I investigated the expression of the cytokeratin (CK)19 gene during carcinogenesis in the oral cavity using 49 cases of squamous cell carcinoma (SCC), 3 cases of erythroplakia (EP), 4 cases of the leukoplakia (LP), 7 cases of LP with epithelial dysplasia, 3 cases of LP without epithelial dysplasia, and 10 cases of normal gingiva. Total-RNA was extracted form biopsy materials and examined by the reverse transcription polymerase chain reaction (RT-PCR) and Northern blot. CK 19 mRNA was expressed in every sample by RT-PCR. The Northern blot test showed it was strongly positive in SCC, moderately positive in EP and LP with epithelial dysplasia and slightly positive in LP without epithelial dysplasia and in normal gingiva. CK 19 gene expression was slightly different in each SCC. However, its expression in oral SCC showed no correlation with the primary site, TNM classification or histological differentiation. These results indicate that the CK 19 gene in EP and LP with epithelial dysplasia and cancer cells is more actively transcripted than in normal cells, implying that it is an important factor in carcinogenesis of oral squamous cell epithelium.

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We studied the filament formation of periodontopathic bacterial cells induced by β-lactam antibiotics, and the macropharge phagocytosis of these cells. Nine β-lactam antibiotics, 5 species of Porphyromonas (6 strains), 6 species of Prevotella (6 strains), and rat peritoneal macrophages were used. Cells of 6 Prevotella strains were markedly elongated by 1/64〜1/2MIC of aztreonam (AZT) treatment. Cells with long filaments of 5 of the Porphyromonas strains were observed after treatment with the same concentration of latamoxef, piperacillin and cefteram. All of the β-lactam used caused cells of the treated bacterial strains to form spheroplasts. The phagocytosis ratio and phagcytosis index of macrophages to elongated cells that resulted from the AZT treatment were reduced one half and one third, respectively, compared with normal cells. These results suggest that Porphyromonas and Prevotella cells were elongated after subMIC treatment with certain β-lactam anatibiotics. In addition, these cells became more resistant to macrophage phagocytosis.

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To assess the clinical application of magnetic attachments, we examined 132 patients with magnetic attachment dentures and recorded the number of magnetic attachments, denture design and prognosis of abutment teeth. We found that the abutment teeth with magnetic attachments were usually canines. In 66% of the cases, the magnets were added to dentures already in use. The number of magnetic attachments on each denture was usually 1 or 2. When we investigated changes in the Gingival Index, Probing depth of the abutment teeth and condition of the denture, few cases had a poor outcome. These findings suggest that magnetic attachments are beneficial for denture retention and stability, and that adding magnetic attachments to a denture in use is very effective.

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Dental caries is an infectious disease caused by bacteria indigenous to the oral cavity. Because it is an endogenous infection, its initiation is affected by factors other than bacterial pathogenicity, such as host and dietary substrates. Dental caries is initiated by demineralization of tooth enamel caused by organic acids produced in dental plaque bacteria that ferment dietary carbohydrates. Among dental plaque bacteria, mutans streptococci are considered the principal etiological agents of human dental caries, because they possess various pathogenic characteristics and can induce experimental caries in animals. An important first step in pathogenesis involves adherence of mutans streptococci to the tooth surface. This process is mediated by sucrose-independent and -dependent adherence mechanisms. Sucrose-independent adherence is mainly due to cell surface polymers, especially cell surface fibrillar portein antigen designated as antigen l/ll, B, lF, P1, SR, MSL-1 or PAc. The ability of mutans streptococci to convert sucrose into water-soluble and -insoluble glucose polymers appears to play an important role in the colonization of tooth surfaces. This process is catalyzed by a group of enzymes called glucosyltransferases. The acidogenicity of these organisms is considered to be one of the major determinants of their cariogenicity. Furthermore, tolerance of acid environment is of major importance in the ecology of dental plaque and the pathogenesis of dental caries. Mutans streptococci cause dental caries by various cariogenic factors. In this symposium, Idiscussed recent information about cell surface fibrillar protein antigen, glucosyltransferase and acid tolerance, including proton-ATPase of mutans streptococci.

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Carious lesions result from the demineralization of enamel exposured to acid produced by plaque bacteria. When exposed to glucide, plaque bacteria readily produce an acidic environment as a byproduct of their normal metabolic activity. In order to inhibit this acid formation and reduce caries, we developed sweeteners that plaque bacteria are incapable of fermenting into cariogenic acid. If coupling sugar, fructooligosaccharide, aspartame and similar products are low- or non-cariogenic, we think that xylitol is an anti-cariogenic substitute. Xylitol inhibits the growth of plaque bacteria and reduces the amount of plaque and number of Streptococcus mutans. This is because it inhibits their glycolytic system and production of futile xylitol.

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It is now generally recognized that dental caries is an infectious disease that causes localized destruction of teeth and is induced mainly by acids produced in dental plaque. Understanding the de- and re-mineralization that occurs as an interaction between plaque and the enamel is important for understanding the caries process and caries prevention. It depends on the plaque pH and is based on chemical reactions. This report describes the de- and re-mineralization of the enamel structure that occurs during the caries process. Atomic force microscope (AFM) and scanning electron microscope (SEM) observations performed after acid challenge demonstrated the structural pathways, such as enlarged crystal interspaces and prism junctions at the surface layer of the subsurface enamel lesion. Remineralized crystals around the enlarged crystal spaces were detected by the AFM technique at the surface layer after the acid challenge. SEM observation of the subsurface layer of the lesion showed destruction of the enamel crystals, remineralized crystals, diffused mineral destruction in the prism core, and destruction of interprismatic substances. Understanding these structural changes during the caries process will aid in the scientific prevention of dental caries.

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Dental caries are classified histopathologically into enamel caries, dentin caries and cementum caries. We observed these caries using established methods and confocal laser scanning microscopy (CLSM). In early enamel caries, subsurface decalcification was observed, demineralization and remineralization occurred, and several zones could be distinguished. Using CLSM, the remaining enamel rod structures were observed in the surface zone. Destruction of enamel rods was seen in the body of the lesion. Enamel rods and cross striations were observed clearly in the dark and translucent zones. The lesion progressed along the enamel rods in two patterns : one along the heads of enamel rods, and the other along the tails. Another mode of progression in enamel caries was along the incremental Retzius lines and enamel lamellae. However, on the basis of radiographic studies there was no direct correlation between the occurrence of enamel lamellae and caries. Once dental caries reached the dentino-enamel junction, they quickly undermined sound enamel. In dentin caries, the lesion progressed along the dentinal tubules and lateral branches, and softened dentin was observed. Cuboidal or rhomboid-shaped mineral crystallites were observed by SEM in the dentinal tubules beneath the carious lesion. Therefore, the dentinal tubules seemed to be related both to demineralization and remineralization. Cementum caries progressed along Sharpey's fibers, the lamellated appearance began to disappear, and the surface of the cementum was destroyed.

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