There’s strong agreement that any significant injury, such as a tear in the knee’s shock-absorbing meniscus, can lead to arthritis. A lifetime of repetitive motion, such as deep-knee bends, also boosts risk. The medical community has also blamed simple wear and tear on the body, like tires gradually wearing out on a car. A new study at Stanford’s School of Medicine puts that view in question.
Osteoarthritis affects 27 million Americans — and one-half of all people over the age of 70. There is no treatment to slow its progression; aspirin and other medicines simply ease the pain. Joint replacement is the only cure. The study headed by Dr. William Robinson, associate professor of immunology and rheumatology, suggests the problem is not just injury, but the body’s response to it.
When the body senses damage to cartilage — even tiny microscopic tears, without symptoms — a primitive arm of the immune system kicks into gear. This system, called the “complement system,” also protects against viruses and bacteria. It cranks out inflammatory proteins and little enzymes, which attack the joint. This continues for years, even decades.
In their study, the team compared the levels of proteins in the joint fluid of patients with arthritis to those of healthy patients. Arthritic patients had more proteins – “accelerators” of this process, with fewer “brakes.” They also looked at the genes that are the recipes for these proteins. In arthritic patients, the genes were more active.
Experiments in mice confirmed this view of the process. A strain of a bioengineered mouse that lacked this inflammatory generating process seemed protected against arthritis — even when their cartilage was damaged.
Since these proteins also protect again infection, it is not possible to eliminate them. However understanding the mechanism should bring the finding of a cure that much nearer.
In the meantime, the advice is to maintain your weight, exercise to strengthen joints and follow a healthy diet.