The introduction of the computed tomograph in the 1970s revolutionized medical diagnosis by initiating the transition from analogue to digital imaging. During this period, more specialized equipment for image processing was developed, such as cathoderay tubes for image display, special sensors for image acquisition, and storage devices for image archiving. Digital imaging systems designed exclusively for use in dentistry were developed in the latter half of the 1980s. Some are now being clinically applied under conditions of close scrutiny to determine diagnostic accuracy, image quality, and radiation exposure to patients. This article reviews the enabling technologies of digital systems used in dentistry, and focuses upon intraoral digital imaging systems, concepts for digital image acquisition, and variations in radiation dose and their effects on diagnostic accuracy of caries detection.

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The neuron innervating the hamster submandibular (SM) gland was identified in the superior cervical ganglion (SCG) in vitro by recording the antidromic response using the intracellular recording technique. After the cellular response was recorded, methylene blue was injected iontophoretically into the neuron from the recording electrode, and the location of the cell soma was determined. The salivatory neurons of the SM gland were in the small- to medium-sized group of the entire cell population of the SCG. The cell size was 36.3×24.4μm (mean, n=45). The postganglionic fibers were entirely unmyelinated (mean: 0.34m/sec at 28-30°C, n=141). Eighty-seven percent of the cells were distributed in the central one-third of area between the external carotid nerve origin and the caudal pole in the SCG. The resting membrane potential, membrane input resistance, membrane time constant and membrane input capacitance of the salivatory neuron were as follows: -49.2±7.6mV (n=102), 52.9±23.6MΩ(n=71), 8.0±3.4msec (n=71) and 147±50pF (n=71). Fast- and slow-excitatory postsynaptic potentials (EPSPs) were evoked, but not slow-inhibitory postsynaptic potentials (IPSPs). The fast EPSP was 13.1±5.7mV in amplitude and 46.2±17.1msec in duration (n=35). The slow EPSP(20Hz, 5sec) was 6.9±11.9mV in amplitude and 101±43sec in duration (n=16). The directly-evoked spike was 63.0±11.9mV in amplitude and 5.9±1.3msec in duration (n=54). The spike after-hyperpolarization (AHP) was 12.5±3.5mV in amplitude and 353±161msec in duration. Na⁺ and Ca²⁺ channels were involved in the spike generation. The voltage-dependent K⁺ channels (delayed rectifier), A channels and rapidly Ca²⁺-activated K⁺ channels (BK channels) regulated the spike-falling phase. The delayed rectifiers, A channels, and BK and SK (slowly Ca²⁺-activated) channels were involved in generation of spike-AHP. Muscarine suppressed the Ca²⁺ component of spike via muscarinic receptors.

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The purpose of this study was the fabrication of titanium powder sheets to enable the application of sintered titanium alloys as metal denture bases. The effects of titanium particle shape and size, binder content, and plasticizer content on the surface smoothness, tensile strength and elongation of titanium powder sheets was investigated. To select a suitable ratio of powdered metal contents for application as a metal denture base, the effects of aluminum content in Ti sheets and various other powder metal contents in Ti-Al sheets on the density, sintering shrinkage, and bending strength were evaluated. Based on the results of the above experiments, we developed a mixed powder sheet composed of 83Ti-7Al-10Cr with TA-45 titanium powder (atomized, -45μm), and 8 mass% binder content. This titanium alloy sheet had good formability and ductility. Its sintered titanium alloy had a density of 3.2g/cm³, sintering shrinkage of 3.8%, and bending strength of 403 MPa. The titanium alloy sheet is clinically acceptable for fabricating denture bases.

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We experienced a case with severe enamel defects of both the deciduous teeth and all the permanent teeth. In order to clarify the etiology of enamel defects in this patient, we performed a DNA analysis in addition to conventional examinations. Although we suspected a variety of systemic factors causing enamel defects, there was no evidence suggesting disturbances of amelogenesis. In the present case, we suspected a mutation in the amelogenin gene and performed nucleotide sequencing of the exons of the amelogenin gene, but we could not find any evidence of mutation. We suggest that a mutation of some other gene related to enamel formation or the adventitious factors contributed to the amelogenesis imperfecta in this case.

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This case report describes an ameloblastic fibro-odontoma arising from a calcifying odontogenic cyst (COC) in the mandible of a twenty-three-year old male. The patient was referred to the Department of Oral Surgery, Tokyo Dental College, on March 30th, 2000, complaining of a painful swelling, which had appeared three weeks earlier on his left mandibular molar region. In a pathological view, the lesion was a round cyst the size of a chicken-egg, dark red in color, and surrounded by a thick membrane. The cyst had an epithelium of varying thickness which included many ghost cells and an enamel-like structure on the inside, and a thick wall of connective tissue with an ameloblastic fibro-odontoma on the outside. Enamel organ-like epithelial islands were structured radially in the form of strands with immature dentin. Cytokeratin 19 was strongly immunoreactive in the epithelium of the lesion; osteopontin and osteocalcin reacted in the mesenchymal cells and weakly in the epithelial element of this tumor.

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