Elderly people suffering with osteoarthritis may have finally found a reason to smile and some hope on the horizon.

Contrary to current wisdom, osteoarthritis is not simply the product of wear and tear. A new study finds it is at least in part driven by the body’s own immune system. This means that the painful condition – thought by many to be irreversible – can perhaps be prevented or cured in humans by blocking the inflammatory processes.

Osteoarthritis, the most common joint disease in the U.S., affects nearly 27 million people, most of them elderly, and is associated with the breakdown of cartilage in joint areas, such as the knees, hips, fingers and spine.

The study, by researchers at Stanford University of Medicine, first demonstrated that humans with osteoarthritis contain a high amount of proteins that are made when the body is under attack by a bacterial or viral infection. These proteins, called the complement system, attack the damaged joints just as they would attack a bacteria or virus. This sets off a cascade of events that result in the inflammation and severe pain associated with osteoarthritis.

The Stanford investigators used genetically-engineered lab mice to determine that the complement system is causally related to the development of osteoarthritis. They showed that if the complement system is disrupted in these mice, the mice are actually protected against osteoarthritis, even when their joints are physically damaged. If the mice contained an over-activated complement system, their arthritis became more severe.

The complement system activates a cluster of proteins called the membrane attack complex (MAC). In osteoarthritis, the MAC facilitates the secretion of enzymes and inflammatory chemicals that chew up cartilage in the joints and spaces between bone cells. The destruction of cartilage causes severe pain when humans with osteoarthritis attempt to move the damaged joint.

With their latest findings, the field of arthritis finally has a specific set of proteins to target – the complement system. The Stanford investigators believe that by tinkering with the complement system earlier in a patient, humans with osteoarthritis could slow the disease progression and perhaps even prevent the disease altogether even before symptoms appear.

“It’s a paradigm change. People in the field predominantly view osteoarthritis as a matter of simple wear and tear, like tires gradually wearing out on a car,” said William Robinson, MD, PhD, the study's senior author.

Currently, the two most popular drugs to treat osteoarthritis are Tylenol (acetaminophen) and Aspirin (ibuprofen), which alleviate some of the inflammation and pain in elderly people but do not treat the disease itself. The nutraceuticals glucosamine and chondroitin are also used by some to protect against the effects of time on joint tissues.

The problem is, however, is that tinkering with the body’s complement system might lead to people being more susceptible to bacterial and viral infections, an outcome that the investigators do not wish to occur. The researchers believe that brief administration of a drug that inhibits the complement system could help treat osteoarthritis without leading to more bacterial and viral infections. More research is needed to come to terms with these issues and to determine if disrupting the complement system helps humans.

This study is published online ahead of print in the journal Nature Medicine.