» Rethinking Osteoarthritis as Just a Wear-and-Tear Disease
Rethinking Osteoarthritis as Just a Wear-and-Tear Disease

Three things are clear from ongoing research: 1) obesity is on the rise in the United States, 2) more people are experiencing osteoarthritis (OA), and 3) there is a direct link between obesity and osteoarthritis.

None of that may surprise you. What is new and notable is the fact that research is showing osteoarthritis (OA) is more than just a wear-and-tear disease. Excess load and weight is certainly a factor. But there may be some "hidden" (less obvious) variables that are just as important (if not more important) contributing to joint degeneration and OA.

What are those less obvious risk factors? Obesity does cause local biomechanical changes in the joint reducing shock absorbing ability and increasing load and force on the joint cartilage. Eventually the joint starts to break down. But fat cells (referred to as adipose tissue) also activate inflammation that is system-wide (throughout the entire body).

It turns out this low-grade inflammation has a direct and pathologic effect on the musculoskeletal system (especially bone and cartilage). Fat is not just a store house of energy. It is also a very active endocrine (hormone producing) gland. Blood tests confirm that this is the case with elevated levels of inflammatory markers measured in obese people.

Scientists haven't fully unraveled how obesity, systemic inflammation, and joint changes are all connected. But they are finding out more and more each day that may eventually help find a drug to prevent or at least manage osteoarthritis. This proinflammatory state of the obese body is also suspected as a contributing cause of hypertension, insulin resistance, and high cholesterol levels.

It is important to note that obesity is not the only reason joint osteoarthritis develops. Age, sex (female), family history, race, previous injury, and lifestyle are all known risk factors for osteoarthritis (OA). That's why OA is considered a multifactorial disease. Of all those risk factors, only obesity is considered modifiable (in other words, a risk factor you can do something about).

There isn't anything you can do to change your age, your past history of injuries, or family history. And even though it can be a challenge, weight loss is one way to change the biomechanical and systemic effects that lead to joint damage and degeneration. In fact, physicians are starting to think of weight loss as one of the most effective treatment approaches to osteoarthritis. Likewise, weight loss can directly affect chronic pain obese people experience from pressure on the surrounding soft tissue structures.

If you are overweight to the point of being considered obese, you know that weight loss isn't easy. Many health care professionals recommend education to prevent weight gain first. But for those whose body mass index (BMI) indicates they are already past 'normal' and in the overweight or obese zone, weight loss is still advised.

Strategies for successful weight loss include diet and exercise, behavioral counseling and incentive programs, and/or possibly bariatric surgery. Slow, gradual, but steady weight loss is always preferred because maintaining weight loss is just as challenging as losing the weight in the first place. Negative side effects of bariatric surgery (e.g., decreased bone mass, increased risk of bone fractures, failure with weight gain) make this approach less desirable.

In summary, joint osteoarthritis is no longer considered just a "wear-and-tear" type of arthritis. Obesity and the excess weight and load associated with obesity are major factors. But now we know there are inflammatory effects of adipose (fat) tissue that also contribute to joint destruction. Weight loss and exercise aren't always easy solutions but they are the most successful in addressing all of the local and systemic effects of obesity.

Reference: Ryan C. Koonce, MD, and Jonathan T. Bravman, MD. Obesity and Osteoarthritis: More Than Just Wear and Tear. In Journal of the American Academy of Orthopaedic Surgeons. March 2013. Vol. 21. No. 3. Pp. 161-169.