets of enamel matrix of the HEBP-injected group. Some small granules immunoreactive to amelogenin antibody were found in the distal portions of the ameloblasts in the HEBP-injected rats. The results indicate that HEBP does not alter amelogenin gene expression over ameloblasts, or the protein's existence in enamel matrix. There appeared to be some accumulation of amelogenin in the HEBP-treated ameloblasts. It is therefore suggested that the enamel hypoplasia in this experiment may not be due to a disturbance in amelogenin synthesis but to a disturbance in a later process, presumably of protein secretion.