| While arthritis has no cure, there are a variety of treatments based on the particular kind of arthritis. Here, a doctor discusses the arthritis patient’s options.
Recently, my colleagues and I were examining x-rays from patients with osteoarthritis (OA) of the femoral joint. These patients were quite young when their OA was first diagnosed. In these OA patients, the disease was clinically significant when they were in their 20s or 30s whereas in the general population OA does not usually present clinically until individuals are in their 40s or 50s. Genetic testing of these individuals indicated that several family members had a similar age onset of OA. The genetic defect is a mutation in the predominating collagen type that makes up the matrix of articular cartilage of synovial joints. In the many cases of inherited OA that we have examined, this precocious form of OA began when patients were in their teens, which often resulted in a bilateral total joint replacement sometime thereafter. Looking at the post-operative x-rays, I remarked to one of my colleagues, tongue-in-cheek, “Well there’s the cure for OA.”
Naturally when we discuss “arthritis cures” we can always include surgical intervention, which removes the dysfunctional joint.
Extraordinary advances in the technological development of joint prostheses and their application leading to joint replacement surgery have improved the quality of life for individuals with advanced arthritis of the peripheral joints.
In this case, the patient’s clinical symptoms improve or are totally alleviated, a so-called “clinical remission” ensues and the patient’s clinical status is sustained over long periods of time. Does such a scenario exist in the therapy of arthritis now, and if not, what novel therapies are being developed to produce such an outcome?
Arthritis is often thought of as one disease, but in reality, while the final common pathway resulting in loss of joint function may be similar for all the arthritides, the pathogenesis or origin of the disease differs depending on which form of arthritis we are considering.
The most common form of arthritis is OA, affecting almost 80 percent of the population over the age of 50. OA has specific risk factors, namely, aging, obesity and repeated mechanical stress or trauma to joints, and so may be considered, in part, a “wear-and-tear” disorder of joints. Rheumatoid arthritis (RA), unlike OA, is an autoimmune disease because the immune system appears to react with self-antigens or self-proteins so that the immune system is activated to react with the body’s own tissue components. Thus, the body treats this response as if the tissue components were foreign proteins such as might occur when the normal immune response reacts to invading bacteria or viruses. There are contributing risk factors in RA as well. These include, allergy to foods, gut substances that might be exposed to peripheral blood, hereditary factors and exposure to certain microbes, which are in part an element of the hyperimmune response in the RA patient.
The final common pathway regardless of pathogenesis for both OA and RA involves inflammation. While OA is slowly progressive, activation of inflammatory cells appears to speed up the rate of progression to joint failure. Chronic inflammation is a hallmark of late-stage OA. Mild to chronic inflammation is a signature of RA at its inception. The proliferation of synovium in RA resulting in pannus causes significant aggressive destruction of cartilage and subchondral bone that is often irreversible. While the joints are mostly affected in RA and OA, in severe RA other organs may also be affected. These include the skin and lungs. The eyes also appear to be particular targets of the immune pathogenesis of RA. Muscle atrophy as a result of disuse is common, but the heart and blood vessels are less likely to be directly affected in RA.
to be continued…