University of Oulu

Listyarifah D, Al-Samadi A, Salem A, et al. Infection and apoptosis associated with inflammation in periodontitis: An immunohistologic study. Oral Dis. 2017;23:1144–1154. https://doi.org/10.1111/odi.12711

Infection and apoptosis associated with inflammation in periodontitis : an immunohistologic study

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Author: Listyarifah, D1,2; Al‐Samadi, A3; Salem, A1,3;
Organizations: 1University of Helsinki, and Helsinki University Central Hospital Department of Medicine, Clinicum Helsinki Finland
2Universitas Gadjah Mada Department of Dental Biomedical Sciences Sleman Indonesia
3University of Helsinki, and Helsinki University Central Hospital Department of Oral and Maxillofacial Diseases Helsinki Finland
4Universitas Gadjah Mada Department of Periodontology Sleman Indonesia
5University of Oulu Department of Diagnostics and Oral Medicine Oulu Finland
6Université Laval Oral Ecology Research Group Quebec QC Canada
7University of Helsinki, and Helsinki University Central Hospital Department of Internal Medicine and Rehabilitation Helsinki Finland
8Karolinska Institutet Division of Periodontology Huddinge Sweden
Format: article
Version: accepted version
Access: embargoed
Persistent link: http://urn.fi/urn:nbn:fi-fe2017120855548
Language: English
Published: John Wiley & Sons, 2017
Publish Date: 2018-08-07
Description:

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.

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Series: Oral diseases
ISSN: 1354-523X
ISSN-E: 1601-0825
ISSN-L: 1354-523X
Volume: 23
Issue: 8
Pages: 1144 - 1154
DOI: 10.1111/odi.12711
OADOI: https://oadoi.org/10.1111/odi.12711
Type of Publication: A1 Journal article – refereed
Field of Science: 313 Dentistry
Subjects:
Funding: This study was supported by Directorate General of Human Resource for Science, Technology and Higher Education of Indonesia, Center for International Mobility (CIMO), Jane and Aatos Erkko Foundation, Selma and Maja- Lisa Selanders fund, Otto A. Malm Foundation, Sigrid Jusélius Foundation, grants from the Helsinki University Hospital Research Foundation, Helsinki, Finland, and the Karolinska Institutes, Stockholm, Sweden.
Copyright information: © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. All rights reserved. This is the peer reviewed version of the following article: Listyarifah D, Al-Samadi A, Salem A, et al. Infection and apoptosis associated with inflammation in periodontitis: An immunohistologic study. Oral Dis. 2017;23:1144–1154. https://doi.org/10.1111/odi.12711, which has been published in final form at https://doi.org/10.1111/odi.12711. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.