Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2001 Apr;30(5 Suppl 2):7-16.
doi: 10.1053/sarh.2001.23704.

Uncoupling of inflammatory and destructive mechanisms in arthritis

Affiliations
Review

Uncoupling of inflammatory and destructive mechanisms in arthritis

W B van den Berg. Semin Arthritis Rheum. 2001 Apr.

Abstract

Objective: To update clinicians on recent advances in the differentiation of the mechanisms of inflammation and cartilage destruction in the pathogenesis of rheumatoid arthritis (RA).

Methods: We present analysis of recent published literature and abstracts that elucidates the independent actions of pivotal proinflammatory cytokines. These experimental data provide the framework for understanding the uncoupling of destructive and inflammatory mechanisms in arthritis.

Results: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator in the inflammation that occurs in RA. Interleukin-1 (IL-1) has a dominant effect on cartilage destruction that occurs later in the disease process. TNF-independent IL-1 production occurs in many RA model situations. Cytokine balance determines the erosive nature of the disease.

Conclusion: IL-1 is at least as important as TNF-alpha in promoting the disease process. The pathways by which the inflammatory and destructive changes occur suggest that targeted anticytokine intervention will arrest the cartilage damage that occurs in patients with RA.

PubMed Disclaimer

MeSH terms

LinkOut - more resources