Researchers at Stanford University have identified 15-PGDH, a protein that increases in activity with age and contributes to the breakdown of joint cartilage. In a study, blocking this protein in older mice led to noticeable thickening of worn knee cartilage and prevented the development of osteoarthritis in younger mice. Remarkably, this recovery did not require stem cells; instead, existing cartilage cells, known as chondrocytes, were reprogrammed into a healthier state. Treated mice exhibited improved mobility and reduced pain. The same treatment also showed promising results in human cartilage samples obtained from knee replacement patients, indicating potential for regrowth and decreased inflammation. Stanford microbiologist Helen Blau expressed excitement over the findings, envisioning a future where joint replacement surgeries may be avoided. The research aligns with other advancements, including a study on semaglutide, which protects joint cartilage, and an injectable treatment being developed at the University of Colorado Boulder that may reverse osteoarthritis. The Stanford team is preparing for clinical trials, supported by previous safety studies on 15-PGDH blockers. The study was published in the journal Science.