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非甾体抗炎药对脂多糖诱导的牙髓和根尖周炎症的影响。

Effect of non-steroidal anti-inflammatory drugs on pulpal and periapical inflammation induced by lipopolysaccharide.

机构信息

School of Dentistry of Ribeirão Preto, University of São Paulo, Avenida do Café, s/n. CEP 14040-904, Ribeirão Preto, São Paulo, Brazil.

Universidade de Pernambuco, Arco Verde, Pernambuco, Brazil.

出版信息

Clin Oral Investig. 2021 Nov;25(11):6201-6209. doi: 10.1007/s00784-021-03919-3. Epub 2021 Apr 1.

DOI:10.1007/s00784-021-03919-3
PMID:33791868
Abstract

OBJECTIVES

The objective of this study was to evaluate the effect of non-steroidal anti-inflammatory drugs (NSAIDs) in controlling pulpal and periapical inflammation in vivo as a potential coadjutant systemic therapy for pulpitis.

MATERIALS AND METHODS

A suspension containing E. coli lipopolysaccharide (LPS; 1.0 μg/μL) was inoculated into the pulp chamber of the first molars of C57BL/6 mice (n = 72), and the animals were treated daily with indomethacin or celecoxib throughout the experimental periods. After 7, 14, 21, and 28 days, the tissues were removed for histopathological, histoenzymology, histometric, and immunohistochemical evaluation.

RESULTS

Inoculation of LPS into the pulp chamber induced the synthesis of the enzyme cyclooxygenase-2 (COX-2) in dental pulp and periapical region. Indomethacin and celecoxib treatment changed the profile of inflammatory cells recruited to dental pulp and to the periapex, which was characterized by a higher mononuclear cell infiltrate, compared to LPS inoculation alone which recruited a higher amount of polymorphonuclear neutrophils. Administration of indomethacin for 28 days resulted in the development of apical periodontitis and increased osteoclast recruitment, unlike celecoxib.

CONCLUSIONS

NSAIDs indomethacin and celecoxib changed the recruitment of inflammatory cells to a mononuclear profile upon inoculation of LPS into the pup chamber, but indomethacin enhanced periapical bone loss whereas celecoxib did not.

CLINICAL RELEVANCE

Celecoxib, a selective COX-2 inhibitor, can change the profile of inflammatory cells recruited to the dental pulp challenged with LPS and might a be potential systemic coadjutant for treatment of pulpitis.

摘要

目的

本研究旨在评估非甾体抗炎药(NSAIDs)在控制牙髓和根尖周炎症方面的作用,将其作为牙髓炎的潜在辅助全身治疗。

材料和方法

将含有大肠杆菌脂多糖(LPS;1.0 μg/μL)的混悬液接种到 C57BL/6 小鼠第一磨牙的牙髓室中(n = 72),并在整个实验期间每天用吲哚美辛或塞来昔布治疗动物。在第 7、14、21 和 28 天,取出组织进行组织病理学、组织化学、组织计量学和免疫组织化学评估。

结果

将 LPS 接种到牙髓室中诱导了牙髓和根尖周区域中酶环氧化酶-2(COX-2)的合成。吲哚美辛和塞来昔布治疗改变了募集到牙髓和根尖周的炎症细胞的特征,与单独 LPS 接种募集更高数量的多形核中性粒细胞相比,募集了更高数量的单核细胞浸润。与塞来昔布不同,吲哚美辛连续 28 天给药导致根尖周病的发展和破骨细胞募集增加。

结论

NSAIDs 吲哚美辛和塞来昔布改变了 LPS 接种到牙髓室后募集的炎症细胞的单核特征,但吲哚美辛增强了根尖周骨丢失,而塞来昔布没有。

临床意义

选择性 COX-2 抑制剂塞来昔布可以改变 LPS 刺激牙髓募集的炎症细胞的特征,可能是牙髓炎治疗的潜在辅助全身治疗药物。

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本文引用的文献

1
Pathogenesis of apical periodontitis: a literature review.根尖周炎的发病机制:文献综述
J Oral Maxillofac Res. 2012 Jan 1;2(4):e1. doi: 10.5037/jomr.2011.2401.
2
[Histopathology and etiopathogenesis of chronic apical periodontitis--periapical granuloma].[慢性根尖周炎——根尖肉芽肿的组织病理学与病因发病机制]
Epidemiol Mikrobiol Imunol. 2011 Jun;60(2):77-86.
MK-886 全身性抑制 5-脂氧合酶加重了小鼠模型中的根尖周炎骨丢失。
BMC Oral Health. 2023 Jan 10;23(1):11. doi: 10.1186/s12903-023-02712-w.