Research progress on molecular signaling pathways related to the pathogenesis of skeletal fluorosis
10.3760/cma.j.cn231583-20240815-00219
- VernacularTitle:氟骨症发病机制相关分子信号通路研究进展
- Author:
Jianbin WANG
1
;
Hongxuan CHEN
;
Jiarong ZHANG
Author Information
1. 遵义医科大学附属医院医药生物技术研究所，遵义 563000
- Publication Type:Journal Article
- Keywords:
Fluorine;
Skeletal fluorosis;
Pathogenesis;
Signaling pathways
- From:
Chinese Journal of Endemiology
2025;44(1):76-81
- CountryChina
- Language:Chinese
-
Abstract:
Fluorine, as one of the important trace elements, has multiple physiological functions and participates in body metabolism. Moderate intake of fluoride is beneficial for human health, while excessive fluoride can lead to dental fluorosis, skeletal fluorosis, and multi-organ damage. Typical symptoms of skeletal fluorosis include bone sclerosis, osteomalacia, osteoporosis, and degenerative changes in articular cartilage. The pathological basis for skeletal changes in fluorosis involves enhanced osteogenesis and accelerated bone turnover, which are comprehensively regulated by multiple signaling pathways. Although the etiology of skeletal fluorosis has been determined, its pathogenic mechanisms remain inconclusive. In recent years, researchers have extensively investigated the signaling pathways involved in skeletal fluorosis development, including Notch, phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), Wnt/β-catenin, Hedgehog, nuclear factor κB (NF-κB), parathyroid hormone (PTH), and insulin signaling pathways, as well as their interactive networks. This article summarizes and reviews the recent research findings, aiming to provide a theoretical foundation for comprehensively understanding the pathogenic mechanisms of skeletal fluorosis and offer insights for scientific prevention of skeletal fluorosis.
