Etiological Mechanisms and Genetic/Biological Modulation Related to PTH1R in Primary Failure of Tooth Eruption

Li, Xiao-xia; Wang, Man-ting; Wu, Zhi-fang; Sun, Qiang; Ono, Noriaki; Nagata, Mizuki; Zang, Xiao-long; Ono, Wanida

doi:10.1007/s00223-024-01227-y

Cited by 1 publication

(1 citation statement)

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“…A previous study on DFCs primarily focused on their role in normal tooth eruption, with limited research concentrating on abnormal eruptions ( 24 ). The role of tooth eruption-related signaling pathways, such as Wnt and TGF-β signaling pathways, in normal tooth eruption has been extensively studied; however, there are few reviews on the mechanisms underlying abnormal signaling pathways in DFCs that result in failed tooth eruption ( 25 , 26 ). Furthermore, numerous studies have summarized the abnormal tooth eruption observed in various genetic diseases and systemic syndrome ( 23 , 25 , 27 – 29 ); however, the pathogenesis of these diseases involves multiple causes, with some specifically implicating the DF in the aberrant tooth eruption process.…”

Section: Introductionmentioning

confidence: 99%

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

Chen,

Ying,

et al. 2024

Mol Med Rep

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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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