Osteoarthritis — the gradual wearing away of the cartilage that cushions joints — is one of the most widespread conditions on the planet, affecting an estimated 500 million people worldwide. Current treatments manage pain but do nothing to address the underlying damage. Joint replacement surgery remains the most definitive option. A study published on November 27, 2025 in the journal Science by researchers at Stanford Medicine in Stanford, California, may point toward something better.
The team discovered that a protein called 15-PGDH acts as what they describe as a "gerozyme" — an enzyme that increases with age and suppresses the body's ability to regenerate tissue. In young mice, 15-PGDH levels in knee cartilage were low; in older mice, they had roughly doubled. When the researchers blocked the protein using an injection in aged mice, the knee cartilage — which had become thin and dysfunctional with age — thickened significantly across the joint surface and began to regenerate. Animals treated this way showed steadier gaits and placed more weight on previously injured legs — signs of reduced pain.
Crucially, the finding extended to human tissue. Samples taken from patients undergoing knee replacement surgery were treated with the same inhibitor and showed early signs of articular cartilage regeneration, alongside reduced expression of cartilage degradation genes.
The study's senior authors, Professor Helen Blau and Professor Nidhi Bhutani, both of Stanford Medicine, described the result as a genuinely new mechanism for adult tissue regeneration. An oral version of the treatment is already in clinical trials for age-related muscle weakness and has shown it is safe and active in healthy volunteers — a development that Blau said she hopes will help accelerate a similar trial for cartilage regeneration.
If that trial confirms what the lab work suggests, the long-term goal — regrowing cartilage and avoiding joint replacement entirely — may no longer be out of reach.