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犬根尖周组织对未感染和感染失活牙髓反应的组织学研究。

Histological study of periradicular tissue responses to uninfected and infected devitalized pulps in dogs.

作者信息

Lin Louis M, Di Fiore Peter M, Lin Jarshen, Rosenberg Paul A

机构信息

Department of Endodontics, Advanced Education Program in Endodontics, New York University College of Dentistry, New York, NY 10010, USA.

出版信息

J Endod. 2006 Jan;32(1):34-8. doi: 10.1016/j.joen.2005.10.010.

DOI:10.1016/j.joen.2005.10.010
PMID:16410065
Abstract

Uninfected necrotic tissue, such as that which follows a myocardial or cerebral infarct, is capable of inducing an inflammatory reaction. Eventually, the infarct is organized by granulation tissue. Why then, does uninfected devitalized pulp tissue, such as in traumatized teeth, not cause periradicular inflammation and does not become organized by granulation tissue? Four beagle dogs were used in this experiment. A total of 48 teeth, which included 24 maxillary and 24 mandibular incisors, were aseptically devitalized, leaving residual pulp tissues in the root canals, and equally divided into two groups. Group A (24 uninfected): A sterile cotton pellet was placed deep into the canal orifice before the pulp chamber and access opening were closed with a layer of zinc-oxide eugenol cement followed by glass ionomer cement. Group B (24 infected): The teeth were left open to the oral cavity for 7 days and then closed with a cotton pellet and zinc-oxide eugenol and glass ionomer cement. The animals were sacrificed one year after the experiment and prepared for histological examination of periradicular tissue responses to uninfected and infected devitalized pulp tissues. The results indicate that uninfected devitalized pulp tissues did not continuously release inflammatory mediators and cause persistent periradicular inflammation over a period of one year. However, infected devitalized pulp tissues induced various degrees of periradicular inflammation. Only the apical few millimeters of uninfected devitalized pulp tissue in the root canals were organized by granulation tissue from vital periodontal ligament tissue.

摘要

未感染的坏死组织,如心肌梗死或脑梗死之后出现的坏死组织,能够引发炎症反应。最终,梗死灶由肉芽组织机化。那么,为什么未感染的失活牙髓组织,比如外伤牙中的牙髓组织,不会引起根尖周炎,也不会由肉芽组织机化呢?本实验选用了4只比格犬。总共48颗牙齿,包括24颗上颌切牙和24颗下颌切牙,在无菌条件下使其失活,根管内留有残余牙髓组织,并将其平均分为两组。A组(24颗未感染牙齿):在髓腔和进入开口封闭之前,将无菌棉球深入放置到根管口,先用一层氧化锌丁香酚水门汀封闭,随后再用玻璃离子水门汀封闭。B组(24颗感染牙齿):让牙齿向口腔开放7天,然后用棉球、氧化锌丁香酚水门汀和玻璃离子水门汀封闭。实验一年后处死动物,制备标本用于组织学检查根尖周组织对未感染和感染失活牙髓组织的反应。结果表明,未感染的失活牙髓组织在一年的时间内不会持续释放炎症介质并引发持续的根尖周炎。然而,感染的失活牙髓组织会引发不同程度的根尖周炎。根管内未感染的失活牙髓组织只有根尖几毫米由来自活力牙周膜组织的肉芽组织机化。

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