Why some people with rheumatoid arthritis have pain without inflammation

Treatment for rheumatoid arthritis has come a long way in recent years. In many cases, a battery of medications can now successfully stymy the inflammatory cells that cause swelling and pain when they infiltrate tissues around the joints.

"These 815 genes are rewiring the sensory nerves, which explains why anti-inflammatory drugs don't work to alleviate pain for these patients," says Orange. The findings may lead to new treatments for these outliers.Rheumatoid arthritis is a tricky chronic disease. Its symptoms -- stiffness, tenderness, swelling, limited motion, and pain -- slowly emerge in the hands, wrists, feet, and other joints. It occurs symmetrically and sporadically, with irregular flare-ups.

GbGMI tests every possible combination of genes in a dataset to determine the optimal set of genes that together associate with a targeted clinical feature -- in this case, pain. Single cell sequencing analysis found that of the four types of fibroblasts in synovial tissue, CD55+ fibroblasts exhibited the highest expression of pain-associated genes. Located in the outer synovial lining, CD55+ cells secrete synovial fluid, allowing for frictionless joint movement. They also expressed thegene, which codes for a protein called Netrin-4. Proteins in the netrin family guide axon growth paths and promote new vascular growth.

"We studied one type, but there are about a dozen. We don't know if all nerves are affected equally. And we don't want to block all sensation. Sensory nerves are important for knowing that you should avoid certain movements and the position of your joint in space, for instance," Orange says.

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