Mechanical Problems or Osteoarthritis

There was a review published in January of 2009 that challenges the conventional thinking that cartilage problems and joint damage that are visible on x-rays are the keys to osteoarthritis, or OA. The authors of this review, saw OA as a painful reaction to mechanical problems, with the muscles surrounding the joint and subchondral bone, the slightly spongy bone under the cartilage, as the main players of OA.

They point to evidence, although this evidence is from small studies, showing that actions to stop excessive mechanical stress on joints can stop OA damage and even allow the regrowth of the bone and cartilage. Even though the replacement tissue may not be as good, it may be good enough for careful movements and a life without pain.

Sources of excessive stress or the force on joints include genetic and developmental defects, obesity, trauma, poor alignment of bones, and tiny missteps or falls, and whether alone or in combination, these can lead to repeated micro-damage to the bone and to the cartilage. The review looks at inflammation as a result of and a secondary contributor to mechanical stress. The unmanageable forces on a joint can chip off minute bits of bone and cartilage and if these bits are ground into the joint they can cause further erosion and then they will attract the attention of the immune system. Our immune system will respond to these bits of bone and cartilage causing inflammation and pain and this response will weaken the tissues even further.

The authors of this review also said that the body has several types of “shock absorbers” to reduce these forces on the cartilage and that the main ones are the muscles around the joint and the subchondral bone. Muscles are like rubber bands, stretching to absorb and disperse the load or force and the subchondral bone cushions the force by releasing fluid out from tiny pores as the force is applied. The micro-damage to the joints occurs when these shock absorbers fail, when reflexes are slow to alert the muscles, when force is applied too quickly, or when the muscles or bones aren't strong enough or healthy enough. Aging, weakness, “micro” missteps, and damaged nerves and reflexes all take a toll on the muscles and joints.

The body's constant repair of the micro-damage may even cause the subchondral bone to be replaced by even more damaged dense tissue, making it less effective in absorbing shock. The overgrowth of the replacement tissue may even cause the cartilage to crack and flake making your osteoarthritis worse.

The authors believe that their colleagues focus too much on x-rays for signs of OA, which can bear little relationship to pain and disability since half of the individuals whose x-rays showed advanced OA, had no pain. Doctors find it difficult to identify the source of pain OA, but their general efforts to reduce the mechanical stress may offer some relief. These efforts include losing weight, preventing injuries, and eliminating chores that require knee bending and heavy loads.

This review should get doctors rethinking about OA. One of the drawbacks is that there has not been a large clinical trial directly and complete testing of the new hypothesis, which is that ongoing mechanical injury is more fundamental to OA than the loss of cartilage.