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Cellular and Molecular Mechanism in Periodontal Diseases II

A special issue of Applied Sciences (ISSN 2076-3417). This special issue belongs to the section "Applied Dentistry and Oral Sciences".

Deadline for manuscript submissions: closed (25 December 2022) | Viewed by 2272

Special Issue Editor


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Guest Editor
Bernhard Gottlieb University Clinic of Dentistry, Medical University of Vienna, 1090 Vienna, Austria
Interests: cellular and molecular mechanisms involved in the homeostasis of periodontal tissue in health and disease—regulation of inflammatory response in periodontitis; host interactions with bacteria and bacterial biofilms; dental stem cells and their role in tissue regeneration and immunomodulation; effect of implant surface characteristics on cell responses
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Special Issue Information

Dear Colleagues,

You are cordially invited to contribute to this Special Issue entitled “Cellular and Molecular Mechanisms in Periodontal Disease”.

Periodontitis is an extremely complex and multifactorial disease, leading to the destruction of all the components of the periodontium, namely, gingiva, periodontal ligament, cementum, and the alveolar bone. It is the main cause of tooth loss and is also associated with several systemic disorders. Nowadays, periodontitis is considered a major public health problem worldwide.

The mechanisms underlying the initiation and progression of periodontal disease are very complex and not entirely understood. The maintaining of oral health depends mainly on the homeostasis between oral microbiome and host immune systems, and its disruption is a major event in the initiation of periodontal disease. Host microbial homeostasis in the oral cavity could be disrupted by ecological, genetic, and epigenetic factors, as well as by subverting the host immune system by some keystone pathogens. The progression of periodontal disease and tissue destruction is mainly forced by the immune response to overgrowing oral biofilms. The initial role of the immune response is the elimination of the invading pathogens, but its initiation, progression, and resolution need to be tightly controlled on the cellular level. A dysregulated immune response is considered to be the major cause of periodontal tissue damage. The immune response is driven by different immune cell types, tissue-resident cells, and numerous pro- and anti-inflammatory cytokines. Understanding the exact mechanisms involved in the progression and control of the immune response is crucially important for the development of new strategies for periodontitis treatment and prevention.

This Special Issue welcomes in vitro, animal, and clinical studies on the cellular and molecular mechanisms involved in the maintenance of oral host–microbe homeostasis and the regulation of the immune response in periodontitis.

Prof. Dr. Oleh Andrukhov
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Applied Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • periodontal disease
  • host–microbial homeostasis
  • periodontal tissue destruction
  • immune response
  • innate immunity
  • polymorphonuclear leukocytes
  • macrophages
  • T cells
  • B cells
  • cytokines
  • regulation of inflammation

Published Papers (1 paper)

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Research

19 pages, 2343 KiB  
Article
Toll-Like Receptors 1/2/4/6 and Nucleotide-Binding Oligomerization Domain-Like Receptor 2 Are Key Damage-Associated Molecular Patterns Sensors on Periodontal Resident Cells
by Yu Chen, Xiao Xiao Wang, Corrie H. C. Ng, Sai Wah Tsao and Wai Keung Leung
Appl. Sci. 2021, 11(11), 4724; https://0-doi-org.brum.beds.ac.uk/10.3390/app11114724 - 21 May 2021
Cited by 2 | Viewed by 1775
Abstract
Background: Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are innate, damage-associated molecular patterns (DAMP) sensors. Their expressions in human periodontal resident cells and reactions toward irritations, such as hypoxia and lipopolysaccharide (LPS), remain not well characterized. This cross-sectional study aimed [...] Read more.
Background: Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are innate, damage-associated molecular patterns (DAMP) sensors. Their expressions in human periodontal resident cells and reactions toward irritations, such as hypoxia and lipopolysaccharide (LPS), remain not well characterized. This cross-sectional study aimed to investigate and characterize TLRs, NOD1/2 and NLRP1/2 expressions at the dento-gingival junction. Methods: Immunohistochemistry screening was carried out on periodontal tissue biopsies sections, while selected DAMP sensors signal and protein expression under Escherichia coli LPS (2 µg/mL) and/or hypoxia (1% O2), 24 h, by human gingival keratinocytes (HGK) or fibroblasts (HGF) were investigated. Results: Positive TLR1/2/4/5/6, NOD1/2 and NLRP1/2 immunostaining were observed in healthy and periodontitis biopsies with apparently more pocket epithelial cells positive for TLR2, TLR4 and NOD1/2. TLR1-6, NOD1/2 and NLRP1/2 messengers were detected in gingival/periodontal biopsies as well as healthy HGK and HGF explants. LPS and/or hypoxia induced signals and protein upregulation of NOD2 in HGKs or TLR1/6 and NOD2 in HGFs. Conclusion: Transcripts and proteins of TLR1/2/4/5/6, NOD1/2 and NLRP1/2 were expressed in human periodontal tissue in health and disease. Putting all observations together, NOD2, perhaps with TLR1/2/4/6, might be considered key, damage-associated molecular pattern sensors on periodontal resident cells. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanism in Periodontal Diseases II)
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