Osteoarthritis (OA) is the most common form of arthritis affecting anywhere from 29-40 million Americans. It is a disease of hyaline cartilage, the gristle that caps the ends of long bones. OA is most often a disease of weight-bearing joints including the neck, low back, hips, and knees. While thought to be a disease due primarily to wear and tear, recent evidence indicates that chronic inflammation, mechanical factors, and central nervous system chemical mediators all play a role in the development and perpetuation of the disease and the symptoms associated with the disease.
The treatment approach to osteoarthritis is, first, to make a diagnosis. Second, non-medicine treatments should be initiated. An example is patient education.
Patients who are overweight need to lose weight. This is because of two reasons. The first is the obvious one which is the relief of mechanical stress on the affected joints. However, a more important reason is that adipocytes (fat cells) produce leptins which are pro-inflammatory chemicals. Leptins aggravate inflammation in joints.
Exercise is an often neglected part of OA therapy. Low impact aerobic exercise conditions muscles and helps the brain produce endorphins and enkephlins which help with pain modulation. Resistance exercise strengthens muscles to help with joint protection. Finally, stretching is critical to maintaining flexibility which aids in reducing joint stress. Often, a physical therapist can assist in designing an exercise program.
Thermal modalities such as ice and moist heat can be of great value for symptomatic relief.
Complementary medicine strategies such as acupuncture, massage, manipulation, self-hypnosis, and such can be useful in certain individuals.
Other treatments that have proven to be useful include transcutaneous electrical nerve stimulation (TENS), medial and lateral foot wedges that help reduce pain with knee OA, and assistive devices such as canes, braces, and walkers.
Once non-medicine treatments have been initiated, medication can also be started. Most people with mild OA can get temporary relief from over-the-counter analgesics and non-steroidal anti-inflammatory drugs (NSAIDS). A plant-based NSAID, flavocoxib (Limbrel), has its advocates. While effective for some, it also has been associated with severe liver toxicity. However, with more severe disease, prescription strength NSAIDS and analgesics such as tramadol and low-grade narcotics may need to be employed. Another class of medications that has been FDA-approved for the pain associated with OA is duloxetine (Cymbalta). The mechanism of action appears to be a suppressive central nervous system effect on pain perception.
Because of toxicity, oral non-steroidal anti-inflammatory drugs seem to be used less than topical NSAIDS now. Topical analgesics such as a lidocaine-impregnated patch are also used for situations such as chronic low back pain.
Much interest has settled complementary therapies for OA. Compounds such as glucosamine, chondroitin, “anti-inflammatory diets”, herbs, MSM, SAMe, homeopathic remedies, and so on. While some of these may help certain individuals, it is difficult at this time to make a blanket recommendation.
Patients with OA may respond to ultrasound-guided joint injections with glucocorticoids. These are temporary “fixes” and should not be administered in the same joint more than three times per year since there is evidence that glucocorticoids weaken cartilage. OA of the knee may also respond to ultrasound-guided injections of lubricants called viscosupplements.
For refractory cases, some physicians have advocated the use of platelet-rich plasma, an ultraconcentrate of whole blood containing a large percentage of platelets. The theory is that because platelets contain a large amount of growth and healing factors, they can be effective for OA. Anecdotal evidence seems to favor this approach although no large randomized trials have been conducted.
Another approach is the use of autologous stem cells. This approach has definite scientific evidence of beneficial effects, mostly in animal models. Small uncontrolled series in humans also appear to show that cartilage regeneration occurs with this therapy.
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