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Arthritis Rheum. 2008 Apr;58(4):1096-106. doi: 10.1002/art.23277.

A type I collagen defect leads to rapidly progressive osteoarthritis in a mouse model.

Author information

National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland 20892-1560, USA.

Erratum in

  • Arthritis Rheum. 2008 Jun;58(6):1888. Fiorientino, N M [corrected to Fiorentino, N M].



This study was undertaken to test the hypothesis that abnormalities of the subchondral bone can result in osteoarthritis (OA).


We used a knockin model of human osteogenesis imperfecta, the Brittle IV (Brtl) mouse, in which defective type I collagen is expressed in bone. OA in individual mice was documented by micro-magnetic resonance imaging (micro-MRI) and micro-computed tomography (micro-CT). Alterations in the knee joints were confirmed by histopathologic and immunohistochemical analysis. In addition, atomic force microscopy (AFM) was used to assess the ultrastructure of the articular cartilage and subchondral bone matrix.


Brtl mice had decreased integrity of bone but initially normal articular cartilage. However, by the second month of life, Brtl mice developed alterations of the cartilage that were characteristic of OA, as documented by micro-CT, micro-MRI, and histologic evaluation. In addition, chondrocyte loss and breakdown of the collagen matrix in the residual cartilage were demonstrated using AFM.


The Brtl mouse model demonstrates that progressive destruction of articular cartilage characteristic of OA may be secondary to altered architecture of the underlying subchondral bone.

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