28 research outputs found

    Chapter 4 : Injury and the Recovery Reaction due to the Penetration of Material into the Mandibular Canal

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    A root canal filling material paste, mainly made of calcium hydroxide and iodoform with the addition of silicone oil, was experimentally introduced into the mandibular canals of dogs. The tissue reactions to the paste were examined by radiography, histopathology, and electron microscopy. The examination results showed that the paste was phagocytosed by macrophages and, in general, was gradually resorbed by the passage of time. The paste was also found to cause heterotopic calcification and/or bone formation within the limited area of original penetration. The histopathological tissue changes of the alveolar nerve tissue were also examined. No injury-related histopathological change was observed as long as the injected paste did not contact alveolar nerve tissue, but tissue damage was observed at sites of direct contact. After removal of degenerated nerved debris by macrophages and Schwann cells, the persisting external membrane or “Schwann tubes” appeared to provide a scaffold for axonal regeneration and Schwann cell proliferation.Editor, Toshiyuki KawakamiLanguage Editor, David M Carlsonviii, 232 p. ill. (some col.

    Chapter 1 : Root Canal Treatment and the Role of Filling Materials

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    Endodontics includes diagnosis and treatment as well as management of pulpal and periapical diseases. Treatment aims to reduce inflammation of the periapical tissues, to dissolve remaining organic material, and to counteract coronal microleakage in the root canal through the use of medication and mechanical instruments. Finally, irrigated root canals should be obturated with filling material and sealer to prevent reinfection.Editor, Toshiyuki KawakamiLanguage Editor, David M Carlsonviii, 232 p. ill. (some col.

    Chapter 3 : An In Vivo Examination of the Fate of the Components of a Root Canal Filling Paste made of Calcium Hydroxide and Iodoform with Silicone Oil

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    Using radioactive compounds, we investigated the fate of the calcium hydroxide and dimethylpolysiloxane (silicone oil) components in a root canal filling paste. The paste was made of calcium hydroxide and iodoform with the addition of silicone oil. Whole body, light, and electron microscopic autoradiographic surveys were used. Additionally, quantitative analysis using a liquid scintillation spectrometer was performed on the component dimethylpolysiloxiane. The calcium component moved to the bone tissue through the body fluid and blood, and some of it was excreted through the digestive tract. The calcium came partly from the calcium components of the paste in both types of heterotopic calcifications: dystrophic and matrix vesicle. Some of dimethylpolysiloxane component also passed into the digestive tract. Furthermore, the dimethylpolysiloxane played some part in the calcification caused by the embedded paste.Editor, Toshiyuki KawakamiLanguage Editor, David M Carlsonviii, 232 p. ill. (some col.

    Involvement of Heat-Shock Proteins During Periodontal Ligament Remodeling

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    Mechanical stress induces various molecules such as heat-shock protein (HSP), which causes structural changes in the proteins in periodontal ligament (PDL). We carried out an experiment to induce traumatic occlusion in mouse PDL and analyzed the expression of HSPs. HSPs investigated acts differently depending on the time of expression. HSPs are constitutively expressed in the PDL and defend cells from stress and maintain homeostasis under normal conditions. During bone addition to the PDL on the tension side, HSP27 and HSP47, HSP70 also acts as molecular chaperone, which assists the maturation of bone morphogenetic proteins and aids osteoblast activation. In HSP 70 and HSP 47, mechanical stress is applied to the PDL on the tension side for a short period of time for alveolar bone repairing, and when abnormality occurs in the collagen structure fibroblasts of PDL, it functions at the injured site, whereby extracellular that promotes abnormal collagen secretion and stores the modified protein in the endoplasmic reticulum, there by controlling the decalcification of PDL. In other words, HSP47 and HSP70 are expressed in PDL fibroblasts on the pressure side damaged by application of mechanical stress and contribute to the repair of collagen tissue by activating PDL fibroblasts, supporting recovery from cell damage

    Bone Marrow Mesenchymal Cell Contribution in Maintenance of Periodontal Ligament Homeostasis

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    In general, remodeling phenomenon of the periodontal ligament (PDL) is occurring in all times. Thus, in the chapter, the word “maintenance” was used, and the chapter title is “Maintenance of Periodontal Ligament Homeostasis.” Our experimental data on the remodeling of the PDL with cell acceleration at the furcation area in this experimental model are recovered using the cells in situ and the bone marrow-derived cells (BMCs). BMC migration into the PDL tissues using green fluorescent protein (GFP) bone marrow-transplanted model mouse was examined. BMCs have abilities of cell migration and differentiation into tissues/organs in the body. The immunohistochemistry revealed that GFP-positive cells were detected in the PDL. GFP-positive cells were also positive to CD31, CD68, and Runx2 suggesting that fibroblasts differentiated into osteoclasts and tissue macrophages. In this way, Notch signaling involvement considered in our tentative examinations revealed that the experimentally induced periodontal polyp was examined; the cytological dynamics of the cells in granulation tissue are mainly from migration of undifferentiated mesenchymal cells of the bone marrow and differentiate into the tissue-specified cells. Furthermore, the data suggest that cell differentiation is due to Notch signaling

    Chapter 3 : Involvement of heat-shock proteins during periodontal logament remondeling.

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    Mechanical stress induces various molecules such as heat-shock protein (HSP), which causes structural changes in the proteins in periodontal ligament (PDL). We carried out an experiment to induce traumatic occlusion in mouse PDL and analyzed the expression of HSPs. HSPs investigated acts diff erently depending on the time of expression. HSPs are constitutively expressed in the PDL and defend cells from stress and maintain homeostasis under normal conditions. During bone addition to the PDL on the tension side, HSP27 and HSP47, HSP70 also acts as molecular chaperone, which assists the matu-ration of bone morphogenetic proteins and aids osteoblast activation. In HSP 70 and HSP 47, mechanical stress is applied to the PDL on the tension side for a short period of time for alveolar bone repairing, and when abnormality occurs in the collagen structure fi broblasts of PDL, it functions at the injured site, whereby extracellular that promotes abnormal collagen secretion and stores the modifi ed protein in the endoplasmic reticulum, there by controlling the decalcifi cation of PDL. In other words, HSP47 and HSP70 are expressed in PDL fi broblasts on the pressure side damaged by application of mechanical stress and contribute to the repair of collagen tissue by activating PDL fi broblasts, supporting recovery from cell damage.Edited by Jane Manakil,282p,illus. : London : IntechOpen, 2019

    歯科矯正学的メカニカルストレスによるマウス歯周組織改造における細胞動態

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    The purpose of the study was to determine the cell dynamics in periodontal ligament in response to mechanical stress during orthodontic movement. Following Waldo’s method, a square sheet of rubber dam was inserted in between the first and second maxillary molars in 10 ddY mice leaving the stress load for 3 hours. After 3 days and at 1 week, cell count on pressure and tension sides of the periodontal ligament was determined. Furthermore, the type of cell present after mechanical stress was identified using GFP bone marrow transplantation mouse model. Immunohistochemistry was carried out at 0 min (immediately after mechanical stress), 24 hours, 1 week, 2 weeks and 6 months. Temporal changes in the expression of GFP-positive bone marrow derived cells were examined. Moreover, double immunofluorescent staining was performed to determine the type of cell in the periodontal ligament. Cell count on the tension side tremendously increased 3 days after mechanical stress. At 1 week, spindle and round cell count increased compared to the control group. These changes were observed on both tension and pressure sides. Cell count on pressure side at 3 days (22.11+/-13.98) and at 1 week (33.23+/-11.39) was higher compared to the control group (15.26+/-8.29). On the tension side, there was a significantly increased at 3 days (35.46+/-11.85), but decreased at 1 week (29.23+/-13.89) although it is still higher compared to the control group (AD+/-SD: 10.37+/-8.69). Using GFP bone marrow transplantation mouse model, GFP positive cell count increased gradually over time in 6 months. GFP positive cells were also positive to CD31, CD68 and Runx2 suggesting that fibroblasts differentiated into osteoclasts and tissue macrophages. In conclusion, mechanical stress during orthodontic movement promoted the increase in the number of cells in the periodontal ligament on both tension and pressure sides. The increase in the number of cells in the periodontal ligament is believed to be due to the migration and cell division of undifferentiated mesenchymal cells.2015博士(歯学)松本歯科大
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