The process is complicated, involving a chain reaction of changes in the joint. The body’s natural reparative process can’t keep up with the multitude of biological and chemical changes that occur in response to injury, explains Stefan Lohmander, MD, PhD, professor of orthopaedics at Lund University Osteoarthritis Research Group and University of Southern Denmark. He says cells begin to die off in the cartilage, and telomeres, which protect chromosomes from deterioration, are diminished, leading to premature aging of cartilage cells. Additionally, the release of various proteins causes altered cell regulation, inflammation and increased bone cell turnover, which can cause bone thinning and/or bone spurs.

What happens next – whether OA develops or not – is influenced by several factors, including genetic variability, gender (women are at higher risk than men), age (people who are older at time of injury are at higher risk), body mass index (BMI), and the type of injury and treatment. 

Researchers are looking for ways to interfere with some of the chemical changes that occur immediately following a trauma. For example, Dr. Buckwalter and his team are targeting some of the causes of cartilage loss, such as oxygen-free radicals and proteins that accumulate with age and degeneration. His studies have so far been in the lab.

Obesity & OA

If you are like most Americans, as the years add up, so do the pounds until – voilà – the arrival and entrenchment of middle-age spread.

One reason that being overweight or obese increases the risk of arthritis is simply biomechanical – the more weight on your joints, the more stress they endure, which in some people results in arthritis. The biomechanical impact of obesity is particularly detrimental when bones are misaligned. 

However, there is another way obesity may increase the chances of developing arthritis, even in non-weight bearing joints, such as those in the hands: Fat tissue releases many chemicals that increase inflammation and affect the joints.

One example is leptin, a hormone that is produced by fat cells and plays a central role in the regulation of fat storage and metabolism. One study found that body fat itself without leptin does not lead to OA. Another study found that higher leptin levels were related to the narrowing of joint space in the hip (a sign of arthritis). And several studies have found that leptin levels correlate with patient self-reported pain scores in OA.

And that’s just one of many chemicals released by fat tissue. Others, such as estrogen and adiponectin, are under study.