化脓性中耳炎骨质重塑的研究进展

Research progress of bone remodeling in suppurative otitis media

鼓室硬化是中耳炎常见的炎性后遗症,鼓室硬化中耳鼓室局部组织发生炎症后,黏膜层毛细血管通透性增加,大量炎性因子深入到黏膜下层和骨质层,引起纤维素性渗出的同时,激活骨质细胞相关受体作用成骨细胞和破骨细胞产生活化或抑制,导致局部钙化及骨化,最终引起鼓室硬化。更加准确地了解鼓室损伤后的修复机理和调控机制是控制过度修复,防控鼓室硬化的关键。本文总结了骨组织代谢过程中的三个主要调控通路:骨形态发生蛋白(bone morphogenetic protein,BMP)、骨桥蛋白(osteopontin,OPN)及护骨素(osteoprotegerin,OPG)/核因子κB受体活化因子配体(receptor activator of NF-κB ligand,RANKL)系统在中耳炎骨质重塑中的作用,为中耳炎鼓室硬化的早期防控提供新的治疗方向。

Tympanosclerosis is a common inflammatory complication of otitis media.After inflammation,the permeability of capillaries in the mucosa increases.A large number of inflammatory factors penetrate into the submucosa and bone layer,causing cellulosic exudation.At the same time,they activate osteoblast-related receptors to act on osteoblasts and osteoclasts.Activation or inhibition leads to local calcification and ossification,and eventually leads to tympanic sclerosis.More accurate understanding of the repair mechanism of tympanic injury is the key to prevent and control tympanic sclerosis.This article summarized three main regulatory pathways in bone metabolism:bone morphogenetic protein(BMP),osteopontin(OPN)and osteoprotegerin(OPG)/receptor activator of NF-κB ligand(RANKL)system,which play an important role in bone remodeling of otitis media.It may provide a new treatment for early prevention and control of tympanic sclerosis in otitis media.