Arthritis Treatment: How Does Being Obese Potentially Affect Arthritis Treatment?

Osteoarthritis (OA) is the most common form of arthritis. It is a condition due to the disruption of hyaline cartilage, the gristle that caps the ends of long bones. Hyaline cartilage consists of a matrix of collagen and proteoglycans (combinations of sugars and proteins). Within this matrix are cells called chondrocytes which are responsible for producing and maintaining the integrity of the matrix.

Triggering factors for the development of osteoarthritis can be such factors as trauma.

Weight also plays a significant role. A study by Messier and colleagues presented at the 2011 meeting of the American College of Rheumatology clearly demonstrated that patients losing 11% of their body weight could experience a 50% reduction in pain related to their OA.

Another key factor in the development of OA is malalignment of the joint. This places excessive stress on the joint. The response is for the chondrocytes to begin to produce chemical messengers called cytokines, metalloproteinases, and other factors that accelerate joint damage. The end result is stoppage of matrix production by the chondrocyte and wearing away of cartilage. There is also evidence that overloading due to malalignment may stimulate bone cells underneath the cartilage to become abnormal.

But that's not all. Obesity is associated with OA in non-weight-bearing areas like the hands.. So being obese may contribute to the development of OA above and beyond mechanical factors.

Scientists are now viewing adipose tissue ("fat") as being an endocrine organ. Adipose tissue produces chemical messengers such as cytokines and adipokines that promote inflammation. These cytokines have been found to be present in the joint tissue of obese patients. The obvious therapeutic action here would be to encourage a patient to lose weight because reduction in the production of these cytokines could assist in symptomatic improvement along with the mechanical relief of just getting weight off the affected joints. So really what happens is an additive beneficial effect of weight loss.

One adipokine that is often mentioned is leptin. Leptin is produced by fat cells. Leptin levels are associated with the amount of body fat a person has but leptin is also regulated by inflammatory messengers. Leptin has a direct effect on cartilage. Normal cartilage doesn't make leptin but osteoarthritic cartilage does. What is perplexing is that leptin is a double-edged sword. While it seems to stimulate the manufacture of growth factors that promote cartilage growth, it also stimulates the production of factors that increase inflammation.

The net effect though seems to favor cartilage degradation.

In summary, the biology of cartilage and OA is experiencing some major new developments that could provide insight into newer therapies.