OA is the most common form of arthritis and affects more than 20 million adults. It’s been estimated that by the age of 70 almost all people have OA to some extent.
OA is a disease of articular cartilage, the gristle that caps the ends of long bones. Cartilage is a complex substance consisting of two basic materials: collagen and proteoglycans and one type of cell- the chondrocyte. Cartilage provides shock absorption as well gliding functions.
With OA, there is premature wear and tear that occurs as a result of a metabolic abnormality that causes the chondrocyte to produce destructive enzymes. There is a complex interplay of the cartilage, the synovium (lining of the joint), and the subchondral bone (the bone that lies underneath the cartilage. The result is premature wear and tear as well as local inflammation.
While OA is primarily a condition that affects weight-bearing joints such as the neck, low back, hips, and knees, it also affects other areas such as the hands and feet, particularly in women.
Risk factors for the development of OA include genetics, trauma (injury to the joint), and weight in the case of weight-bearing areas such as the low back and knees. There is less evidence that weight plays a role in inducing OA of the hips. However, once OA in the hips is present, weight plays a key role in making the symptoms worse.
Symptoms of OA include morning stiffness lasting less than one-half an hour, stiffness during the days with prolonged sitting, crepitus (crunching sounds that accompany joint movement), pain, and joint swelling. Joint fluid, called an “effusion” can develop.
As osteoarthritis progresses, it becomes harder for patients to limber up and to move without pain.
Diagnosis is usually suspected by history and physical examination. While confirmation can be obtained by x-rays, unfortunately, by the time x-ray changes occur in OA, it is late in the course of disease.
While magnetic resonance imaging is much more sensitive for making the diagnosis, because of expense, it is often not used.
Laboratory tests are usually negative or normal.
Current forms of treatment for this condition are inadequate.
While advising a patient who is heavy to lose weight and exercise is admirable and necessary, it is an admonition that is usually ignored.
In addition, other measures such as analgesic medications (pain killers), non-steroidal anti-inflammatory drugs, physical therapy, bracers, and injections of glucocorticoids and viscosupplements provide only temporary and palliative relief.
In a recent report, Madonna Behan writing for Healthday reported, “The number of new-knee procedures doubled over the last decade, reached more than 620,000 in 2009, and the researchers said younger patients — those 45 to 64 — accounted for a disproportionate amount of that growth. In addition, researchers “estimate that nearly 53 percent of men and 52 percent of women diagnosed with symptomatic knee [osteoarthritis] will receive a total knee replacement in their lifetimes.”
Knee replacement surgery is not an innocuous procedure with the potential for complications such as infection, excessive bleeding, blood clots, worsening pain after the procedure, nerve damage, and death.
So what else can be done? Attempts to find a pharmacologic solution, so-called disease modifying anti-osteoarthritis drugs (DMOADS) have been disappointing at best.
The most promising new development is the use of autologous mesenchymal stem cells. These are adult stem cells found within many areas of the body including the bone marrow, fat, deciduous teeth, and periosteum of bone.
Anecdotal reports and small uncontrolled studies in both animal models as well as humans appear promising as a method for slowing down the rate of cartilage loss in knee OA and possibly even allowing for cartilage regeneration.
(Wei N, Beard S, Delauter S, Bitner C, Gillis R, Rau L, Miller C, Clark T. Guided Mesenchymal Stem Cell Layering Technique for Treatment of Osteoarthritis of the Knee. J Applied Res. 2011; 11: 44-48)
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