[Response of exposed pulp to capping agents in germ-free rat molars].

[Response of exposed pulp to capping agents in germ-free rat molars].
复制标题

[无菌大鼠磨牙暴露的牙髓对盖帽剂的反应]。

DOI:
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发表时间:
1983
期刊:
Kokubyo Gakkai zasshi. The Journal of the Stomatological Society, Japan
影响因子:
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通讯作者:
T. Aoki
T. Aoki
中科院分区:
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文献类型:
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作者:
T. Aoki

文献摘要

被引文献

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采用无菌大鼠和常规大鼠,对氢氧化钙或氧化锌和丁香酚粘固剂对牙髓的反应进行了组织病理学研究。用P1/2圆钻通过牙齿近中面暴露上第一磨牙牙髓,并覆盖覆盖剂。观察期为术后1、2、4、7、10、14和28天。得到的结果如下:1)在常规大鼠中,在整个观察期间,由于细菌污染,观察到牙髓严重炎症。牙髓本身对封端剂的反应无法准确评估。2)氢氧化钙覆盖的无菌鼠牙髓,术后28天炎症轻微,钙化管状牙本质桥较高。3)在无菌大鼠牙髓覆盖氧化锌和丁香酚水泥,炎症是中度和相对较差的钙化牙本质桥没有牙本质小管术后28天观察。4)在无菌大鼠中,其牙髓对口腔环境开放,牙髓的反应是所有实验组中最温和的。术后28天,该组牙本质桥的钙化程度略高于氧化锌丁香油粘固粉盖髓。5)牙本质碎片的存在减弱了牙髓组织对试剂的反应,但牙本质桥的形成被延迟。
The response of the dental pulp to calcium hydroxide or zinc oxide and eugenol cement was investigated histopathologically, using the germ-free and conventional rats. The upper first molar pulp was exposed with a p1/2 round bur through the mesial surface of the teeth and covered with the capping agents. The observation period was 1, 2, 4, 7, 10, 14 and 28 days postoperatively. The results obtained were as follows: 1) In the conventional rats, severe inflammation of the pulp was observed as the result of bacterial contamination throughout the observation period. The response of the pulp itself to the capping agents could not be assessed exactly. 2) In the germ-free rat pulp covered with calcium hydroxide, the inflammation was slight and a higher calcified tubular dentin bridge was observed 28 days postoperatively. 3) In the germ-free rat pulp covered with zinc oxide and eugenol cement, the inflammation was moderate and a relatively poorly calcified dentin bridge without the dentinal tubules was observed 28 days postoperatively. 4) In the germ-free rat whose pulp was left open to the oral environment, the response of the pulp was the mildest of all the experimental groups. The calcification of the dentin bridge of this group was slightly higher than that of the pulp capped with zinc oxide and eugenol cement 28 days postoperatively. 5) The presence of the dentin chips weakened the response of the pulp tissue to the agent, but the formation of the dentin bridge was delayed.