高血糖和氧化应激在糖尿病和衰老过程中加剧，导致骨骼中先进糖基化和糖氧化终产物（AGEs/AGOEs）的过度积累。AGEs/AGOEs被认为是解释糖尿病、衰老和骨质疏松引起骨骼脆性增加的“缺失环节”，其中骨质量和/或跌倒发生率的增加不能完全解释骨折危险性的增加。AGEs/AGOEs通过改变有机基质（胶原和非胶原蛋白）、矿物质和水含量干扰骨骼周转，破坏骨质的质量。AGEs和AGOEs也与其他疾病（如阿尔茨海默病、昼夜节律紊乱和癌症）中的骨骼脆性有关。本综述论述了AGEs和AGOEs在骨骼中的积累以及对骨质和骨折的影响，以及如何在临床前和临床调查中针对AGEs/AGOEs进行抑制或清除，以预测和管理糖尿病、骨质疏松和骨折不足。版权所有 © 2023 Elsevier Inc. 发布。

Hyperglycemia and oxidative stress, enhanced in diabetes and aging, result in excessive accumulation of advanced glycation and glycoxidation end products (AGEs/AGOEs) in bone. AGEs/AGOES are considered to be "the missing link" in explaining increased skeletal fragility with diabetes, aging, and osteoporosis where increased fracture risk cannot be solely explained by bone mass and/or fall incidences. AGEs/AGOEs disrupt bone turnover and deteriorate bone quality through alterations of organic matrix (collagen and non-collagenous proteins), mineral, and water content. AGEs and AGOEs are also associated with bone fragility in other conditions such as Alzheimer's disease, circadian rhythm disruption, and cancer. This review explains how AGEs and AGOEs accumulate in bone and impact bone quality and bone fracture, and how AGES/AGOEs are being targeted in preclinical and clinical investigations for inhibition or removal, and for prediction and management of diabetic, osteoporotic and insufficiency fractures.Copyright © 2023. Published by Elsevier Inc.