Osteoarthritis is the most common form of joint disease, a condition that causes joints to become painful and stiff. It can happen to any joint when the cartilage cushioning the ends of bones breaks down or wears away. Currently, there are no approved drugs to slow or stop the underlying disease. But there is a promising development from an unexpected quarter—a blood thinner.
Researchers led by Chuan-ju Liu from the Department of Orthopedics and Rehabilitation at Yale University School of Medicine screened a library of nearly 1,000 approved drugs for compounds that could suppress the inflammatory signals underlying osteoarthritis.
Although inflammation is normally part of the body’s response to injury, persistent low-level inflammation in joints can contribute to the gradual breakdown of cartilage.
Unexpected discovery
Of the 980 drugs tested, three stood out because they could suppress two key inflammatory signals involved in osteoarthritis. Further testing whittled them down to one: a medication called dabigatran, which is a blood thinner used to prevent clots and strokes.
To see what effect dabigatran might have on osteoarthritic joints, the researchers tested it on mice and macaques with surgically induced osteoarthritis. The drug was injected directly into the mice’s affected joints, while the macaques received it orally.
The results, published in the journal Science Translational Medicine, were encouraging.
In mice, dabigatran reduced cartilage damage and signs of joint inflammation. The animals also showed less pain-related behavior and could move more freely.
Meanwhile, in the macaques, the drug helped preserve cartilage and improved their ability to walk. There was also less abnormal hardening of the bone beneath the cartilage.
Behind the results
But how was a blood thinner producing these effects? To find out, the researchers looked more closely at how dabigatran interfered with the inflammatory processes involved in osteoarthritis.
They discovered that the drug acted on a protein called BIG2, which helps control the movement of cell surface receptors. These receptors receive chemical signals that can trigger inflammation.
Dabigatran affected two of these receptors, known as TNFR1 and IL-1R1, in different ways to reduce inflammation. It encouraged the release of TNFR1 from cells and promoted the breakdown of IL-1R1, which made the cells less responsive to both inflammatory signals.
“This coordinated regulation of receptor availability represents a previously unrecognized approach to dampening inflammatory signaling and restoring chondrocyte homeostasis,” commented the study authors.
However, the findings are still at an early stage. The treatment has not been tested in people with osteoarthritis, and there are concerns that dabigatran could cause bleeding.
“Nonetheless, comprehensive safety studies evaluating infection and bleeding risk, as well as long-term tolerability, will be required before clinical translation.” https://medicalxpress.com/news/2026-11-blood-thinner-osteoarthritis.html
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