Pathogenesis of bone erosions in rheumatoid arthritis.

[Guest guest]

Curr Opin Rheumatol 2002 Jul;14(4):406-10

Pathogenesis of bone erosions in rheumatoid arthritis

Goldring SR.

Beth Israel Deaconess Medical Center, Harvard Medical School, and New

England Baptist Bone and Joint Institute, Harvard Institutes of

Medicine, Boston, Massachusetts, USA.

Focal marginal joint erosions represent the radiographic hallmark of

rheumatoid arthritis (RA). These bone changes are characteristically

localized to the joint margins, but in addition, regions of focal bone

resorption can be detected in the subchondral bone adjacent to the bone

marrow space into which the synovial inflammatory tissues have extended.

Because progressive destruction of the periarticular bone contributes

significantly to joint dysfunction and disability in patients with RA,

there is considerable interest in developing a better understanding of

the pathologic mechanisms involved in this process and in developing

therapies that can arrest these events. Previous analysis of joint

tissues from patients with RA have provided morphologic evidence that

osteoclasts are the cell types that mediate the focal bone resorption

associated with the rheumatoid synovial lesion. Additional recent data

from animal models have helped to further implicate these cells in the

pathogenesis of focal bone erosions. Furthermore, analysis of RA

synovium and joint tissues from animal models of inflammatory arthritis,

as well as cell and tissues culture studies, have helped to define the

cytokines and inflammatory mediators that are involved in the

recruitment and activation of bone resorbing cells associated with focal

bone erosions. These findings provide a rational framework for

developing targeted therapies that can specifically inhibit or slow the

progressive focal bone destruction associated with the rheumatoid

synovial lesion.

PMID: 12118176