New Drug Treatment For Rheumatoid Arthritis Specifically Targets Cartilage

Researchers have uncovered a novel Rheumatoid Arthritis treatment method that directly targets the cells responsible for cartilage damage in the joints.

A specific rheumatoid arthritis (RA) drug that directly targets damage-causing cells may sound too good to be true — but it isn’t science fiction. Researchers from the La Jolla Institute for Allergy and Immunology and their colleagues from the University of California San Diego have uncovered a novel drug therapy that specifically focuses on the kinds of cells that are responsible for cartilage damage in affected joints of RA patients.

 Their findings, published in the current issue of Science Translational Medicine, have the potential to unleash a whole new world of RA medications that could alleviate symptoms and improve disease outlook with less complicated side effects. While current RA pharmaceuticals focus on the immune system, this new class of therapies would work on a different target to slow disease progression, prevent severe joint damage, and reduce inflammation without slowing or suppressing the immune system like many treatments do.

“Unfortunately, for around 40 percent of patients, immune-targeted therapies are not sufficient to bring them into full remission,” said Bottini. “If we could add a drug that acts on a different target without increasing immune suppression it could be very valuable.”

How Will the New Drugs Be Different?

These new drugs will be unique in that they target fibroblast-like synoviocytes (FLS), which are the specialized cells in the synovial joint lining. They line the joints to provide lubrication and cushioning, preventing against and repairing injuries. However, once activated, like during the autoimmune process of RA patients, the cells can actually attack the healthy cartilage and tissue surrounding the joint. In patients with RA, the synoviocytes are what cause the most joint and cartilage destruction, yet, until now, no drug approach has targeted them directly.

Taking it a step further, even if biologics or immunosuppressants have an RA patient’s immune activity under control, synoviocytes can still cause structural, skeletal damage to the patient’s joints. This may explain why some patients still experience pain and disability while inflammation rates and swelling are relatively under control.

The novel drug target that these researchers have identified will work on altering the enzyme receptor response that triggers the destructive activity of synoviocytes, using a sort of molecular decoy. Scientists envision this new method of treatment being used either in lieu of, or in addition to, existing RA therapies.

According to Dr. Bottini, “The ultimate goal is to use biologics that target synoviocytes in combination with treatments that suppress the immune system, such as methotrexate or anti-TNF, to address all three aspects of rheumatoid arthritis: swollen joints as a result of inflammation, cartilage damage, and bone damage.”

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