Osteoarthritis (OA) is both a degenerative and progressive disorder that is the result of the breakdown of the cartilage cushions that sit between the bone surfaces in the joints, causing pain and stiffness. It is the most common form of arthritis and often leads to the development of bony spurs and cysts in various joints.

The joints in the hands, knees, hips, neck and spine are the most affected by OA. Osteoarthritis is a significant cause of disability in middle-aged to older adults, causing limitation in mobility, and decreased ability to work and to care for oneself. The symptoms can create a vicious cycle of decreasing movement that in turn leads to increased pain, loss of muscle tone and further disability.

Rather than assuming OA is an inevitable result of aging, people can decrease their risk, and perhaps slow its progression, by making diet and lifestyle changes.

Physical therapy to improve mobility and strengthen surrounding muscles is often prescribed to treat osteoarthritis, along with medications to target pain and inflammation. Both may reduce the symptoms of OA, but they are not cures. Surgical interventions to reduce bone spurs and joint degeneration include arthroscopy and joint replacement.

For a long time it was believed that osteoarthritis was the result of wear and tear on the joints over years. This view is beginning to change, however: a recent study reviewing the current literature on this subject highlights a different source of the joint destruction seen in OA.

OA is often worse in people who are overweight, and this had been assumed to be the result of the additional stress bearing a heavier load puts on their joints. But the disease is also severe in overweight patients' non-weight bearing joints, such as the hands. This observation suggested that being overweight may bring on the disease in a biochemical/metabolic way, rather than purely mechanical one.

The cells in your joints are metabolically active, that is, they use nutrients and produce metabolic products. As such, their function and health are influenced by the cellular environment around them. If the cells that make up the joint tissue are exposed, for example, to the abnormal metabolic conditions commonly seen in obesity, they can produce substances such as inflammatory compounds, metabolic by-products and immune modulators that are harmful to the cells that make up the joint cushions.

These biochemical processes can lead to the joint changes that are observed in osteoarthritis. Researchers have noted that when joint cells are metabolically stressed, they produce too much glucose. The extra glucose is converted into lactic acid. The presence of high levels of lactic acid in the surrounding tissue can lead to inflammation and pain in the joint space, and produce the signs and symptoms of OA.

This is how a poor diet, sedentary life style and being overweight can contribute to the development of osteoarthritis by actually changing the biochemical functioning of the cells in the joints. These changes lead to immune and inflammatory responses which destroy normal tissue and cause the joint breakdown characteristic of the disease.

These findings are highly significant for at least two reasons. First, they suggest that rather than assuming OA is an inevitable result of aging, people can decrease their risk and perhaps slow its progression, by making diet and lifestyle changes. Second, as some of the metabolic and biochemical mediators of these changes are identified, scientists will eventually be able to create drugs to specifically combat the process and prevent its progression.

The researchers believe that weight, diet, lifestyle, exercise and attention to metabolic health are all key factors that are within our control and should be addressed in the battle against OA. People can take a more active role in protecting themselves against this debilitating disease, rather than assuming it is inevitable. This will benefit both individuals and society, as both suffering and health care spending will be decreased.

The study is published in Nature Reviews Rheumatology.