Lee GW. Aberrant bone formation and dysregulated bone homeostasis in ankylosing spondylitis. World J Stem Cells 2025; 17(5): 106934 [DOI: 10.4252/wjsc.v17.i5.106934]
Corresponding Author of This Article
Gun Woo Lee, MD, PhD, Associate Professor, Department of Orthopedic Surgery, Yeungnam University College of Medicine, No. 170 Hyunchung-ro, Namgu, Daegu 42415, South Korea. gwlee1871@gmail.com
Research Domain of This Article
Medicine, Research & Experimental
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (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: http://creativecommons.org/licenses/by-nc/4.0/
World J Stem Cells. May 26, 2025; 17(5): 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
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 Orthopedic 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
Abstract
Ankylosing spondylitis (AS) is a chronic, progressive, systemic autoimmune disease characterised by spinal stiffness and ocular, cardiac, intestinal, and peripheral joint involvements. Genetics, infectious agents, and immune-mediated inflammatory processes have all been hypothesized to contribute to AS pathogenesis, but the precise aetiology remains elusive. Recent studies have identified biological and cellular factors that correlate with the onset and progression of AS. This has provided avenues of research that may help elucidate disease mechanisms and lead to advances in therapeutic interventions. This study aimed to examine some of the findings from recent molecular studies, focusing on the molecular mechanism and associated factors such as interleukin-17, tumor necrosis factor-alpha, receptor activator of nuclear factor-kappa B/receptor activator of nuclear factor-kappa B ligand/osteoprotegerin pathway, and related microRNAs to gain insight into aberrant bone formation in AS and potential approaches to its prevention. This editorial also addresses the contribution of osteoclasts to bone pathology in AS. The author examined the molecular pathways governing osteoclast differentiation and activity, with particular emphasis on relevant cytokines and immune cell interactions. A comprehensive understanding of these mechanisms is essential for the development of targeted therapies to mitigate excessive bone resorption and pathological skeletal remodeling in AS.
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.
