氟斑牙发病分子信号通路研究进展

Progress in molecular signal pathway of dental fluorosis

氟斑牙是儿童时期摄入过量氟化物而引起的慢性口腔氟中毒表现。目前氟斑牙发病的分子机制尚不明确。成釉细胞是牙齿组织中对氟化物最敏感的细胞,氟通过对分子信号通路中关键分子的作用,影响成釉细胞增殖和分泌功能,导致氟斑牙形成。本文综述了近年来分子信号通路[丝裂原活化蛋白激酶(MAPK)、转化生长因子-β(TGF-β)/Smad、Wnt、Foxo1/Runx2]及应激途径(内质网应激及氧化应激)与氟斑牙发生的关系,以期在分子层面上,深入了解氟斑牙的发病机制,为氟斑牙的防治提供新思路。

Dental fluorosis is a manifestation of chronic oral fluorosis caused by excessive fluoride intake in childhood.At present,the molecular mechanism of dental fluorosis is still unclear.Ameloblasts are the most sensitive cells to fluoride in tooth tissue.Fluoride affects the proliferation and secretion of ameloblasts through the role of key molecules in the molecular signal pathways,leading to the formation of dental fluorosis.This paper reviews the relationship between the molecular signal pathways[mitogen-activated protein kinase(MAPK),transforming growth factor-β(TGF-β)/Smad,Wnt,Foxo1/Runx2],stress pathways(endoplasmic reticulum stress and oxidative stress)and the occurrence of dental fluorosis in recent years,in order to deeply understand the pathogenesis of dental fluorosis at the molecular level,and provide new ideas for the prevention and treatment of dental fluorosis.