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Biology
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Understanding the Molecular Basis of Genetic Dental Diseases
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Understanding the Molecular Basis of Genetic Dental Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 633

Special Issue Editor

Dr. Yuta Chiba

E-Mail Website
Guest Editor
Division of Pediatric Dentistry, Department of Community Social Dentistry, Tohoku University Graduate School of Dentistry, Sendai, Japan
Interests: developmental biology; molecular biology; bioinformatics; tooth development; dental anomaly; genetic diseases

Special Issue Information

Dear Colleagues,

Genetic dental diseases are caused by disruption of tooth development processes, and they show various symptoms depending on the cause of disturbance; for example, abnormality in number of teeth, shape of teeth, quality of teeth (e.g., enamel hypoplasia), abnormality in periodontal tissues, and tooth eruption. Furthermore, dental anomalies are often accompanied by inherited systemic diseases. However, the molecular basis of genetic dental diseases is not fully understood, and only a few of the genes responsible for genetic dental diseases have been identified. This Special Issue, entitled “Understanding the Molecular Basis of Genetic Dental Diseases”, aims to uncover novel findings on tooth development and contribute to clarifying the pathogenesis of genetic dental diseases. For this Special Issue, we warmly invite authors to submit original research papers and review articles focusing on the molecular basis of dental diseases and tooth development.

Dr. Yuta Chiba
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • genetic diseases
  • dental anomaly
  • genetic abnormality related to dental diseases
  • tooth development
  • molecular biology of tooth development

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Published Papers (1 paper)

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Research

16 pages, 10651 KiB  
Article
Impact of Amelogenesis Imperfecta on Junctional Epithelium Structure and Function
by Kevin Lin, Jake Ngu, Susu Uyen Le and Yan Zhang
Biology 2025, 14(7), 853; https://doi.org/10.3390/biology14070853 (registering DOI) - 14 Jul 2025
Abstract
The junctional epithelium, which lines the inner gingival surface, seals the gingival sulcus to block the infiltration of food debris and pathogens. The junctional epithelium is derived from the reduced enamel epithelium, consisting of late developmental stage ameloblasts and accessory cells. No prior [...] Read more.
The junctional epithelium, which lines the inner gingival surface, seals the gingival sulcus to block the infiltration of food debris and pathogens. The junctional epithelium is derived from the reduced enamel epithelium, consisting of late developmental stage ameloblasts and accessory cells. No prior studies have investigated whether defective ameloblast differentiation or enamel matrix formation affects junctional epithelium anatomy or function. Here, we examined the junctional epithelium in mice exhibiting amelogenesis imperfecta due to loss-of-function mutations in the major enamel matrix protein amelogenin (Amelx−/−) or the critical enamel matrix protease KLK4 (Klk4−/−). Histological analyses demonstrated altered morphology and cell layer thickness of the junctional epithelium in Amelx−/− and Klk4−/− mice as compared to wt. Immunohistochemistry revealed reduced ODAM, laminin 5, and integrin α6, all of which are critical for the adhesion of the junctional epithelium to the enamel in Amelx−/− and Klk4−/− mice. Furthermore, we observed altered cell–cell adhesion and increased permeability of Dextran-GFP through the mutants’ junctional epithelium, indicating defective barrier function. Reduced β-catenin and Ki67 at the base of the junctional epithelium in mutants suggest impaired mitotic activity and reduced capacity to replenish continuously desquamated epithelium. These findings highlight the essential role of normal amelogenesis in maintaining junctional epithelium homeostasis. Full article
(This article belongs to the Special Issue Understanding the Molecular Basis of Genetic Dental Diseases)
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