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Osteoarthritis treatments provide hope

Would it be fair to say that good health is a desirable goal, one that is pursued by many? Because heart disease is rampant, cardiac fitness is typically part of the plan on the road to optimal health. But how do you achieve this very desirable objective if you can’t walk or stand without pain? For so many, the simple act of walking is the best form of exercise, but cannot comfortably be performed. Cardiologists all tell their patients the same thing: get out and walk, for your heart, for your health.

One of the most common reasons for an inability to walk comfortably is arthritis. As most people are aware, there are many different kinds, but too often the diagnosis is simply “arthritis,”without a discussion of what type, what can be done, and what the prognosis is.

Unfortunate, since there are many options for treatment, and the degree of disability suffered is very dependent on the specific type. Statistically-speaking, osteoarthritis is the most common, by a large factor, so this is generally the reason most are unable to pursue their fitness goals.

Perhaps the most important change in the study and treatment of osteoarthritis over the past several decades has been in attitudes, rather than knowledge.

OA has changed from being a boring, degenerative form of joint pathology, for which nothing can be done, to an exciting clinical disorder of the joints that can be manipulated and improved. What has led to this change? What new information has been discovered?

Historically, diagnosing osteoarthritis was made by examining the affected part clinically, with certain changes in joint anatomy being characteristic of this disease, and on x-ray.

Joints affected by OA experience localized areas of cartilage destruction. As this process advances, narrowing of the joint space is observed on X-ray. Thus, it should not be surprising that interest in OA focused on these destructive changes because all we had to go on was X-ray, as well as the observable developments in the shape and configuration of the part. An obsession with these two specific facets of the disease set the field back, perpetuating a negative view of the condition among clinicians.

This explains why, during the earlier years of study on articular cartilage, fundamental research into OA was dominated by biochemists and cellular biologists who did wonders in sorting out the biology of cartilage, but largely failed to understand that OA is primarily a mechanical problem.

This is a new paradigm, with many researchers and physicians believing it is now possible to alter the course of the disease by changing the mechanics of the particular structure.

There was a failure to appreciate the importance of older observations that OA pathology is joint-specific, not a generalized, systemic condition. It has been noted for some time the damage only occurs in habitually loaded areas of a joint. Unfortunately, that change has yet to be fully embraced or endorsed by many clinicians dealing with musculoskeletal disorders, or by the vast numbers of people in the community with pain and disability associated with their OA. However, because perception is everything, one of the greatest challenges has been to spread the word about this wonderful opportunity to alter the course of the disease.

The joint is a mechanical structure, and the key to understanding OA is abnormal mechanical stress. Joint failure is the biologic response of a joint to mechanical insult, an attempt by the joint to repair the damage caused by local abnormalities in force per unit area. The abnormalities in biochemistry of a joint, such as degradative enzymes, toxic free radicals and various other substances developing in and around an “arthritic” joint, are rather the result of this attempted repair. Finally, our thinking about osteoarthritis is moving from concerns about the biochemistry of the cartilage to the biomechanics of the whole joint.

Osteoarthritis would not pose so much of a problem if it was not associated with pain and disability. Oddly, sometimes it is and sometimes it is not. We have known for years that many people in the community have radiographic evidence of severe OA but have no symptoms. Every clinician has noted this. Yet many remain wedded to the biomedical model of the disease–the belief that disease causes tissue damage, and this results in symptoms. That thinking is still apparent in the rather desperate attempts that some researchers are currently making to show that if we could only image or assess the pathology of OA better, we would find that there is a good correlation between joint changes and symptoms. But pain is not always the result of these typical joint changes.

Everyone knows that OA is common, and that it can be asymptomatic. What is less well known is the fact that many of those who become symptomatic never seek any medical help for their OA-related problems. Because we have confined our studies to patients with OA, meaning those who have sought treatment from a health care professional, we have developed a strangely biased view of the condition. One of the biggest changes that has occurred over the last 50 years has been the development of population-based studies of OA, from which we have gained new insights into the risk factors for OA, its progression (or lack thereof), and outcomes. One of the more important findings from such studies has been the fact that OA is not necessarily a progressive, worsening disorder.

Many researchers are now offering a new hypothesis, which claims that OA is caused by increased forces across a local area of a joint. These abnormal forces can be due to several factors. There may be abnormal anatomy (which you may be born with or can be acquired), and this anomaly leads to an increased focused area of stress, with the overall load across the joint being normal.

Another possibility is the presence of an excessive load on the joint, which may develop either acutely or chronically. This might be the result of an injury, such as might occur during sports, or with chronic condition such as obesity. Of course, a combination of the two, abnormal anatomy and excess load, can both be at play. This latter situation might be the case when an obese person has a slightly deformed joint, or a poorly aligned extremity.

If these new concepts about OA are accurate, how does one change the course of this very common and sometimes debilitating condition? Is it possible that by altering the mechanics of specific joints, the course and frequency of this disease could be changed for the better? If the statistics are examined, this is not a treatment approach typically utilized.

By and large, we wait until the disease is symptomatic and severe enough that replacement of the joint is the treatment of choice. What if we could recognize this condition in the early stages, and then take appropriate action? This is the new paradigm mentioned earlier, a ground-breaking concept only recently proposed.

Stay tuned for the next article, in these very pages, in which this theory, actual prevention of osteoarthritis, will be discussed and dissected.

Editor’s note: Dr. Conway McLean is a podiatric physician now practicing foot and ankle medicine in the Upper Peninsula, having assumed the practice of Dr. Ken Tabor. McLean has lectured internationally on surgery and wound care, and is board certified in both, with a sub-specialty in foot orthotic therapy. Dr. McLean welcomes questions, comments and suggestions at drcmclean@penmed.com.

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