Arthritis Treatment: The Role of Weight Loss In Osteoarthritis Treatment

Osteoarthritis (OA) is the most common form of arthritis and affects more than 20 million Americans. It is a condition that affects hyaline articular cartilage, the tough gristle that caps the ends of long bones.

Hyaline cartilage consists of a matrix made up of a combination of proteoglycans (complexes of proteins and sugars) and chondrocytes. Chondrocytes are cartilage cells that manufacture matrix under normal circumstances. They are responsible for nourishing the matrix as well.

However, when OA develops, a distinct change in the milieu of the joint environment occurs. Chondrocytes begin to elaborate destructive enzymes causing cracks in the cartilage, the synovium (lining of the joint) becomes inflamed, and the underlying bone becomes hard and forms spurs.

What causes OA to develop is usually injury or trauma. In any event an injury to the joint appears to be the inciting factor. Genetics play a role as well.

As OA progresses, biomechanical factors come into play. And this is where obesity plays a huge role in the worsening of disease. While overloading of the joint is the obvious major consideration, there is now abundant evidence that fat itself acts as an "organ" that perpetuates inflammation.

"Adipokines" are chemical messengers produced mainly by adipocytes (fat cells). The major adipokine is a substance called leptin. Leptin is interesting because it has contradictory actions. While it appears to help with the synthesis of growth factors that stimulate cartilage growth, it also appears to lead to the production of inflammatory proteins that cause further cartilage deterioration.

But that's not all. There are other adipokines that make a significant contribution in this cascade of events. Adipopnectin also seems to promote inflammation in arthritis. It causes the cartilage matrix to degrade and also promotes the manufacture of destructive enzymes.

Visfatin levels are also associated with cartilage degradation. Resistin promotes inflammation.

These fat produced proteins may explain why symptoms in people with OA who are overweight seem to get better with loss of body fat rather than just with weight reduction.

The bottom line is that OA is more than just a mechanical disease. Abnormal fat metabolism appears to lead to the production of factors that cause further cartilage loss and deterioration.

These new developments confirm the long held belief that people with symptomatic OA who carry excess fat may benefit from fat reduction.

These findings have been substantiated in real life clinical trials. Richette and colleagues (Richette P, et al. Ann Rheum Dis. 2011; 70: 139-140) demonstrated that obese individuals with knee OA who underwent gastric banding surgery not only had improvements in their symptoms but also blood levels of adipokines plummeted along with other inflammatory markers.