Newly Identified Cadherin Molecule Implicated in Joint Damage in Rheumatoid Arthritis

Scientists supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) have made an important discovery about the cause of joint damage in rheumatoid arthritis (RA), one of the most common and debilitating joint diseases. They have identified a new target for therapeutic development to slow or prevent joint damage, perhaps without the side effects of many current arthritis medications.

RA, a disease that affects an estimated 2.1 million Americans, is thought to occur when the body’s normally protective immune system mistakenly attacks the thin membrane that lines the joint. In healthy joints, that membrane, called the synovium, secretes a fluid that nourishes and lubricates the joint. “It is essential for joint function,” says David M. Lee, M.D., of Brigham and Women’s Hospital in Boston and lead author of the new study published in the journal Science. In RA, however, white blood cells of the immune system infiltrate the synovium. “We think these cells drive inflammation in the joint,” he says. “But at the same time, the synovium shows a number of other abnormal features. It overgrows and starts attaching to the bone and cartilage.” Unchecked, the synovial tissue can erode the cartilage and bone, leading to joint damage and malformation.