Mice that don't produce lubricin, a thin film of protein found in the cartilage of joints, showed early wear and higher friction in their joints, a new study led by Brown University researchers shows.
This link between increased friction and early wear in joints is a first; no other team of scientists has proven this association before. The finding, published in Arthritis & Rheumatism, sheds important light on how joints work. The discovery also suggests that lubricin, or a close cousin, could be injected directly into hips, knees or other joints inflamed from arthritis or injury – a preventive treatment that could reduce the need for painful and costly joint replacement surgery.
In an editorial that accompanies the journal article, orthopedics researchers from Rush University Medical Center in Chicago call the research an “important contribution to the field” and note that the use of biomolecules like lubricin to prevent joint wear “could have a substantial clinical impact, if successful.”
Gregory Jay, M.D, a Rhode Island Hospital emergency physician and an associate professor of emergency medicine and engineering at Brown, led the research. For 20 years, Jay has studied lubricin's role as a “boundary lubricant” by reducing friction between opposing layers of cartilage inside joints. In this new work, Jay and his colleagues set out to answer the next question: Does reducing friction actually prevent wear, or surface damage, in joints?
To find out, Jay and his team studied cartilage from the knees of mice that don't produce lubricin. Directly after birth, the cartilage was smooth. But in as little as two weeks, researchers found, the cartilage began to show signs of wear. Under an electron microscope, scientists could see that the collagen fibers that cartilage is composed of were breaking up, giving the surface a rough, frayed appearance. This damage is called wear, an early sign of joint disease or injury.