Inflammation: A key factor in the pathogenesis of osteoarthritis

Osteoarthritis (OA) is no longer seen as a degenerative disease. Low grade chronic inflammatory processes lead to cartilage damage.

Understanding joint tissue destruction in OA will hint at new therapeutic targets

Osteoarthritis (OA) is no longer seen as a degenerative disease. Low grade chronic inflammatory processes lead to cartilage damage.

In the past, OA was simply considered a degenerative “wear and tear” process. However, the pathogenesis of OA is much more complex. The new paradigm of OA as a chronic low-grade inflammatory disease began with the detection of the catabolins, a low molecular weight peptide that subsequently was named Interleukin (IL)-1, which is released by synovial tissue. IL-1, IL-6, and TNF-α play a key role in its pathogenesis. “Altered biomechanics promote inflammation,” explained Prof. Steven B. Abramson, NYU School of Medicine, New York (NY/USA).

The OA group consists of two distinct populations, the fast progressors, and the non-progressors. Only, 10 to 20% of all OA patients are rapidly progressing. Therefore, it is of key importance to find biomarkers that predict progression. Patients with symptomatic OA often have high prostaglandin (PG) E2 and C reactive protein levels.

In another trial, patients with more than a 3-fold elevation of IL-1 had higher levels of pain, assessed in the WOMAC Index total score. Plasma levels of IL-1 receptor antagonist were associated with the severity and progression of symptomatic knee osteoarthritis in a causal fashion, independent of other risk factors, in a recent trial.

By understanding the mechanisms driving joint tissue destruction in OA, hopefully, new targets for therapy are emerging, that might be able to halt the progression of OA.

Symposium “Management of OA: Beyond the guidelines”, 2017 ACR/ARHP Annual Meeting, November 3- 8 2017, San Diego (CA/USA).

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