Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥1,600,000 (Direct Cost: ¥1,600,000)
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Research Abstract |
Periapical lesions have been shown to be induced mainly by local immune defense reactions against bacterial infection and inflammatory reactions. It has also been shown that the immune system and tissue repair are impaired in older animals : especially, T-cell dependent, cell mediated immunity reacts less efficiently with increasing age. Thus, ageing may be one of factors influencing the process of periapical lesions. Our aims here were to compare localizations of immunocompetent cells after experimental periapical lesions in molar teeth between young and old rats, and to elucidate the effects of ageing on the processes of periapical lesions. Eighteen old (16 month-old) and eighteen young (2 month-old) male Wistar rats were used. To induce periapical lesions, a pulpectomy was performed on the mandlbular first molar. Then, their own excrement dissolved in a sterile broth medium was infused into the root canal. At 4, 7, 14 and 28 days after pulp treatment, the animals were anaesthetized w
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ith pentobarbital and perfused with 4% parafolmaldehyde solution. In each animal, the mandibles were dissected free, immersed in the same fixative solution for a day, and then decalcified in 14% EDTA solution at 4℃ for 2 months. The mandibles were embedded in paraffin wax. Mesio-distal, longitudinal sections were cut serially at a thickness of 5 μm. Immunoperoxidase staining was done on sections by the use of monoclonal antibodies OX-6 (anti-class II molecules) , ED1 (a pan-macrophage antibody, reactive also with dendritic cells), and ED2 (anti-tissue macrophages). The present observation indicated that the processes of experimental periapical lesions were different between young and old rats. In the old rats, the inflammatory reactions around the periapical lesions appeared to be less severe, and to become chronic, and the repair tended to delay, as compared with the young rats. (1) localization of ED1-positive cells : In 16 month-old rats, there appeared to be many ED1-positive mononuclear and polynuclear cells in periapical lesions and surrounding tissues at 4 and 7 days ; at 14 and 28 days, ED1-positive polynuclear cells were still seen adjacent to bone surfaces from apical to apex. In 2 month-old rats, at 28 days ED1-positive cells appeared to decrease. (2) localizations of ED2 and 0X6-positive cells : In 16 month-old rats, distributions and numbers of ED2 and 0X6-positive cells appeared to be similar from 4 to 14 days, but the positive cells tended to increase at 28 days in the periodontal ligament at apical and mid-root levels. In 2 month-old rats, there appeared to be no differences in localizations of those positive cells between 7 and 28 days. We assume that the chronic inflammatory reactions in the old rats may be due to the impairment with ageing of the immune mechanisms where macrophages, lymphocytes, and plasma cells play main roles. Less
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