Stanford scientists reverse joint aging

Researchers at Stanford University have identified a critical protein, 15-PGDH, that contributes to the breakdown of joint cartilage as people age. This protein's increased activity interferes with the body's natural tissue repair and inflammation reduction processes.

In laboratory experiments, scientists administered a drug to block 15-PGDH in older mice with worn cartilage, observing significant thickening. The treatment also prevented the development of osteoarthritis in younger, injured mice. Notably, this regeneration occurred without stem cells, by reprogramming existing cartilage cells.

Further tests on human knee cartilage samples from patients awaiting replacement surgery demonstrated regrowth and decreased inflammation following the same treatment. These findings, published in the journal Science, suggest a potential pathway to avoid joint replacement surgeries. The team is preparing for clinical trials, building on prior safety data for 15-PGDH blockers.