- Paper Report
- Open Access
TRANCE/RANKL in bone erosion in arthritis
- Riako Masuda1
© Biomed Central Ltd 2002
- Received: 14 January 2002
- Accepted: 15 January 2002
- Published: 21 January 2002
- Bone erosion
- cartilage destruction
- serum transfer model
Although joint destruction is a complication of severe rheumatoid arthritis (RA), the definitive pathogenic mechanisms have yet to be elucidated. TRANCE/RANKL has been characterized as an essential factor not only for osteoclastogenesis, but also for the viability of dendritic cells resulting in the activation and proliferation of T cells. A significant reduction of bone erosion is seen in the adjuvant arthritis model after blockade of TRANCE/RANKL. To exclude the influence of T cell-dendritic cell interactions on this process, the authors generated inflammatory arthritis in TRANCE/RANKL-deficient mice using a serum transfer model bypassing the requirement for T cell activation.
Following serum transfer, inflammation developed in TRANCE/RANKL knockout mice similarly to matched littermates; however, bone erosion was dramatically reduced in the knockout mice. In contrast, erosion of cartilage could not be prevented. These results suggest that osteoclasts play a critical role in the pathogenesis of bone erosion in RA independent of T cell-dendritic cell interactions, but that the mechanism of cartilage destruction, as well as the factors which drive the inflammatory process, appears to be different from those of bone erosion.
TRANCE/RANKL-deficient mice, serum transfer model of arthritis, micro CT imaging, haematotoxylin and eosin staining, toluidine blue staining, fluorescent staining
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