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Molecular Insight into Oral Health: Disease and Medicine

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: 20 August 2026 | Viewed by 552

Special Issue Editor


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Guest Editor
Department of Medical Neurobiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8558, Japan
Interests: oral medicine

Special Issue Information

Dear Colleagues,

The meaning of “oral health” is broad. The oral cavity cannot be considered healthy if it is not clean, and nor can it in the presence of diseases and symptoms such as swelling or pain. In the promotion of oral health, it is necessary to consider not only the state of oral hygiene but also the factors that promote or hinder it.

For instance, the congenital or medical suppression of salivation impairs self-cleaning by saliva, resulting in poor oral hygiene. Motor or cognitive impairments, resulting from conditions such as Parkinson’s disease or dementia, may prevent adequate oral cleaning. Consequently, the mouth becomes dirty, halitosis and caries are more likely to occur, and periodontal disease is more likely to progress. Additionally, dental and occlusal disorders are a major cause of oral health problems.

Conversely, fluoride and xylitol can prevent dental caries, and oral care drugs can promote oral health by preventing the development and progression of dental caries and periodontal disease.

In this Special Issue, we aim to compile the results of studies on biomolecules and bacterial molecules. We are also seeking to compile review articles on these molecules’ mechanisms of action, pathogenesis, and the diagnosis and treatment of the factors, diseases, and symptoms that affect oral health.

Dr. Norio Sogawa
Guest Editor

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Keywords

  • oral health
  • disease
  • molecular medicine
 

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Published Papers (1 paper)

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Research

22 pages, 11232 KB  
Article
DPP-Mediated Interaction of TAZ/β-Catenin Promotes the Differentiation of DPSCs into Odontoblasts
by Yinghua Chen, Adrienn Petho, Amudha Ganapathy, Velavan Bakthavachalam, Cassandra Villani and Anne George
Int. J. Mol. Sci. 2026, 27(10), 4599; https://doi.org/10.3390/ijms27104599 - 20 May 2026
Viewed by 144
Abstract
Dental pulp tissue contains mesenchymal stem/progenitor cells that possess high proliferative potential for self-renewal. They are neural-crest derived cells and exhibit multi-lineage differentiation properties. These progenitor stem cells are now recognized as being vital to the dentin regeneration process following injury. Understanding the [...] Read more.
Dental pulp tissue contains mesenchymal stem/progenitor cells that possess high proliferative potential for self-renewal. They are neural-crest derived cells and exhibit multi-lineage differentiation properties. These progenitor stem cells are now recognized as being vital to the dentin regeneration process following injury. Understanding the molecular mechanisms that mediate the differentiation of adult stem cells into odontoblasts and their use in the repair of the dentin–pulp complex is of significant interest in regenerative dental medicine. Dentin Phosphophoryn (DPP), synthesized and processed predominantly by the odontoblasts, functions both as a structural and signaling protein. We had previously demonstrated that DPP activates NF-κB and promotes Wnt5a expression in dental pulp stem cells. In this context, we observed that DPP can activate TAZ, a biologically potent transcriptional coactivator which serves as a downstream element of the NF-κB signaling cascade. Furthermore, binding of NF-κB p65 subunit to the TAZ promoter was facilitated by DPP stimulation, and their interaction was confirmed by ChIP analysis. In addition, DPP-dependent activation of the TAZ/TEAD reporter was confirmed by luciferase activity in DPSCs. Co-immunoprecipitation analysis confirmed the in vivo interaction between TAZ and β-catenin with DPP stimulation. This regulatory complex facilitated TAZ to bind to the conserved TEAD binding motifs of key gene targets involved in odontogenic differentiation such as RUNX2, OSX, OCN, ALP, BMP4, and WNT5A. Some of these genes also contain binding sites for the TCF/LEF transcription factors that interact with the Wnt effector, β-catenin. Activation of TAZ and β-catenin resulted in the upregulation of odontoblast gene expression and reduced expression in the presence of the TAZ–TEAD protein complex inhibitor. Using mandibles of DSPP KO and WT mice, we confirmed reduced TAZ and β-catenin protein levels in the dental pulp cells and in the odontoblasts of DSPP KO mice when compared with WT. Thus, DPP, an extracellular matrix protein, provides biological cues to activate the TAZ signaling pathway that can stimulate the terminal differentiation of DPSCs into functional odontoblasts. Full article
(This article belongs to the Special Issue Molecular Insight into Oral Health: Disease and Medicine)
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