1990 Fiscal Year Final Research Report Summary
A Basic and Clinical Study on the Pathogenesis and Nature of the Periapical Lesions.
| Project/Area Number |
01304046
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| Research Category |
Grant-in-Aid for Co-operative Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Conservative dentistry
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
SUNADA Imao Tokyo Medical and Dental University Faculty of Dentistry Emeritus Professor, 歯学部, 名誉教授 (50005013)
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| Co-Investigator(Kenkyū-buntansha) |
SAITO Tsuyoshi Nihon University School of Dentistry Professor, 歯学部, 教授 (60059235)
MATSUMOTO Hiroshi Nagasaki University School of Dentistry Professor, 歯学部, 教授 (30013923)
NAGASAWA Hisashi Kyushu University Faculty of Dentistry Professor, 歯学部, 教授 (10013848)
NAKAMURA Jiro Tsurumi University School of Dental Medicine Professor, 歯学部, 教授 (90064336)
AONO Masao Kyushu University Faculty of Dentistry Professor, 歯学部, 教授 (70037498)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Periapical Lesion / Anaerobic Bacteria / Endotoxin / Immunocompetent Cell / Inflammatory Cell / Cytokaine / Ultrasonic Debridement / Endodontic-Periodontic Pathosis |
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| Research Abstract |
Sunada found that some macrophage-like cells infiltrated into the experimentally induced periapical lesions, and that most of them were Ia-antigen positive. Uno reported that superoxidating process was related to the pathogenesis of the periapical lesions. Kawanami revealed most of endotoxin in the root apex was found in the root canal and the superficial layer of the dentinal wall. Ueno demonstrated that the perfect disinfection of the root canal was essential for the reduction of periapical inflammation. Tamazawa made interesting findings concerning the clinical success of the root canal treatment. Maita found the correlation of putrescine concentration in the root canal system with clinically observed pain in patients with periapical lesions. Saito demonstrated that the phagocytic ability of polymorphonuclear leukocytes in the exudation from periapical pathosis was weaker than that in the peripheral blood flow. K. Matsumoto observed some inflammatory cells in the periapical lesion u
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sing an electron microscope. Nakamura found that there was some correlations between clinical symptoms and periapical pathological changes. Ebisu identified anaerobic bacteria even in the prepared root canals, and suggested that there were correlations between the presence of bacteria and clinical symptoms. Murayama showed that the numbers and species of bacteria in the root canal were much less than those in the periodontal pockets. Yamamoto and Soh found that the enlargement of the root canal using ultrasonic apparatus was more effective than any other enlarging method, while it produced much more extruded substance beyond the apical foramen. Aono demonstrated that a lot of IgG-containing cells in the experimentally induced periapical lesions. Nagasawa showed the similarity of the root end structures between the rat and human maxillary first molars. H. Matsumoto showed the difficulties of producing heat-induced periapical lesions. Nagaoka recognized that Bacteroides species caused the periapical inflammation, and suggested that the immunological process played an important role in its development. Less
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