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