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牙周炎中与炎症相关的感染和细胞凋亡:一项免疫组织化学研究。

Infection and apoptosis associated with inflammation in periodontitis: An immunohistologic study.

机构信息

Department of Medicine, Clinicum, University of Helsinki, and Helsinki University Central Hospital, Helsinki, Finland.

Department of Dental Biomedical Sciences, Faculty of Dentistry, Universitas Gadjah Mada, Sleman, Indonesia.

出版信息

Oral Dis. 2017 Nov;23(8):1144-1154. doi: 10.1111/odi.12711. Epub 2017 Aug 7.

DOI:10.1111/odi.12711
PMID:28686335
Abstract

OBJECTIVE

Evidence of increased apoptosis is observed in periodontitis and may be associated with destruction of the periodontal tissue caused by the increased cell death, with the release of danger signals and subsequent stimulation of the proinflammatory processes. However, the exact mechanisms associated with these processes remain unclear. This study aimed to investigate the presence of the periodontal pathogen Treponema denticola, apoptosis, high mobility group box 1 as a damage-associated molecular pattern, and several inflammatory markers in periodontitis and gingivitis subjects.

MATERIALS AND METHODS

Soft tissue specimens from gingival tissues of periodontitis and gingivitis patients were used for immunohistochemical and immunofluorescence staining of T. denticola chymotrypsin-like proteinase (CTLP), apoptosis markers, high mobility group box 1, Toll-like receptor 4, inflammatory cell markers, and proinflammatory cytokines.

RESULTS

Treponema denticola was detected in all periodontitis-affected tissues. This was associated with a significant increase in the number of apoptotic cells, including macrophages, alterations in the expression of high mobility group box 1 and its receptor, and increased levels of proinflammatory cytokines compared with gingivitis.

CONCLUSIONS

In summary, the presence of T. denticola (especially its CTLP), apoptosis, high mobility group box 1, and inflammatory markers suggests their potential involvement in the pathogenesis of periodontitis.

摘要

目的

在牙周炎中观察到细胞凋亡增加的证据,并且可能与细胞死亡增加导致的牙周组织破坏有关,细胞死亡会释放危险信号,随后刺激炎症过程。然而,与这些过程相关的确切机制仍不清楚。本研究旨在研究牙周病原体密螺旋体、凋亡、高迁移率族蛋白 1 作为损伤相关分子模式,以及几种炎症标志物在牙周炎和牙龈炎患者中的存在情况。

材料和方法

使用牙周炎和牙龈炎患者牙龈组织的软组织标本进行密螺旋体蛋白酶(CTLP)、凋亡标志物、高迁移率族蛋白 1、Toll 样受体 4、炎症细胞标志物和促炎细胞因子的免疫组织化学和免疫荧光染色。

结果

密螺旋体在所有受牙周炎影响的组织中均被检测到。这与凋亡细胞数量的显著增加有关,包括巨噬细胞,高迁移率族蛋白 1 及其受体的表达改变,以及与牙龈炎相比,促炎细胞因子水平的升高。

结论

综上所述,密螺旋体(尤其是其 CTLP)、凋亡、高迁移率族蛋白 1 和炎症标志物的存在表明它们可能参与牙周炎的发病机制。

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