The cartilage repaired itself once they flipped one switch

Stanford Medicine researchers have identified a protein that roughly doubles in aging joints and blocks cartilage from healing, and found that switching it off regrew the smooth, load-bearing tissue that osteoarthritis destroys. The protein, called 15-PGDH, degrades a molecule that drives repair. Block the protein, and repair resumes. In older mice given a small-molecule inhibitor, thinned cartilage grew thicker. Human tissue taken from knee replacement surgeries responded after just one week of treatment. The surprise was how it happened. The team went in expecting stem cells and did not find them. Instead, the cartilage cells already sitting in the joint quietly shifted their gene expression and got back to work. "We were looking for stem cells, but they are clearly not involved," said Helen Blau, senior author of the study, published in Science. Osteoarthritis affects hundreds of millions of people, and no approved drug treats the cartilage loss itself. A human cartilage trial is the next step.