Open Access

Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review)

  • Authors:
    • Jiahao Chen
    • Ying Ying
    • Huimin Li
    • Zhuomin Sha
    • Jiaqi Lin
    • Yongjia Wu
    • Yange Wu
    • Yun Zhang
    • Xuepeng Chen
    • Weifang Zhang
  • View Affiliations

  • Published online on: July 15, 2024     https://doi.org/10.3892/mmr.2024.13292
  • Article Number: 168
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The dental follicle (DF) plays an indispensable role in tooth eruption by regulating bone remodeling through their influence on osteoblast and osteoclast activity. The process of tooth eruption involves a series of intricate regulatory mechanisms and signaling pathways. Disruption of the parathyroid hormone‑related protein (PTHrP) in the PTHrP‑PTHrP receptor signaling pathway inhibits osteoclast differentiation by DF cells (DFCs), thus resulting in obstructed tooth eruption. Furthermore, parathyroid hormone receptor‑1 mutations are linked to primary tooth eruption failure. Additionally, the Wnt/β‑catenin, TGF‑β, bone morphogenetic protein and Hedgehog signaling pathways have crucial roles in DFC involvement in tooth eruption. DFC signal loss or alteration inhibits osteoclast differentiation, affects osteoblast and cementoblast differentiation, and suppresses DFC proliferation, thus resulting in failed tooth eruptions. Abnormal tooth eruption is also associated with a range of systemic syndromes and genetic diseases, predominantly resulting from pathogenic gene mutations. Among these conditions, the following disorders arise due to genetic mutations that disrupt DFCs and impede proper tooth eruption: Cleidocranial dysplasia associated with Runt‑related gene 2 gene mutations; osteosclerosis caused by CLCN7 gene mutations; mucopolysaccharidosis type VI resulting from arylsulfatase B gene mutations; enamel renal syndrome due to FAM20A gene mutations; and dentin dysplasia caused by mutations in the VPS4B gene. In addition, regional odontodysplasia and multiple calcific hyperplastic DFs are involved in tooth eruption failure; however, they are not related to gene mutations. The specific mechanism for this effect requires further investigation. To the best of our knowledge, previous reviews have not comprehensively summarized the syndromes associated with DF abnormalities manifesting as abnormal tooth eruption. Therefore, the present review aims to consolidate the current knowledge on DFC signaling pathways implicated in abnormal tooth eruption, and their association with disorders of tooth eruption in genetic diseases and syndromes, thereby providing a valuable reference for future related research.
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September-2024
Volume 30 Issue 3

Print ISSN: 1791-2997
Online ISSN:1791-3004

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Spandidos Publications style
Chen J, Ying Y, Li H, Sha Z, Lin J, Wu Y, Wu Y, Zhang Y, Chen X, Zhang W, Zhang W, et al: Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review). Mol Med Rep 30: 168, 2024.
APA
Chen, J., Ying, Y., Li, H., Sha, Z., Lin, J., Wu, Y. ... Zhang, W. (2024). Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review). Molecular Medicine Reports, 30, 168. https://doi.org/10.3892/mmr.2024.13292
MLA
Chen, J., Ying, Y., Li, H., Sha, Z., Lin, J., Wu, Y., Wu, Y., Zhang, Y., Chen, X., Zhang, W."Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review)". Molecular Medicine Reports 30.3 (2024): 168.
Chicago
Chen, J., Ying, Y., Li, H., Sha, Z., Lin, J., Wu, Y., Wu, Y., Zhang, Y., Chen, X., Zhang, W."Abnormal dental follicle cells: A crucial determinant in tooth eruption disorders (Review)". Molecular Medicine Reports 30, no. 3 (2024): 168. https://doi.org/10.3892/mmr.2024.13292