Any discussion about arthritis must begin with a definition of the disease. Seemingly simple on the surface, actually defining the disease becomes difficult due to the imprecise language physicians are accustomed to using. One of the quandaries medicine has found itself in is terminology. Doctors understand each other because they are in the business and have come to know what other physicians mean through common experience. That has led doctors to believe that their language is precise and as such should be easily understood by patients and others willing to dissect the terms and learn what they mean. This is not the case at all and is readily observable in the terms used to describe arthritis.
The word “arthritis”, when broken into its roots, simply means joint inflammation. That sounds straightforward enough until you consider that Rheumatoid Arthritis (RA) is defined as an inflammatory disease, while Osteoarthritis (OA) is not. If they are both arthritis then they should both be due to inflammation of the joint making them both inflammatory diseases, right? Wrong! The word inflammation is being used in two different ways. In the general definition of arthritis, it refers to swelling, redness, warmth, and tenderness; all the things we associate with inflammation. When used in regards to RA, however, inflammation refers to the activation of the immune system against the body. Because medical terminology is not as precise as doctors think, we are forced to come up with our own definitions of RA and OA.
I think the best way to start is to define arthritis as joint damage that leads to permanent discomfort, pain, or change in function. In other words if it hurts and/or does not work right and it is a place where two or more bones come into contact with each other then we will call it arthritis. Thus, any joint can be affected by arthritis because any joint can sustain injury. Arthritis is a blanket term that includes many different diseases that all affect the joints. Most people are familiar with Osteoarthritis and Rhemuatoid arthritis, but are less familiar with psoriatic arthritis, septic arthritis, lupus arthritis, gouty arthritis, and several others. There are many ways to injure the joints, and though we will focus on OA and RA in this article, it is important to realize that these are not the only diseases that affect the joints and that it is important to discern the true cause of the disorder so that the appropriate treatment can be provided. Fro this article, we will start with RA because, believe it or not, it is the easier of the two to explain. Understanding RA will help us to understand OA.
RA is a systemic inflammatory disease with its most obvious and common manifestations occurring in specific joints of the body. What this means is that RA, while primarily a disease of the joints, affects other systems of the body as well. The designation “inflammatory disease” means that it is an autoimmune disorder that activates segments of the body’s immune system, which, instead of fighting invading infections, turn against the body itself. Simply put RA is an autoimmune disease that can affect the entire body, but is predominately a disease of the joints.
No one is quite sure what the event begins the chain reaction that ultimately leads to RA and joint damage, great deal of the chain itself is understood. Nevertheless, by understanding at least some of the sequence of events that leads to RA, medicine has been able to develop very effective treatments in the last 10 to 15 years that can stop the progress of the disease in most people. In very brief terms, RA results from over production of cells in the joints called fibroblasts and macrophages. This overproduction leads to growth and swelling of the protective lining of the joints and results in damage to the bones of the joint and the structures designed to protect the joint and maintain its function. The overall results are loss of joint function, joint derangement, tendon laxity, and crippling if untreated. Systemic manifestations of RA can include lung damage, increased risk of heart disease and heart attack, kidney damage, liver damage, eye problems, and anemia.
RA has a genetic component. There is definite evidence that RA is at least partially inherited from one’s ancestors and that changes in DNA predispose a person to developing RA. It is important to stress that the genetic predisposition is necessary, but not sufficient for the development of RA. In other words, just because your parents had RA does not mean that you are destined to get it, though it does increase the probability that you will. Twin studies help us to determine exactly how much of the RA is due to genetics and how much is not. The studies are based on the fact that while identical twins share 100% of their DNA, fraternal (or non-identical) twins do not. A disease that is 100% inherited that affects one of the identical twins would also affect the other. On the other hand, a disease that is 100% inherited affects both fraternal twins only a certain percentage (less than 100%) of the time because their DNA is not identical. Thus, by looking at large groups of identical and fraternal twins, we can get an idea of just how much of the disease development can be attributed to inheritance and how much cannot. According to the Primer on the Rheumatic Diseases published by the Arthritis Foundation the following is known about heredity in RA. In 30% of identical twin groups, if one has RA, the other will have RA. This is 3.5 times higher than in fraternal twins. This means several things. First, there is a genetic component to RA because identical twins share the disease more often than do fraternal twins. Second, genetics alone are not enough to cause RA because identical twins (who share 100% of their DNA) only both develop RA 30% of the time. Thus, we can conclude that the genetic predisposition to RA exists, but that alone is not enough to cause a person to develop the disease. There is some other factor that a person who is predisposed must be affected by in order to develop the disease. The problem is that no one knows what that other factor is. While doctors attempt to determine what ultimately leads a person with a genetic predisposition to develop RA so that the disease can be prevented, treatments that slow of stop the progression of the disease are currently available.
The determination of whether you have RA occurs via physical examination and laboratory testing. The physical exam will focus on the following:
1. Morning Stiffness – People with RA tend to complain of stiffness in the joints of the hands, wrists, and ankles that is worse in the morning and takes an hour or more to “loosen up.” The stiffness does not have to occur in the morning, but rather is related to immobilization (i.e. how long it has been since you have moved the joints). RA gets better with movement and worse with rest. The stiffness is directly related to how long the joint is immobile. The long you don’t move it, the longer it will take to “loosen up.” Morning stiffness is usually a problem because you have been asleep all night and not using the joints.
2. Warm, red, swollen joints – A warm joint tends to connote inflammation, which could be due to several processes, but in the setting of other signs of RA, helps to increase the probability your doctor is on the right track.
3. Structural changes – Changes in the ligaments and tendons that help to support the joints and maintain their architecture leads to characteristic deformities. Given pretty names like swan neck and boutonniere deformity, these deformities are not usually painful, but have a characteristic appearance unique to RA.
4. The affected joints. While RA can affect any joint in the body, it often has a unique pattern of doing so. First of all, the disease is almost always symmetric. In other words, if your right knee is affect then so is you left. If the middle joints of the first and second fingers on your right hand are affected, then so will be those same joints on the left hand. Second, RA tends to affect the first two joints of each finger and spare the joint furthest from the hand. OA tends to affect his last joint, but skip the middle joint.
Laboratory testing usually includes blood tests, x-rays, and possibly an aspiration of fluid from the affected joints. The blood tests are used to look for several things. First, the ESR (erythrocyte sedimentation rate) is measured. ESR is a general measure of inflammation in the body and is elevated in inflammatory diseases such as RA. While not specific to RA, a normal value will rule the disease out. Next the rheumatoid factor (RF) level is measured. According to the Primer on the Rheumatic Diseases, RF is an abnormal protein that is found in about 85% of people with RA. Not having RF does not rule out RA, but having it makes the disease much more likely. There are a few diseases that also lead to a production of RF, so those must be ruled out with other testing. Other laboratory tests to check for anemia and some other blood problems that occur in RA may also be performed if you exhibit symptoms. Some of these other blood problems include too much antibody, a propensity for clotting, and overproduction of certain types of cells. X-rays will be performed to determine if there is any permanent damage and also to rule out other types of arthritis, like OA. It is quite possible to have more than one type of arthritis. A joint aspiration may also be done to rule out gout or infection.
The diagnosis of RA is made on a clinical basis. While laboratory tests and x-rays may help, the diagnosis rests upon the physical exam and what you tell your doctor. Ultimately, this is also the way that the effectiveness of treatment will be assessed as well. The laboratory tests are not reliable ways of determining treatment success or failure, which will instead be based upon your symptoms and how you are feeling.
The basic premise underlying the treatment of RA rests upon the fact that it is an autoimmune disease caused by over-activation of the body’s defense system. The treatments are therefore aimed at suppressing the immune system, or parts of it, in order to suppress the disease. The mainstays of treatment are divided into two rough categories, though they overlap considerably. The first of these categories includes treatments that relieve pain, but do not change the course of the disease. These treatments include NSAIDs (like Naprosyn, Ibuprofen, and Celebrex), narcotics (like Percocet), and hot/cold compresses. These relieve pain, but do not alter the progression of the disease.
The second rough class is referred to as Disease-Modifying Antirheumatic Drugs (DMARDs). DMARDs are known to slow the progression the disease (which will lead to pain relief) and can even prevent complications from arising if started early enough in the course of RA. Several DMARDs are listed below along with benefits and drawbacks.
1. Corticosteroids – this includes drugs like prednisone, which are general anti-inflammatory drugs. They do delay joint damage, but are not terribly effective. Furthermore, they have very serious side-effects that limit their long-term use, such as bone erosion, weight gain, diabetes, etc. Corticosteroids are often most effective for getting the disease under control when it is severe and are thus used intermittently during disease flares or when initiating another therapy and waiting for it to take effect.
2. Methotrexate – Methotrexate is the mainstay of treatment for RA. According to the Primer on the Rheumatic Diseases, methotrexate provides a 60 – 70% improvement when used alone. Often it is used as first line therapy and then other drugs are added on top of it to bring the disease fully under control and slow progression. It is important to note that methotrexate alone will slow RA progression, but will not stop it completely. Methotrexate is extremely safe for long-term use and has been extensively studied to determine efficacy and safety. Methotrexate is very affordable.
3. Anti-TNF alpha Agents – These include such drugs as Etanercept (Enbrel), infliximab (Remicade), and Humira. These drugs work by suppressing on TNF alpha, one of the chemical messengers used by the body to promote inflammation. By blocking TNF alpha, these drugs block the system that leads to inflammation and thus RA. These agents are extremely effective in halting the progression of RA. However, they have some serious side effects, including an increased risk of infection (especially tuberculosis) and increased risk of demyelinating syndromes (which affect the brain and nervous system). These drugs are also very expensive, costing in the range of $1000 per dose or up to several thousand dollars per year. They are currently reserved for severe RA that does not respond to Methotrexate or other DMARDs. While they do carry risk, the experience with these drugs is extensive and they are known to be effective.
4. Other DMARDs – other DMARDs include Hydroxychloroquine, Sulfasalazine, Azathiorpine, Cyclosporine, and Leflunomide among others.
Research into the cause/causes of RA is ongoing. Prevention would be the most successful method of treating RA, but until we know that exact cause that is not possible. Currently, medications to treat and retard the disease are very effective, but not without risks and side effects. We are light-years ahead in the treatment of RA compared to only 20 or 30 years ago. In another 20 or 30 years, we may very well have a cure. Until such time, early detection will remain essential to preventing complications and a close relationship with a qualified physician will help you to ensure that everything possible is done for you.
It used to be that OA was referred to as the wear-and-tear arthritis. It was presumed to be due to injury and over-use and the reason some people got it and other did not was simply luck. The unlucky injured the joint in such a way so as to lead to arthritis and the lucky did not. Well, wear-and-tear is only part of the story. It turns out that what we know about OA is the opposite of what we know about RA. In RA we know the chain of events that leads to joint damage, but we do not know that primary cause. In OA we know that primary cause (i.e. over-use/injury) but we do not know that process that leads to some people developing OA and some people recovering joint function. There is at least some genetic component to OA, thought what that is is not clear. It turns out, that just like RA, some people are more susceptible to developing OA than others are. The difference is that in RA, the predisposition is necessary but not sufficient to develop the disease while in OA, the predisposition is neither necessary nor sufficient. In other words, it you put enough strain on a joint over time, you will get OA even if you do not have a predisposition. However, if you do have a predisposition, it will take less strain to cause OA than in a person without a predisposition. Finally, even with the predisposition, you are not guaranteed to get OA, because you many not put the necessary strain on the joint to do so. In the end, we can say that OA is due to wear-and-tear, but some of us can take a beating more than others. In fact, for some of us, the daily motions of life are enough to cause OA.
The general process by which OA occurs is that the protective cartilage at the ends of bones where they form joints becomes damaged and breaks down. This breakdown results in bone on bone movement, which leads to pain, fractures, bone spurs, etc. Our understanding of OA is rapidly increasing and it may be that this wear-and-tear hypothesis will ultimately be proven wrong. For now, it is the best we have to work with and there is truth to the fact that taking care to avoid injury to joints and avoiding repetitive stresses can help to prevent OA from occurring in the future.
Tests for OA generally include the physical exam, blood work, and x-rays. The physical exam looks to see if the signs of RA and other arthritidies are absent, as they should be in OA. For instance, morning stiffness in OA lasts less than 10 minutes on average compared to the hour or more of RA. Also, OA gets worse with use of the joint while RA improves. The exam will also be used to help judge the extent of OA, how it affects movement, and what the ultimate treatment strategy will be. X-rays are used to look for evidence of fracture and damage (CT or MRI may be used if the diagnosis is uncertain for your doctor is concerned that something else in addition to OA is affecting the joint). Blood tests are used to rule out other form of arthritis. In addition, so diseases like osteoporosis and thyroid disease can lead to OA and need to be ruled out as well. If you have one of these diseases, correcting that can lead to resolution of the OA in some cases.
Treatment for OA is aimed at alleviating pain, correcting factors that may contribute to advancement of the disease, and ultimately at replacing or repairing the joint if appropriate and possible. Pain relief for OA ranges from NSAIDs (e.g. Ibuprofen or Celebrex), Narcotics (e.g. Percocet),, local injections, nerve blocks, and braces. Any of all of these may be employed to help manage the pain associated with OA. Local injections can be of several types and a quick discussion is warranted.
1. Corticosteroids – This refers to the injection of steroids such as kenalog and cortisone directly into the affected joint, usually in conjunction with a local anesthetic. The anesthetic provides immediate relief while the steroid provides longer-term relief (on the order of days to months depending on the person). Local injection of steroids helps to avoid the systemic problems of these drugs such as weight gain, immune suppression, and insulin resistance. The efficacy of such therapy is highly dependent on the individual patient.
2. Viscosupplementation – This refers to the injection of substances that mimic the normal lubrication found in a joint. In most cases, this refers to a molecule called to as hyaluronan which is used by the body to lubricate cartilage surfaces and help them glide over one another more easily. The theory is that by adding more of this substance to the joint, the joint will move more freely and there will be a decrease in pain. Studies have not been conclusive about the effectiveness of this therapy, but the risks are minimal and it does appear to work for some people. It is often used as a stop-gap to postpone the need for surgery (usually this can be done for about a year).
Other treatments are aimed at correcting factors that can contribute to OA or lead to its advancement. Such things include, posture, muscle strength, weight, etc. A physician may prescribe weight loss, physical therapy, or occupational therapy. Weight loss is single most important factor in helping to alleviate symptoms of OA and prevent further progression.
Finally, surgery is employed is several way to repair the joint, replace the joint, or to alleviate pain through alteration. In general, surgery includes one of two approaches. Arthroscopic surgery is done with the aid of tiny cameras and instruments and allows the surgeon to make small incisions meaning less pain and quicker healing time. These procedures are often used to inspect joints visually, remove damaged cartilage, or make small repairs to the cartilage, ligaments, or tendons. The other general type of surgery is total joint arthroplasty or replacement of the damaged joint with an artificial joint. These types of surgeries used to be delayed until absolutely necessary due to the prolonged recovery time, cost, and relatively short life-span of the artificial joints. Advances in science have lead to joints that now last an average of 20 years and often as long as 30. Thus, a person who gets a total knee or hip replacement in his/her 40’s will be 60 or 70 before another is required. The benefits in pain reduction and range of motion are dramatic and have led to an increase in the use of this type of surgery. Joints that can be replaced include: knees, shoulders, hips, ankles, elbows, fingers, and even some places in the spine now.
Arthritis is a general term that can apply to just about any joint injury that would otherwise be permanent without some sort of treatment. We have discussed OA and RA, how they develop, how they are diagnosed, and how they are treated. However, there are other, less common types of arthritis that are no less devastating than OA and RA. It is important to find a qualified physician, such as a rheumatologist, who can help make sense of your symptoms and start you on the road to recovery.
Arthritis Foundation. Primer on the Rheumatic Diseases. Chapters 9 and 13