Li B, Wei W, Zhang YL, Zhang XX. Effects of hyperglycemia on the bone microenvironment in diabetic osteoporosis. World J Diabetes 2026; 17(7): 121312 [DOI: 10.4239/wjd.121312]
Corresponding Author of This Article
Xi-Xu Zhang, MD, Professor, Department of Endocrinology, The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, No. 60 Huanghe North Street, Shenyang 261000, Liaoning Province, China. 13287683505@163.com
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Endocrinology & Metabolism
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review-article
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Li B, Wei W, Zhang YL, Zhang XX. Effects of hyperglycemia on the bone microenvironment in diabetic osteoporosis. World J Diabetes 2026; 17(7): 121312 [DOI: 10.4239/wjd.121312]
World J Diabetes. Jul 15, 2026; 17(7): 121312 Published online Jul 15, 2026. doi: 10.4239/wjd.121312
Effects of hyperglycemia on the bone microenvironment in diabetic osteoporosis
Bo Li, Wei Wei, Yan-Long Zhang, Xi-Xu Zhang
Bo Li, Wei Wei, Yan-Long Zhang, Department of Orthopedics, The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 261000, Liaoning Province, China
Xi-Xu Zhang, Department of Endocrinology, The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 261000, Liaoning Province, China
Co-corresponding authors: Yan-Long Zhang and Xi-Xu Zhang.
Author contributions: Zhang YL and Zhang XX contributed equally to this work, as they are co-corresponding authors; Wei W wrote the manuscript; Zhang YL and Zhang XX designed the research; Li B, Wei W, Zhang YL and Zhang XX have read and approved the final manuscript.
AI contribution statement: No AI tools, including but not limited to ChatGPT, Grammarly, or DeepL, were used in the preparation of this manuscript. No portion of the main text of the manuscript was AI-generated. The entire text was written by the authors. No images in the manuscript were generated by AI. We would like to clarify that we did not use any AI tools to generate, edit, or assist in the file “answering-reviewers”. The content was written entirely by the authors manually, based on our own work and understanding. Furthermore, in responding to the reviewers' comments point by point, we did not use any AI tools. All responses were written directly by the authors without any AI assistance.
Conflict-of-interest statement: The authors declare that they have no conflict of interest.
Corresponding author: Xi-Xu Zhang, MD, Professor, Department of Endocrinology, The Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, No. 60 Huanghe North Street, Shenyang 261000, Liaoning Province, China. 13287683505@163.com
Received: March 23, 2026 Revised: April 17, 2026 Accepted: May 21, 2026 Published online: July 15, 2026 Processing time: 110 Days and 15.4 Hours
Abstract
With the global surge in diabetes mellitus prevalence, diabetic osteoporosis (DOP) has become a pressing public health challenge because it markedly increases fracture risk and impairs bone repair capacity. The bone microenvironment, a dynamic ecosystem that maintains skeletal integrity, undergoes profound pathological changes under chronic hyperglycemia: Excessive reactive oxygen species production induced by high glucose and accumulation of advanced glycation end products together trigger oxidative stress and chronic low-grade inflammation in the bone microenvironment (e.g., activation of the nuclear factor-kappa B signaling pathway). These processes, by inhibiting osteoblast differentiation, enhancing osteoclast activity, and damaging microvascular supply, disrupt the coupled balance of bone remodeling. This article aims to systematically review the effects of hyperglycemia on the bone microenvironment and its molecular mechanisms, clarify the pathological basis of DOP, and provide a theoretical foundation for identifying new targets for prevention, treatment, and clinical intervention.
Core Tip: Diabetic osteoporosis (DOP) poses a major health challenge, elevating fracture risk. Chronic hyperglycemia is central to DOP pathogenesis, instigating oxidative stress via excessive reactive oxygen species and advanced glycation end products, plus inflammation involving the nuclear factor-kappa B signaling pathway within the bone microenvironment. This disrupts bone remodeling. Understanding these molecular mechanisms is crucial for developing innovative prevention and treatment strategies for DOP.
