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Updated: Mar 8, 2026
Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
Published on: March 18, 2022
Attenuation of subchondral bone abnormal changes in osteoarthritis by inhibition of SDF-1 signaling
1Institute of Orthopedic Diseases and Department of Orthopedics, The First Affiliated Hospital, Jinan University, Guangzhou, PR China; Department of Orthopaedics & Traumatology, Li Ka Shing Institute of Health Sciences and Lui Che Woo Institute of Innovative Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong Special Administrative Region; The CUHK-ACC Space Medicine Centre on Health Maintenance of Musculoskeletal System, The Chinese University of Hong Kong, Shenzhen Research Institute, Shenzhen, PR China.
Background:
Current conservative treatments for osteoarthritis (OA) are largely symptoms control therapies. Further understanding on the pathological mechanisms of OA is crucial for new pharmacological intervention.
Objective:
In this study, we investigated the role of Stromal cell-derived factor-1(SDF-1) in regulating subchondral bone changes during the progression of OA.
Methods:
Clinical samples of different stages of OA severity were analyzed by histology staining, micro-CT, enzyme-linked immunosorbent assay (ELISA) and western blotting, to compare SDF-1 level in subchondral bone. The effects of SDF-1 on human mesenchymal stem cells (MSCs) osteogenic differentiation were evaluated. In vivo assessment was performed in an anterior cruciate ligament transaction plus medial meniscus resection in the SD rats. The OA rats received continuous infusion of AMD3100 (SDF-1 receptor blocker) in osmotic mini-pump implanted subcutaneously for 6 weeks. These rats were then terminated and subjected to the same in vitro assessments as human OA samples.
Results:
SDF-1 level was significantly elevated in the subchondral bone of human OA samples. In the cell studies, the results showed SDF-1 plays an important role in osteogenic differentiation of MSCs. In the OA animal studies, there were less cartilage damage in the AMD3100-treated group; microCT results showed that the subchondral bone formation was significantly reduced and so did the number of positive Nestin or Osterix cells in the subchondral bone region.
Conclusions:
Higher level of SDF-1 may induce the subchondral bone abnormal changes in OA and inhibition of SDF-1 signaling could be a potential therapeutic approach for OA.
Insights
Stromal cell-derived factor-1 (SDF-1) is elevated in osteoarthritis (OA) subchondral bone, driving bone changes and cartilage damage. Inhibiting SDF-1 signaling may offer a new therapeutic strategy for OA.
Area of Science:
- Orthopedics
- Rheumatology
- Cell Biology
Background:
- Current osteoarthritis (OA) treatments primarily manage symptoms.
- Understanding OA's pathological mechanisms is vital for developing new pharmacological interventions.
Purpose of the Study:
- Investigate the role of Stromal cell-derived factor-1 (SDF-1) in subchondral bone changes during OA progression.
- Evaluate SDF-1's impact on mesenchymal stem cell (MSC) osteogenic differentiation.
Main Methods:
- Analyzed human OA samples (histology, micro-CT, ELISA, Western blotting) for SDF-1 levels.
- Assessed SDF-1 effects on human MSCs in vitro.
- Used an OA rat model (ACL transaction + medial meniscus resection) treated with an SDF-1 receptor blocker (AMD3100).
Main Results:
- SDF-1 levels were significantly elevated in human OA subchondral bone.
- SDF-1 influenced MSC osteogenic differentiation.
- AMD3100 treatment reduced cartilage damage and subchondral bone formation in OA rats, with fewer Nestin/Osterix positive cells.
Conclusions:
- Elevated SDF-1 may drive abnormal subchondral bone changes in OA.
- Inhibiting SDF-1 signaling presents a potential therapeutic approach for OA treatment.
