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Oral Medicine and Immunity 2.0
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Oral Medicine and Immunity 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (15 February 2024) | Viewed by 3513

Special Issue Editor

Dr. Kenichi Kumagai

E-Mail Website
Guest Editor
Department of Oral and Maxillofacial Surgery, Dentistry and Orthodontics, The University of Tokyo Hospital, Tokyo 113-8655, Japan
Interests: clinical immunology; cancer immunity; oral mucosal disease; T cell receptor; oral microbiome; temporomandibular disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The oral cavity is the port of entry to the gastrointestinal and respiratory tracts, characterised by the juxtaposition of soft and hard tissues, and it is continuously subject to challenges by the external environment, such as foreign antigens or material.

Oral microbial communities are now seen as the fundamental etiological agent in oral diseases through their interface with host inflammatory responses. Thus, it is essential to understand the molecular mechanisms and pathogenicity of oral diseases in terms of immunological and microbiological perspectives.

Oral medicine is concerned with the diagnosis and management of oral diseases, including oral mucosal disease, oral cancer, salivary gland disorders, temporomandibular disorders, and the oral manifestations of systemic and infectious diseases. This Special Issue aims to cover all areas of oral medicine to study various oral diseases in terms of immunological and microbiological perspectives.

Dr. Kenichi Kumagai
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

  • oral immunity
  • oral microbiology
  • oral mucosal disease
  • oral cancer
  • salivary gland disorders
  • temporomandibular disorders
  • oral manifestations of systemic and infectious diseases
  • T cell
  • B cell
  • microbiome

Related Special Issue

Published Papers (2 papers)

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Research

16 pages, 16867 KiB  
Article
Increased RBP4 and Asprosin Are Novel Contributors in Inflammation Process of Periodontitis in Obese Rats
by Yuwei Zhang, Yifei Zhang, Yutian Tan, Xiao Luo and Ru Jia
Int. J. Mol. Sci. 2023, 24(23), 16739; https://doi.org/10.3390/ijms242316739 - 25 Nov 2023
Viewed by 1244
Abstract
There is a significant comorbidity between obesity and periodontitis, while adipokines are pivotal in the immunoinflammatory process, which may play a role in this special relationship. We aimed to assess the effect of adipokines as mediators in the progression of periodontitis in obese [...] Read more.
There is a significant comorbidity between obesity and periodontitis, while adipokines are pivotal in the immunoinflammatory process, which may play a role in this special relationship. We aimed to assess the effect of adipokines as mediators in the progression of periodontitis in obese Sprague Dawley rats. Rats were divided into four groups: normal body weight with and without periodontitis and obesity with and without periodontitis. Experimental obesity and periodontitis were induced by a high-fat diet or ligaturing, and the effect was measured using metabolic and micro-computed tomography analysis and histological staining. Compared with the other three groups, the group of periodontitis with obesity (OP) had the heaviest alveolar bone absorption, the largest increase in osteoclasts, the utmost inflammatory cell infiltration and the highest expressions of pro-inflammatory cytokines and nuclear factor-kappa B ligand (RANKL); meanwhile, its expression of the osteogenesis-related gene was the lowest among the four groups. The expressions of leptin, visfatin, resistin, retinol-binding protein 4 (RBP4) and asprosin were upregulated, while adiponectin was decreased significantly in OP. The strong positive associations between the periodontal or circulating levels of RBP4 (or asprosin) and the degree of alveolar resorption in experimental periodontitis and obese rats were revealed. The upregulated expression of inflammation biomarkers, the corresponding degradation in connective tissue and the generation of osteoclasts in periodontitis were activated and exacerbated in obesity. The elevated level of RBP4/asprosin may contribute to a more severe periodontal inflammatory state in obese rats. Full article
(This article belongs to the Special Issue Oral Medicine and Immunity 2.0)
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12 pages, 3201 KiB  
Article
Sirt6 Activation Ameliorates Inflammatory Bone Loss in Ligature-Induced Periodontitis in Mice
by Myung Jin Lee, Hyang Hwa Ryu, Jae Won Hwang, Jung Ryul Kim, Eui-Sic Cho, Jin Kyeong Choi and Young Jae Moon
Int. J. Mol. Sci. 2023, 24(13), 10714; https://doi.org/10.3390/ijms241310714 - 27 Jun 2023
Cited by 4 | Viewed by 1747
Abstract
Periodontitis is an inflammatory disease caused by microorganisms that induce the destruction of periodontal tissue. Inflamed and damaged tissue produces various inflammatory cytokines, which activate osteoclasts and induce alveolar bone loss and, eventually, tooth loss. Sirt6 expression suppresses inflammation and bone resorption; however, [...] Read more.
Periodontitis is an inflammatory disease caused by microorganisms that induce the destruction of periodontal tissue. Inflamed and damaged tissue produces various inflammatory cytokines, which activate osteoclasts and induce alveolar bone loss and, eventually, tooth loss. Sirt6 expression suppresses inflammation and bone resorption; however, its role in periodontitis remains unclear. We hypothesized that Sirt6 has a protective role in periodontitis. To understand the role of Sirt6 in periodontitis, we compared periodontitis with ligature placement around the maxillary left second molar in 8-week-old control (C57BL/6J) male mice to Sirt6-overexpressing Tg (Sirt6Tg) mice, and we observed the resulting phenotypes using micro-CT. MDL801, a Sirt6 activator, was used as a therapy for periodontitis through oral gavage. Pro-inflammatory cytokines and increased osteoclast numbers were observed in alveolar bone tissue under periodontitis surgery. In the same condition, interestingly, protein levels from Sirt6 were the most downregulated among sirtuins in alveolar bone tissue. Based on micro-CT and CEJ-ABC distance, Sirt6Tg was observed to resist bone loss against ligature-induced periodontitis. Furthermore, the number of osteoclasts was significantly reduced in Sirt6Tg-ligated mice compared with control-ligated mice, although systemic inflammatory cytokines did not change. Consistent with this observation, we confirmed that bone loss was significantly reduced when MDL801, a Sirt6 activator, was included in the ligation mouse model. Our findings demonstrate that Sirt6 activation prevents bone loss against ligature-induced periodontitis. Thus, a Sirt6 activator may provide a new therapeutic approach for periodontitis. Full article
(This article belongs to the Special Issue Oral Medicine and Immunity 2.0)
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