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

IF 3.3 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Calcified Tissue International Pub Date : 2024-08-01 Epub Date: 2024-06-04 DOI:10.1007/s00223-024-01227-y
Xiao-Xia Li, Man-Ting Wang, Zhi-Fang Wu, Qiang Sun, Noriaki Ono, Mizuki Nagata, Xiao-Long Zang, Wanida Ono
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Abstract

Primary failure of eruption (PFE) is a rare disorder that is characterized by the inability of a molar tooth/teeth to erupt to the occlusal plane or to normally react to orthodontic force. This condition is related to hereditary factors and has been extensively researched over many years. However, the etiological mechanisms of pathogenesis are still not fully understood. Evidence from studies on PFE cases has shown that PFE patients may carry parathyroid hormone 1 receptor (PTH1R) gene mutations, and genetic detection can be used to diagnose PFE at an early stage. PTH1R variants can lead to altered protein structure, impaired protein function, and abnormal biological activities of the cells, which may ultimately impact the behavior of teeth, as observed in PFE. Dental follicle cells play a critical role in tooth eruption and root development and are regulated by parathyroid hormone-related peptide (PTHrP)-PTH1R signaling in their differentiation and other activities. PTHrP-PTH1R signaling also regulates the activity of osteoblasts, osteoclasts and odontoclasts during tooth development and eruption. When interference occurs in the PTHrP-PTH1R signaling pathway, the normal function of dental follicles and bone remodeling are impaired. This review provides an overview of PTH1R variants and their correlation with PFE, and highlights that a disruption of PTHrP-PTH1R signaling impairs the normal process of tooth development and eruption, thus providing insight into the underlying mechanisms related to PTH1R and its role in driving PFE.

Abstract Image

原发性牙齿萌出失败的病因机制以及与 PTH1R 相关的遗传/生物调节。
原发性牙齿萌出失败(PFE)是一种罕见的疾病,其特征是磨牙/臼齿无法萌出到咬合平面,或对正畸力无法做出正常反应。这种病症与遗传因素有关,多年来已被广泛研究。然而,其发病机制仍未完全明了。对PFE病例的研究证据表明,PFE患者可能携带甲状旁腺激素1受体(PTH1R)基因突变,基因检测可用于早期诊断PFE。PTH1R 变异可导致蛋白质结构改变、蛋白质功能受损和细胞生物活性异常,最终可能影响牙齿的行为,正如在 PFE 中观察到的那样。牙泡细胞在牙齿萌出和牙根发育中起着关键作用,其分化和其他活动受甲状旁腺激素相关肽(PTHrP)-PTH1R 信号的调节。在牙齿发育和萌出过程中,PTHrP-PTH1R 信号还能调节成骨细胞、破骨细胞和牙髓细胞的活动。当 PTHrP-PTH1R 信号通路受到干扰时,牙泡的正常功能和骨重塑就会受到损害。本综述概述了 PTH1R 变体及其与 PFE 的相关性,并强调 PTHrP-PTH1R 信号通路的中断会损害牙齿发育和萌出的正常过程,从而让人们深入了解与 PTH1R 有关的潜在机制及其在驱动 PFE 中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Calcified Tissue International
Calcified Tissue International 医学-内分泌学与代谢
CiteScore
8.00
自引率
2.40%
发文量
112
审稿时长
4-8 weeks
期刊介绍: Calcified Tissue International and Musculoskeletal Research publishes original research and reviews concerning the structure and function of bone, and other musculoskeletal tissues in living organisms and clinical studies of musculoskeletal disease. It includes studies of cell biology, molecular biology, intracellular signalling, and physiology, as well as research into the hormones, cytokines and other mediators that influence the musculoskeletal system. The journal also publishes clinical studies of relevance to bone disease, mineral metabolism, muscle function, and musculoskeletal interactions.
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