Trauma

When a bone is injured, it often mends quickly with no further problems. But unlike bone and most other tissues, articular cartilage lacks blood vessels, nerves and lymphatics, channels that carry lymph – a clear fluid that bathes and nourishes body tissues. As a result, injured cartilage doesn’t heal well.

Damage to the joint can lead to joint instability, which can cause cartilage to wear excessively. It also sets of chemical changes in the joint that the body’s natural reparative process can’t keep up with. Cartilage cells begin to die and telomeres – regions at the end of chromosomes involved in their replication and stability – shorten.

For as many as 50 percent of people who suffer cartilage injuries, the result is osteoarthritis, which may begin as soon as three months after a severe injury or decades after a minor one, says Joseph A. Buckwalter, MD, professor and chair of the Department of Orthopaedic Surgery at the University of Iowa Hospitals and Clinics in Iowa City, Iowa.

The risk of OA development following injury is influenced by the type of injury as well as an individual’s characteristics, such as age, sex and body mass index.

Findings Could Lead to New Therapies

While there are currently no therapies to stop OA or its progression, research into these factors could eventually lead to new ways to treat – or even prevent – OA and to target preventive efforts and therapeutics to people at greatest risk.

For example, an understanding of the chemical changes that occur in the joint following injuries could lead to therapies to interfere with those changes. Dr. Buckwalter and his team are targeting some of the molecular causes of cartilage loss. Their studies are moving into animal models.

Findings about leptin’s role in OA suggest that maintaining a healthy weight may help OA in more ways beyond reducing mechanical stress and that a low-fat diet – or therapies to interfere with leptin – could eventually prove useful for managing the disease, says Guilak. “If we know that some inflammatory mediator, whether it is leptin or something downstream of leptin, causes the joint damage, we could potentially take this one step further and interfere with that process,” he says.

Genetic findings could have multiple implications as well. “We hope that by learning about gene mutations we will eventually be able to define a therapeutic approach to these diseases, either by manipulating the gene itself or by downstream manipulation to modify the effects of the mutation,” says Dr. Moskowitz.