Scientists are getting closer to finding a way to fix damaged knees and protect people from arthritis. A new discovery shows how ageing changes our joints, and it could lead to treatments that help keep them healthier for longer.
Arthritis is a painful condition that makes joints swell, stiffen, and become inflamed. It affects millions of people in the UK and around the world, and for many, it slowly gets worse over time. Right now, there is no cure. Most treatments only help manage the pain, and in serious cases, people may need joint replacement surgery. But there is some hope. Researchers at Stanford University say they may have found a new way to help cartilage repair itself, which could change how arthritis is treated in the future.
Cartilage is a smooth, rubbery tissue that cushions joints like the knees, hips and shoulders. It allows bones to move easily without rubbing together. The issue lies in cartilage’s inability to self-repair once it sustains damage from injury, sports, or ageing. Over time, this damage can lead to arthritis, where bones grind against each other, causing pain and loss of movement.
The Stanford team developed a new drug that targets a protein in the body linked to ageing. This protein, called 15-PGDH, becomes more active as we get older and has been associated with a gradual decline in how well tissues function.
In earlier studies, scientists found that high levels of this protein were linked to muscle weakness in ageing mice. When researchers blocked the protein, older mice gained muscle strength and endurance. On the other hand, when young mice were made to produce more of it, their muscles shrank.
These findings led scientists to wonder whether the same protein might also be affecting cartilage. To test this, researchers used a drug designed to block 15-PGDH. They injected it into mice, either into the body or directly into the knee joint. The results were striking. In older mice, cartilage that had worn down with age began to thicken again, showing signs of regeneration.
The treatment also worked in mice with knee injuries similar to ACL tears, a common sports injury that often leads to arthritis later in life. Mice that received the drug twice a week for four weeks after injury were far less likely to develop osteoarthritis. They were also able to put more weight on the injured leg, suggesting less pain and better joint function. In contrast, mice that did not receive the drug developed severe arthritis within just a few weeks. Researchers also noticed that treated mice showed fewer signs of inflammation in their cartilage and a shift back toward a more “youthful” cartilage profile.
To see if the findings might apply to humans, the team tested the drug on cartilage taken from patients undergoing knee replacement surgery. After just one week of treatment in the lab, the human cartilage showed early signs of regeneration and reduced inflammation.
Professor Helen Blau, who led the study, said the discovery could change how doctors think about treating joint damage. She explained that the drug does not rely on creating new cells but instead helps existing cartilage cells change their behaviours and start repairing tissue again.
Dr Nidhi Bhutani, a co-author of the study, added that this shift in cell activity could have a major impact on real-world treatments. Importantly, early clinical trials of a similar drug targeting the same protein have already shown it to be safe in healthy volunteers when used for muscle weakness.
The researchers now want to test this treatment in people to see if it can help the body repair damaged cartilage and stop arthritis from developing. If it works, it could help millions of people avoid long-term joint pain and may even reduce the need for joint replacement surgery later in life.
