Osteoarthritis has traditionally been thought to be an inevitable result of wear and tear. But it's now clear the immune system is playing a leading role.
Orthopaedic surgeon Constance Chu has spent her career seeking ways to prevent osteoarthritis from developing after a knee injury.
Stanford scientists have dug up a defect at the heart of rheumatoid arthritis: a faulty "anchor" that should be tethering a key molecule to the spot inside immune cells where it has to be in order to do its job. It seems this defect can be reversed with a not yet commercially available small-molecule drug.
Rheumatoid arthritis and coronary artery disease share a common culprit: an important type of immune cell, called a macrophage, that has gone haywire. Stanford investigators have zeroed in on a molecular defect in macrophages' metabolic process that drives both disorders.