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Periarticular bone loss in antigen-induced arthritis.

Journal article
Authors Cecilia Engdahl
Catharina Lindholm
Alexandra Stubelius
Claes Ohlsson
Hans Carlsten
Marie Lagerquist
Published in Arthritis and rheumatism
Volume 65
Issue 11
Pages 2857–2865
ISSN 1529-0131
Publication year 2013
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Centre for Bone and Arthritis Research
Institute of Medicine, Department of Internal Medicine and Clinical Nutrition
Pages 2857–2865
Language en
Links dx.doi.org/10.1002/art.38114
Subject categories Endocrinology, Rheumatology and Autoimmunity

Abstract

Objective: Bone loss in arthritis is a complex process including bone erosions, periarticular and generalized bone loss. The antigen-induced arthritis (AIA) model is mainly used to study synovitis and joint destruction, including bone erosions, while periarticular bone loss is less investigated. The main aim of this study was to characterize and establish AIA as a model for periarticular bone loss. We also determined the importance of NADPH oxidase 2 (NOX2) derived reactive oxygen species (ROS) for periarticular bone loss. Methods: AIA was induced in one knee by a local antigen injection and the other knee was used as non-arthritic control. At termination the knees were collected for histology. Periarticular bone mineral density (BMD) was investigated using peripheral Quantitative Computed Tomography (pQCT). Flow cytometry analyses were performed on synovial and bone marrow cells. Results: AIA resulted in decreased periarticular trabecular BMD and increased frequencies of preosteoclasts, neutrophils and monocytes in the arthritic synovial tissue. Arthritis resulted in an elevated capability to produce ROS. However, AIA induction in Ncf1(*/*) mice, lacking NOX2 derived ROS, and control mice resulted in similar reduction in periarticular trabecular BMD. Conclusions: AIA resulted in periarticular bone loss associated with local effects on inflammatory cells and osteoclasts. Furthermore, using this model, we conclude that NOX2 derived ROS production is not essential for inflammation-mediated periarticular bone loss. Thus, AIA can be used as a model to investigate the pathogenesis of local inflammation-mediated bone loss. © 2013 American College of Rheumatology.

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