The purpose of this study was to investigate the abnormalities of articulation and the effectiveness of speech training in the hearing-impaired children. Twenty-one hard-of-hearing children were selected as subjects, who were ten or eleven years old and had impaired hearing by congenital causes or postnatal diseases before two years of age. The subjects were divided into two groups ; the group A, consisting of ten hard-of-hearing children with average hearing losses between 51dB and 85dB in the better ear and, the group B, eleven children with average losses greater than 86dB in the better ear. They were tested by three methods, namely articulation test, sound spectrogram and air-dynamic measurements during phonation, before and after speech training of two years duration. The articulation test was carried out by three speech therapists on the spoken sound phonated by the subject reading one of the three test card-decks, each consisting of sixty-seven Japanese monosyllabic sounds arranged at random. Nasal and oral air flow rates and oral air pressure during phonation were examined by means of electro-transducer and recorded by paper oscillogram. Results were as follows : 1. The most probable cause of mistakes in spoken sounds was discooperation of vocal sound and orally composed sound (s-factor), the second was the lack of stability of oral resonance for vowel production (v-factor), and the least one was the inaccuracy of orally composed sound (o-factor). 2. The lack of stability of aspiration before and during phonation was pointed out as one of the causes of inaccurate vowels, and the poor control of intraoral air pressure was revealed on phonation of pressure consonants. 3. The effectiveness of speech training was shown largely in improvement of o-factor, somewhat in v-factor, and a little in s-factor of some consonants. 4. So far as o-factor was concerned, speech training was more effective in group A than in group B, but concerning s-factor and v-factor, no difference was shown in effectiveness between the groups.

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In dental casting technique, it has been said that the metal shrinkage should be fully compensated with the same amount of expansion obtained by setting and heating the investment bulk. However, some reports have recently pointed out the anisotropy and heterogeneity of the latter. So, the author measured the displacement of 'crystobalite' investment material in the casting ring and the dimensional change of 'K-metal' casting under the conditions very close to the clinical practice to know the actual circumstances of shrinkage compensation. The displacement of two inner portions of 'crystobalite' investment in the casting ring was measured along its axis by using differential transformer, of which the core was connected to a plate embeded in the investment bulk balancing by a bob so that no gravitative effect might work. Net setting expansion of the investment bulk under the plate was generally greater at higher W/P ratio and more than 3% when the ring was lined with an appropriate number of wet asbestos layers. It increased as the number of asbestos layers increased up to a certain critical value, which was lesser at higher W/P ratio. Dimensional changes of several important portions as well as volume change of crown type and MOD type castings were also evaluated with reference to those of the wax pattern. Even in case that setting expansion by itself of the investment exceeded 3%, the casting could not always become larger than the wax pattern in every portion. Although asbestos lining had remarkable enlarging effects on the dimensions along ring radius and anyhow supported the shrinkage compensation, thickness and volume of casting could almost never become larger than those of the wax pattern even with 4 layers of asbestos. Nevertheless, at least the inside dimensions of crown and MOD castings could be sufficiently larger than those of the wax pattern under certain proper conditions. Such castings could well be fit to the model. Therefore, it may be concluded that the well-fitting casting can be produced due to a favorable deformation even with considerable shrinkage as a total.

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Organic mercury poisoning was caused in rats by inducing methylmercuric chloride with per os administration. Pathological changes of the sensory receptor-apparatus for taste were investigated both light and electron microscopically and the following results were obtained. 1. The methylmercury induced in rats caused disorders of the taste buds as a sensory receptor apparatus for taste. The most characteristic changes were observed on the taste bud cells in which severe exhausion due to cell degeneration occurred resulting a consequential atrophy of the taste buds. 2. Light microscopically, the cells revealed their degenerative appearances such as pyknosis, karyolysis, karyorrhexis and swelling of the cytoplasm. 3. Electron microscopically, it became difficult to differentiate type 1 cells (light cell) from type 2 cells (dark cell), because the difference of density between the two kinds of cells decreased during the degenerative course. In the taste bud cell cytoplasm, a particular change of mitochondrial matrices appeared revealing a wormeating spot-like, translucent lesions. These lesions developed in later stage to vacuolarization of the mitochondria with an additional change of loss of cristae. Similar vacuolarization occurred in endoplasmic reticulum and Golgi element. Therefore, whole cytoplasm was observed being occupied by vacuolated organelles in the end stadium. In contrast, the nuclei of the taste bud cells increased remarkably their densities which were regarded to correspond with pyknosis in the light microscopic changes. Some of the severely affected cells were supposed to come to final cell destruction. 4. The same kind of mitochondrial degeneration as that in the taste bud cells appeared also in the nerve endings. Changes of neurotubules came thereafter. 5. No severe affections were found on the squamous epithelial cells surrounding the taste buds. But slight vacuolarization was detectable in some of the epithelial cell mitochondria. So that, the degenerative appearancte of the taste buds formed a sharp conrast with intact views of the surrounding tissues. We understand that our findings of the disturbance of the taste buds which was caused by methylmercury are important because our results found in this experiment are not only the first presentation of pathological changes which can explain the mechanism of taste disturbance in human Minamata disease, but it will suggest a direction of future investigation for other sensory disturbances in methylmercury poisoning.

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Distribution of methylmercury in tissue cells in dental fields of adult and fetal rats during the process of dental development and its time course change were compared and the following results were obtained. 1. Many tissues and cells in the oral cavity could be exposed to methylmercury in various degrees. 2. Intongue, relatively intense deposition of methylmercury was noted in the mucous membrane of the tip and body of the tongue and in the lingual muscles. Especially in the former, the mechanism of excretion of methylmercury along with epithelial desquamation was suggested. 3. Among the perioral tissues, the deposition was not as intense in the epidermis as in lingual mucous membrane, but deposition and accumulation of methylmercury was noted in the hair. In the muscle tissues of the same portion, the deposition was almost as intense as in the lingual muscle. 4. In the parotid gland, marked deposition was noted in the glandular cells and ducts in the initial period of administration. This was followed by a rapid decrease as time progressed. An excretory mechanism via the saliva is suggested indicating recontamination in the oral cavity. 5. The dental tissues of mature rats showed the lowest mercury uptake among the tissues studied. 6. Tissues and cells in the process of dental development, on the other hand, readily take up methylmercury. The main findings included the following : 1) Intense deposition is generally seen in the epidermal tissues of ectodermal origin in the lamina-shaped stage and bud-shaped stage. Along with the formation of the enamel organ, intense deposition is seen in the inner enamel epithelial cells. 2) In tissues of mesodermal origin, marked deposition of methylmercury was noted in the tissue cells of mesenchymal nature along with formation of the dental papilla, and a considerable uptake was noted in the odontoblasts. 7. Through each period of dental development, such findings of deposition of methylmercury gives a suggestion on the pathogenesis of dental developmental anomaly in patients with fetal Minamata disease.

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1. df-t Rate The rate was higher in the male than in female. The rate was higher in the upper jaw than in lower jaw through both sexes. 2. df-t Rate of individual teeth Upper jaw : The df-t rate of deciduous central incisor was the highest followed by deciduous first molar, deciduous second molar, deciduous lateral incisor and deciduous canine in this order through both sexes. Lower jaw : The rate was higher teeth of anterior part than in posterior part of jaw, and this difference was more remarkable in lower jaw than in upper jaw through both sexes.

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Supernumerary deciduous teeth was found in a girl of 3 years and 2 months. Teeth erupted in both sides of lower incisor region. As to the frequency of supernumerary appearance deciduous tooth, Okamoto (1941) reported that it occurred once in tens of thousands, Ikuta (1925) reported 2 cases in 23, 600 and Fukada (1957) failed to see any in 10, 149 subjects examined. It shoud be noted that all these supernumerary tooth, as they appeard in so few instances, occurred in the upper frontal teeth, except that which was reported by Tochihara (1956) to have ocurred in the lower frontal teeth. Two theories have been advanced as to possible origin of the supernumerary tooth in the deciduous dentition, of which the one is based on the ontogenetic dysplasia and the other based on the phylogenetic atavism. In view of our findings on the position of the tooth erupted and the shape and size of the tooth itself, we would like to favor the theory advanced by Fujita (1958) for the origin of the supernumerary tooth as being the result of a morphological disturbance that occurred in the dental lamina.

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Developmental anomalies of the teeth may be classified according to severity as anomalies, malformations and monstrosities, some abnormalities are determined largely by intrinsic factors (heredity and mutation) and others by extrinsic factors (physical and chemical agents, endocrine dystunction and infection). Certain teratologic lesions are apparent at birth but some noncongenital defect are not predetermined, resulting entirely from postnatal environmental influences on the still developing structures. Recently we experienced a rare case of 12 years old male infant who had fusion in mandibular anterior region, congenital missing teeth and enamel hypoplasia. 1. Fused teeth was complete fusion between 1^^__| and 2^^__|. 2. Congenital missing teeth were [numerical formula]. 3. Enamel hypoplasia was apparent on [numerical formula]. One fundamental cause of this anomaly may be attributed to the Fujita's theory of phylogenetic consideration, but some other factors such as developmental and nutritional disturbances due to measles, varicella and parotitis epidemica in the period of his dental growth, also affected to the formation of such a serious dental anomaly.

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