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Review
. 2006 May;54(5):1357-60.
doi: 10.1002/art.21813.

Molecular mechanisms of cartilage destruction: mechanics, inflammatory mediators, and aging collide

Richard F Loeser
Review

Molecular mechanisms of cartilage destruction: mechanics, inflammatory mediators, and aging collide

Richard F Loeser. Arthritis Rheum. 2006 May.
No abstract available

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Figures

Figure 1
Figure 1
Factors acting on articular cartilage during the development of osteoarthritis (OA). The image of OA tissue is from a toluidine blue–stained section and demonstrates classic OA features including loss of matrix staining and loss of cells in the upper zone of the cartilage with clusters of chondrocytes in the deeper zone. These clusters can contain cells in various stages of cell division, hypertrophic differentiation, and death. Adapted from ref. .
Figure 2
Figure 2
Theoretical model for pathways involved in cartilage destruction during the development of osteoarthritis. Excessive mechanical forces stimulate the chondrocyte directly or indirectly through signals generated by matrix damage, including generation of matrix fragments. The resultant activation of signaling pathways, including reactive oxygen species (ROS) generation, results in increased production of cytokines, chemokines, and proteolytic enzymes. This catabolic response to injury serves to degrade the damaged matrix. Matrix degradation results in release of growth factors stored in the matrix that would normally feed back on the cell and shut down the catabolic pathways. However, aged chondrocytes have an insufficient response to growth factor stimulation, and this results in continued matrix destruction from unbalanced catabolic and anabolic activity.
See this image and copyright information in PMC

Comment on

References

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