By comparing and contrasting differential gene expression in the synovium of Osteoarthritis versus “normal” subjects, the researchers noticed upregulation of genes involved in RA inflammation and Osteoporosis bone resorption.
It is known that OA is inflammatory, and IL1 is a major cytokine player in this process, but even if OA is viewed as a lesser inflammatory state than RA or JIA, the expensive targeted therapies against IL1, IL6 or TNF are unlikely to be used longterm in a slow-moving disease like OA.
Osteoclast directed therapies are far cheaper and stand a far better chance of a day in the sun.
This GWAS (Genome Wide Association Study) compared the differential gene expression between OA subjects with better preserved cartilage against those with more severely degenerative cartilage.
Not surprisingly, those with worse disease expressed higher levels of genes associated with inflammation.
Osteoarthritis fully deserves the “itis” suffix, and as in so many (probably all) life processes (yes: atherosclerosis, fatty liver, Alzheimer’s and cancers are all inflammatory), inflammation is key to repair and disease.
