Effects of ageing on localizations of immunocompetent cells in periapical lesions in the rat mandibular molar

根尖周围病变主要是由局部免疫防御反应和炎症反应引起的。研究还表明，老年动物的免疫系统和组织修复受损：特别是，t细胞依赖性、细胞介导的免疫反应随着年龄的增长效率降低。因此，衰老可能是影响根尖周病变进程的因素之一。我们的目的是比较年轻和年老大鼠磨牙根尖周病变后免疫活性细胞的定位，并阐明衰老对根尖周病变过程的影响。选用18只16月龄雄性Wistar大鼠和18只2月龄雄性Wistar大鼠。为了诱发根尖周围病变，对下颌第一磨牙进行了牙髓切除术。然后，将他们自己的粪便溶解在无菌肉汤培养基中注入根管。牙髓处理后4、7、14和28天，用戊巴比妥麻醉动物，并灌注4%的聚甲醛溶液。每只动物的下颌骨均游离解剖，在同一固定液中浸泡1天，然后在14% EDTA溶液中4℃脱钙2个月。下颌骨用石蜡包裹。中、远端、纵向切片依次切割，厚度为5 μm。利用单克隆抗体OX-6（抗II类分子）、ED1（泛巨噬细胞抗体，也与树突状细胞反应）和ED2（抗组织巨噬细胞）对切片进行免疫过氧化物酶染色。本研究结果表明，实验性尖周病变的发生过程在年轻大鼠和老年大鼠之间存在差异。在老年大鼠中，与年轻大鼠相比，根尖周围病变周围的炎症反应似乎不那么严重，并且变成慢性的，并且修复倾向于延迟。(1) ed1阳性细胞的定位：16月龄大鼠在4天和7天时，在根尖周围病变及周围组织中出现了许多ed1阳性的单核和多核细胞；在第14和28天，ed1阳性的多核细胞从骨尖到骨尖邻近骨表面。在2月龄大鼠中，28天ed1阳性细胞出现减少。(2) ED2和0x6阳性细胞的定位：16月龄大鼠，4 ~ 14天时，ED2和0x6阳性细胞的分布和数量基本一致，但28天时，牙周韧带根尖和中根水平的阳性细胞有增加的趋势。在2个月大的大鼠中，这些阳性细胞的定位在7天和28天之间似乎没有差异。我们认为老年大鼠的慢性炎症反应可能是由于巨噬细胞、淋巴细胞和浆细胞起主要作用的免疫机制随着年龄的增长而受损。少

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 … More 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