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Sarah Davidson
"The embryonic origins of site-specific arthritis" published in Nature Immunology, provides new insight into one of the long-standing mysteries of rheumatoid arthritis: why inflammation targets certain joints while leaving others relatively unaffected.
Rheumatoid arthritis is an autoimmune disease that causes pain, swelling and stiffness when the immune system attacks the synovium, the tissue lining the joints. Over time, this inflammation can damage cartilage, bone and surrounding tissues.
The study compared two finger joints that differ in their susceptibility to rheumatoid arthritis. Researchers compared distal finger joints - known as proximal interphalangeal (PIP) joints, which are commonly affected by the disease, and the distal interphalangeal (DIP) joints near the fingertips, which are usually spared. They found that the PIP joints contained larger synovial volume and higher levels of PI16-positive (PI16+) fibroblasts, a specialised type of connective tissue cell. These differences were established before birth, suggesting that the tissues themselves may play an important role in determining where disease occurs.
Christopher Buckley, Kennedy Professor of Translational Rheumatology at the University of Oxford, said: 'For decades we have known that rheumatoid arthritis selectively targets particular joints, but one of the great unanswered questions is why? Our findings suggest that the answer lies not only in the immune system but also in the tissues themselves. The cellular and structural characteristics established during development may help determine where inflammation takes hold later in life.'