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Periarticular bone loss in antigen-induced arthritis
Cecilia Engdahl1, Catharina Lindholm, Alexandra Stubelius
1University of Gothenburg, Gothenburg, Sweden.
Arthritis and Rheumatism
|August 7, 2013
Summary
Antigen-induced arthritis (AIA) causes periarticular bone loss. This study found that NADPH oxidase 2 (NOX-2)-derived reactive oxygen species (ROS) are not essential for this bone loss, establishing AIA as a model for investigation.
Area of Science:
- Rheumatology
- Orthopedics
- Immunology
Background:
- Arthritis involves complex bone loss, including periarticular and generalized loss.
- The antigen-induced arthritis (AIA) model primarily studies synovitis and joint destruction.
- Periarticular bone loss in AIA requires further characterization.
Purpose of the Study:
- To characterize AIA as a model for periarticular bone loss.
- To investigate the role of NADPH oxidase 2 (NOX-2)-derived reactive oxygen species (ROS) in AIA-induced periarticular bone loss.
Main Methods:
- Arthritis was induced in mice via antigen injection; control knees were used for comparison.
- Histologic assessment, peripheral quantitative computed tomography (pQCT) for bone mineral density (BMD), and flow cytometry were performed.
- ROS production capability was assessed in arthritic and control mice, including Ncf1-/- mice lacking NOX-2.
Main Results:
- AIA led to decreased periarticular trabecular BMD and increased inflammatory cells (preosteoclasts, neutrophils, monocytes).
- Arthritis induction increased ROS production capability.
- Similar periarticular trabecular BMD reductions were observed in Ncf1-/- mice and controls, indicating NOX-2 independence.
Conclusions:
- AIA induces periarticular bone loss linked to local inflammatory cell and osteoclast activity.
- NOX-2-derived ROS are not essential for inflammation-mediated periarticular bone loss in this model.
- AIA is suitable for studying the pathogenesis of local inflammation-mediated bone loss.

