Promoting Cartilage Stem Cell Activity to Improve Recovery from Joint Fracture.

摘要

It has been assumed that chondrocytes killed by mechanical injury to articular cartilage are never replaced and that the resulting hypocellularity contributes to post-traumatic osteoarthritis. However, we found that nonviable areas in an explant injury model were repopulated within 7-14 days by cells that appeared to migrate from the surrounding matrix. We hypothesized that the migrating population included chondrogenic progenitor cells drawn to injured cartilage by alarmins released from dead chondrocytes. Injuries that caused chondrocyte death stimulated the emergence and homing of chondrogenic progenitors via RAGE-mediated chemotaxis. Moreover, when supplied with a fibrin matrix chondrogenic progenitor cells regenerated cartilage in a chondral defect. Thus, we confirmed an endogenous mechanism that may be leveraged to repair cartilage defects in vivo that might otherwise lead to progressive cartilage loss.