Copyright
©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Stem Cells. May 26, 2025; 17(5): 106934
Published online May 26, 2025. doi: 10.4252/wjsc.v17.i5.106934
Published online May 26, 2025. doi: 10.4252/wjsc.v17.i5.106934
Aberrant bone formation and dysregulated bone homeostasis in ankylosing spondylitis
Gun Woo Lee, Department of Orthopedic Surgery, Yeungnam University College of Medicine, Daegu 42415, South Korea
Gun Woo Lee, Institute for Quantitative Health Science & Engineering, East Lansing, MI 48824, United States
Author contributions: Lee GW wrote, revised the manuscript, and approved the final manuscript published.
Supported by 2024 Yeungnam University Research Grant.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Gun Woo Lee, MD, PhD, Associate Professor, Department of Ortho pedic Surgery, Yeungnam University College of Medicine, No. 170 Hyunchung-ro, Namgu, Daegu 42415, South Korea. gwlee1871@gmail.com
Received: March 11, 2025
Revised: April 3, 2025
Accepted: May 7, 2025
Published online: May 26, 2025
Processing time: 76 Days and 17.4 Hours
Revised: April 3, 2025
Accepted: May 7, 2025
Published online: May 26, 2025
Processing time: 76 Days and 17.4 Hours
Core Tip
Core Tip: In ankylosing spondylitis (AS), osteoclasts contribute significantly to pathological bone resorption and remodeling. The receptor activator of nuclear factor-kappa B/receptor activator of nuclear factor-kappa B ligand/osteoprotegerin signaling axis, inflammatory cytokines such as interleukin-17 and tumor necrosis factor-alpha, and immune cells such as T helper type 17 and macrophages are central to osteoclastogenesis in AS. Elucidation of the mechanisms governing osteoclast differentiation, activation, and dysregulation in AS is essential for the development of targeted therapeutic strategies that modulate aberrant bone remodeling.