Effects of microtrauma on joint structural changes in the Curdlan-injected SKG mouse model of ankylosing spondylitis
4 affiliations
- 1Hanyang University Institute for Rheumatology Research (HYIRR), Hanyang University, Seoul, South Korea
- 2Department of Anatomy & Cell Biology, College of Medicine, Hanyang University, Seoul, South Korea
- 3Department of Biology, College of Natural Sciences, Soonchunhyang University, Asan, Chungcheongnam-do, South Korea
- 4Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, South Korea
Abstract
Although microtrauma is considered a potential environmental factor in the development of ankylosing spondylitis (AS), there is a lack of experimental research regarding its precise contribution to disease pathogenesis. To induce physiological microtrauma, the right ankles of SKG mice were immobilized for a week using surgical plaster and a pipette tip to stimulate compensatory mechanical overload in the contralateral limb. Following the removal of the immobilization, the mice were intraperitoneally injected with 3 mg of Curdlan. In this model, the non-immobilized left ankle served as the microtraumatized group, while the immobilized right ankle served as the internal control. Arthritis severity was clinically scored weekly for 5 weeks. At 6 weeks, ankle, hip, and sacroiliac (SI) joint changes were evaluated using histological and micro-CT analyses. The microtraumatized (left) ankles of Curdlan-injected SKG mice exhibited exacerbated arthritis severity, synovitis, and enthesitis compared with the control ankles. Micro-CT analysis revealed a significantly elevated inflamed bone volume in the microtraumatized ankles. Immunohistochemistry showed markedly higher expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the synovium and enthesis of the microtraumatized ankles. Notably, distant pathological changes, including proteoglycan loss and joint space narrowing, were also observed in the left hip joints. Collectively, these findings indicate that compensatory microtrauma significantly exacerbates joint inflammation and pathological bone destruction in the Curdlan-injected SKG mouse model, highlighting mechanical stress as a critical aggravating factor in AS progression.
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BibTeX
@article{lee2026effects,
title = {{Effects of microtrauma on joint structural changes in the Curdlan-injected SKG mouse model of ankylosing spondylitis}},
author = {Seung Hoon Lee and Dongju Kim and Chanhyeok Jeon and Hye-Ryeong Jo and Jeehee Youn and Sungsin Jo and Tae-Hwan Kim},
journal = {PLOS One},
year = {2026},
month = oct,
doi = {10.1371/journal.pone.0360912},
url = {https://doi.org/10.1371/journal.pone.0360912},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Effects of microtrauma on joint structural changes in the Curdlan-injected SKG mouse model of ankylosing spondylitis
AU - Seung Hoon Lee
AU - Dongju Kim
AU - Chanhyeok Jeon
AU - Hye-Ryeong Jo
AU - Jeehee Youn
AU - Sungsin Jo
AU - Tae-Hwan Kim
PY - 2026
DA - 2026/10/15
JO - PLOS One
DO - 10.1371/journal.pone.0360912
UR - https://doi.org/10.1371/journal.pone.0360912
AB - Although microtrauma is considered a potential environmental factor in the development of ankylosing spondylitis (AS), there is a lack of experimental research regarding its precise contribution to disease pathogenesis. To induce physiological microtrauma, the right ankles of SKG mice were immobilized for a week using surgical plaster and a pipette tip to stimulate compensatory mechanical overload in the contralateral limb. Following the removal of the immobilization, the mice were intraperitoneally injected with 3 mg of Curdlan. In this model, the non-immobilized left ankle served as the microtraumatized group, while the immobilized right ankle served as the internal control. Arthritis severity was clinically scored weekly for 5 weeks. At 6 weeks, ankle, hip, and sacroiliac (SI) joint changes were evaluated using histological and micro-CT analyses. The microtraumatized (left) ankles of Curdlan-injected SKG mice exhibited exacerbated arthritis severity, synovitis, and enthesitis compared with the control ankles. Micro-CT analysis revealed a significantly elevated inflamed bone volume in the microtraumatized ankles. Immunohistochemistry showed markedly higher expression of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) in the synovium and enthesis of the microtraumatized ankles. Notably, distant pathological changes, including proteoglycan loss and joint space narrowing, were also observed in the left hip joints. Collectively, these findings indicate that compensatory microtrauma significantly exacerbates joint inflammation and pathological bone destruction in the Curdlan-injected SKG mouse model, highlighting mechanical stress as a critical aggravating factor in AS progression.
SN - 1932-6203
ER -