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Molecular Mechanisms of Periodontal Disease 3.0
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Molecular Mechanisms of Periodontal Disease 3.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 10102

Special Issue Editor

Prof. Dr. Mikihito Kajiya

E-Mail Website
Guest Editor
Department of Periodontal Medicine, Applied Life Sciences, Institute of Biomedical & Health Sciences, Graduate School of Biomedical & Health Sciences, Hiroshima University, Minami-ku, Hiroshima, Japan
Interests: stem cells; bone biology; signal transduction; cytokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Periodontitis is a chronic inflammatory disease characterized by lymphocytic infiltration and alveolar bone destruction, along with tooth loss. Accumulated lines of evidence suggest that such destructive inflammation is elicited by the host innate and adaptive immune response to periodontal biofilm-associated multiple microorganisms. In addition, several inflammatory cytokines produced from lymphocytes, leukocytes, fibroblasts, and gingival epithelial cells in the context of host immune responses have been identified as key molecules inducing periodontal tissue destruction. More specifically, proinflammatory cytokines, including IL-6 and IL-17, facilitate the RNAKL expression level in fibroblasts or lymphocytes, which results in the induction of bone resorption. However, despite advances in our understanding of its etiology, scientific endeavors to fight against periodontal disease have progressed little. Accordingly, it is necessary to deepen our understanding of the molecular mechanisms of the immune system against oral microorganisms, in order to develop preventive or therapeutic regimens. To this end, this Special Issue, which is a continuation of a previous successful Special Issue on the molecular mechanisms of periodontal disease, focuses on novel immune reaction systems from the molecular level (microbe, microRNA, inflammatory cytokine signaling cascade, etc.) to the cellular level (Th1, Th2, Th17, Treg, and B cells activity, osteoclastogenesis, dendritic cells and monocytes immune response, the role of fibroblasts/epithelial cells in inflammation, etc.) in mouse periodontal disease models.

Dear everyone—I am delighted to inform you that our second Special Issue, “Molecular Mechanism of Periodontal Disease 2.0”, was a massive success due to your great efforts and scientific contributions. This continuous success encourages me to relaunch the following Special Issue, ver 3.0, which will deepen our knowledge of periodontitis and encourage the development of novel promising therapies.

Prof. Dr. Mikihito Kajiya
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • periodontitis
  • immune response
  • periodontal pathogens
  • bone resorption
  • RANKL

Related Special Issues

Published Papers (5 papers)

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Research

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14 pages, 21200 KiB  
Article
IL-1 Generated by Oral Squamous Cell Carcinoma Stimulates Tumor-Induced and RANKL-Induced Osteoclastogenesis: A Possible Mechanism of Bone Resorption Induced by the Infiltration of Oral Squamous Cell Carcinoma
by Yuki Fukawa, Kou Kayamori, Maiko Tsuchiya and Tohru Ikeda
Int. J. Mol. Sci. 2023, 24(1), 688; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24010688 - 30 Dec 2022
Cited by 1 | Viewed by 1522
Abstract
We previously observed a novel osteoclastogenesis system that is induced by oral squamous cell carcinoma (OSCC) cells, which target osteoclast precursor cells (OPC) without upregulation of the master transcriptional factor of osteoclastogenesis, NFATc1. Here, we analyzed inflammatory cytokines that were preferentially expressed in [...] Read more.
We previously observed a novel osteoclastogenesis system that is induced by oral squamous cell carcinoma (OSCC) cells, which target osteoclast precursor cells (OPC) without upregulation of the master transcriptional factor of osteoclastogenesis, NFATc1. Here, we analyzed inflammatory cytokines that were preferentially expressed in one of the osteoclastogenic OSCC cell lines, namely NEM, compared with the subclone that had lost its osteoclastogenic properties. Based on a gene expression microarray and a protein array analyses, IL-1, IL-6, IL-8, and CXCL1 were chosen as candidates responsible for tumor-induced osteoclastogenesis. From the results of the in vitro osteoclastogenesis assay using OPCs cultured with OSCC cells or their culture supernatants, IL-1 was selected as a stimulator of both OSCC-induced and RANKL-induced osteoclastogenesis. The IL-1 receptor antagonist significantly attenuated osteoclastogenesis induced by NEM cells. The stimulatory effects of IL-1 for OSCC-induced and RANKL-induced osteoclastogenesis were effectively attenuated with cannabidiol and denosumab, respectively. These results suggest that IL-1 secreted from OSCC cells stimulates not only tumor-induced osteoclastogenesis targeting OPCs but also physiological RANKL-induced osteoclastogenesis, and this may be the biological mechanism of bone resorption induced by the infiltration of OSCC. These results also suggest that IL-1 inhibitors are candidates for therapeutic agents against bone resorption induced by OSCC. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 3.0)
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15 pages, 2923 KiB  
Article
Proof-of-Principle Study Suggesting Potential Anti-Inflammatory Activity of Butyrate and Propionate in Periodontal Cells
by Ana Flávia Piquera Santos, Lara Cristina Cunha Cervantes, Layla Panahipour, Francisley Ávila Souza and Reinhard Gruber
Int. J. Mol. Sci. 2022, 23(19), 11006; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231911006 - 20 Sep 2022
Cited by 8 | Viewed by 2011
Abstract
Short-chain fatty acids (SCFAs) are potent immune modulators present in the gingival crevicular fluid. It is therefore likely that SCFAs exert a role in periodontal health and disease. To better understand how SCFAs can module inflammation, we screened acetic acid, propionic acid, and [...] Read more.
Short-chain fatty acids (SCFAs) are potent immune modulators present in the gingival crevicular fluid. It is therefore likely that SCFAs exert a role in periodontal health and disease. To better understand how SCFAs can module inflammation, we screened acetic acid, propionic acid, and butyric acid for their potential ability to lower the inflammatory response of macrophages, gingival fibroblasts, and oral epithelial cells in vitro. To this end, RAW 264.7 and primary macrophages were exposed to LPSs from Porphyromonas gingivalis (P. gingivalis) with and without the SCFAs. Moreover, gingival fibroblasts and HSC2 oral epithelial cells were exposed to IL1β and TNFα with and without the SCFAs. We report here that butyrate was effective in reducing the lipopolysaccharide (LPS)-induced expression of IL6 and chemokine (C-X-C motif) ligand 2 (CXCL2) in the RAW 264.7 and primary macrophages. Butyrate also reduced the IL1β and TNFα-induced expression of IL8, chemokine (C-X-C motif) ligand 1 (CXCL1), and CXCL2 in gingival fibroblasts. Likewise, butyrate lowered the induced expression of CXCL1 and CXCL2, but not IL8, in HSC2 cells. Butyrate further caused a reduction of p65 nuclear translocation in RAW 264.7 macrophages, gingival fibroblasts, and HSC2 cells. Propionate and acetate partially lowered the inflammatory response in vitro but did not reach the level of significance. These findings suggest that not only macrophages, but also gingival fibroblasts and oral epithelial cells are susceptive to the anti-inflammatory activity of butyrate. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 3.0)
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9 pages, 1813 KiB  
Article
TGF-β Signalling Mediates the Anti-Inflammatory Activity of Enamel Matrix Derivative In Vitro
by Layla Panahipour, Mariane Beatriz Sordi, Zahra Kargarpour and Reinhard Gruber
Int. J. Mol. Sci. 2022, 23(17), 9778; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23179778 - 29 Aug 2022
Cited by 3 | Viewed by 1565
Abstract
Enamel matrix derivative (EMD) prepared from extracted porcine fetal tooth material can support the regrow of periodontal tissues. Previous findings suggest that EMD has anti-inflammatory properties and TGF-β activity in vitro. However, the anti-inflammatory activity of EMD is mediated via TGF-β has not [...] Read more.
Enamel matrix derivative (EMD) prepared from extracted porcine fetal tooth material can support the regrow of periodontal tissues. Previous findings suggest that EMD has anti-inflammatory properties and TGF-β activity in vitro. However, the anti-inflammatory activity of EMD is mediated via TGF-β has not been considered. To this aim, we first established a bioassay to confirm the anti-inflammatory activity of EMD. The bioassay was based on the RAW 264.7 macrophage cell line and proven with primary macrophages where EMD significantly reduced the forced expression of IL-6. We then confirmed the presence of TGF-β1 in EMD by immunoassay and by provoking the Smad2/3 nuclear translocation in RAW 264.7 macrophages. Next, we took advantage of the TGF-β receptor type I kinase-inhibitor SB431542 to block the respective signalling pathway. SB431542 reversed the anti-inflammatory activity of EMD and TGF-β in a bioassay when IL-6 and CXCL2 expression was driven by the LPS stimulation of RAW 264.7 macrophages. This central observation was supported by showing that SB431542 reversed the anti-inflammatory activity of EMD using IL-1β and TNF-α-stimulated ST2 bone marrow stromal cells. Together, these findings implicate that the TGF-β activity mediates at least part of the anti-inflammatory activity of EMD in vitro. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 3.0)
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11 pages, 2359 KiB  
Article
Platelet-Rich Fibrin Reduces IL-1β Release from Macrophages Undergoing Pyroptosis
by Mariane Beatriz Sordi, Layla Panahipour, Zahra Kargarpour and Reinhard Gruber
Int. J. Mol. Sci. 2022, 23(15), 8306; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23158306 - 27 Jul 2022
Cited by 10 | Viewed by 1877
Abstract
Background: Pyroptosis is a catabolic process relevant to periodontal disorders for which interleukin-1β (IL-1β) inflammation is central to the pathophysiology of the disease. Despite platelet-rich fibrin (PRF) anti-inflammatory properties and its application to support periodontal regeneration, the capacity of PRF to modulate pyroptosis, [...] Read more.
Background: Pyroptosis is a catabolic process relevant to periodontal disorders for which interleukin-1β (IL-1β) inflammation is central to the pathophysiology of the disease. Despite platelet-rich fibrin (PRF) anti-inflammatory properties and its application to support periodontal regeneration, the capacity of PRF to modulate pyroptosis, specifically the production and release of IL-1β, remains unknown. The question arises whether PRF could regulate IL-1β release from macrophages in vitro. Methods: To answer this question, RAW 264.7 macrophages and primary macrophages obtained from murine bone marrow were primed with PRF before being challenged by lipopolysaccharide (LPS). Cells were then analysed for the pyroptosis signalling components by gene expression analyses and IL-1β secretion at the protein level. The release of mitochondrial reactive oxygen species (ROS) was also detected. Results: PRF lowered the LPS-induced expression of IL-1β and NLRP3 inflammasome, caspase-11 and IL-18 in primary macrophages, and IL-1β and caspase-11 in RAW 264.7 cells. Additionally, PRF diminished the secretion of IL-1β at the protein level in LPS-induced RAW 264.7 cells. This was shown through immunoassays performed with the supernatant and further confirmed by analysing the lysates of permeabilised cells. Furthermore, PRF reduced the ROS release provoked by LPS in RAW 264.7 cells. Finally, to enhance IL-1β release from the LPS-primed macrophages, we introduced a second signal with adenosine triphosphate (ATP). In this setting, PRF significantly reduced IL-1β release in RAW 264.7 cells and a trend to diminish IL-1β release in primary macrophages. Conclusion: These findings suggest that PRF can reduce IL-1β release and, at least in part, inhibit pyroptosis-related factors in LPS-challenged macrophages. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 3.0)
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Review

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21 pages, 822 KiB  
Review
Therapeutic and Metagenomic Potential of the Biomolecular Therapies against Periodontitis and the Oral Microbiome: Current Evidence and Future Perspectives
by Simona Santonocito, Salvatore Ferlito, Alessandro Polizzi, Vincenzo Ronsivalle, Rossana Sclafani, Alessandra Valletta, Antonino Lo Giudice, Raffaele Cavalcanti, Gianrico Spagnuolo and Gaetano Isola
Int. J. Mol. Sci. 2022, 23(22), 13708; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232213708 - 08 Nov 2022
Cited by 4 | Viewed by 2076
Abstract
The principles of periodontal therapy are based on the control of microbial pathogens and host factors that contribute to biofilm dysbiosis, with the aim of modulating the progression of periodontitis and periodontal tissue destruction. It is currently known how differently each individual responds [...] Read more.
The principles of periodontal therapy are based on the control of microbial pathogens and host factors that contribute to biofilm dysbiosis, with the aim of modulating the progression of periodontitis and periodontal tissue destruction. It is currently known how differently each individual responds to periodontal treatment, depending on both the bacterial subtypes that make up the dysbiotic biofilm and interindividual variations in the host inflammatory response. This has allowed the current variety of approaches for the management of periodontitis to be updated by defining the goals of target strategies, which consist of reducing the periodontopathogenic microbial flora and/or modulating the host-mediated response. Therefore, this review aims to update the current variety of approaches for the management of periodontitis based on recent target therapies. Recently, encouraging results have been obtained from several studies exploring the effects of some targeted therapies in the medium- and long-term. Among the most promising target therapies analyzed and explored in this review include: cell-based periodontal regeneration, mediators against bone resorption, emdogain (EMD), platelet-rich plasma, and growth factors. The reviewed evidence supports the hypothesis that the therapeutic combination of epigenetic modifications of periodontal tissues, interacting with the dysbiotic biofilm, is a key step in significantly reducing the development and progression of disease in periodontal patients and improving the therapeutic response of periodontal patients. However, although studies indicate promising results, these need to be further expanded and studied to truly realize the benefits that targeted therapies could bring in the treatment of periodontitis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Periodontal Disease 3.0)
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