Osteoarthritis - Article Degenerative Joint Disease; Osteoarthritis arthritis
Osteoarthritis (OA, also known as degenerative arthritis or degenerative joint disease, and sometimes referred to as "arthrosis" or "osteoarthrosis" or in more colloquial terms "wear and tear"), is a condition in which low-grade inflammation results in pain in the joints, caused by wearing of the cartilage that covers and acts as a cushion inside joints. As the bone surfaces become less well protected by cartilage, the patient experiences pain upon weight bearing, including walking and standing. Due to decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax. OA is the most common form of arthritis. The word is derived from the Greek word "osteo", meaning "of the bone", "arthro", meaning "joint", and "itis", meaning inflammation, although many sufferers have little or no inflammation.
OA affects nearly 21 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID (Non-Steroidal Anti-Inflammatory Drugs) prescriptions. It is estimated that 80% of the population will have radiographic evidence of OA by age 65, although only 60% of those will be symptomatic (Green 2001). Treatment is with NSAIDs, local glucocorticoid injections, and in severe cases, with joint replacement surgery. There is no cure for OA, as it is impossible for the cartilage to grow back. Although, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment.
Signs and symptoms
The main symptom is chronic pain, causing loss of mobility and often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associated muscles and tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasm and contractions in the tendons. Occasionally, the joints may also be filled with fluid. Humid weather increases the pain in many patients.
OA commonly affects the hand, feet, spine, and the large weight-bearing joints, such as the hips and knees, although in theory, any joint in the body can be affected. Progressive degeneration of cartilage, technically known as synovium (joint lining), in the knees can lead to them curving outwards in a condition known as "bow legged". As OA progresses, the affected joints appear larger, are stiff and painful, and usually feel worse, the more they are used throughout the day, thus distinguishing it from rheumatoid arthritis.
In smaller joints, such as at the fingers, hard bony enlargements, called Heberden's nodes (on the distal interphalangeal joints) and/or Bouchard's nodes (on the proximal interphalangeal joints), may form, and though they are not necessarily painful, they do limit the movement of the fingers significantly. OA at the toes leads to the formation of bunions, rendering them red or swollen.
Causes of osteoarthritis
Osteoarthritis often affects multiple members of the same family, suggesting that there is hereditary susceptiblity to this condition. A number of studies have shown that there is a greater prevalence of the disease between siblings and especially monozygotic twins, indicating a hereditary basis. In the population as a whole up to 60% of OA is thought to be as a result of genetic factors.
The crucial factor in the development of osteoarthritis is the wearing out and eventual disappearance of synovium, and later, all cartilage of the affected joints.
Osteoarthritis may be divided into two types:
This type of OA is caused by aging. As a person ages, the water content of the cartilage decreases, and the protein composition in it degenerates, thus degenerating the cartilage through repetitive use or misuse. Inflammation can also occur, and stimulate new bone outgrowths, called "spurs" (osteophyte), to form around the joints. Sufferers find their every movement so painful and debilitating that it can also affect them emotionally and psychologically.
- Congenital disorders, such as:
- Cracking jointsâ€”the evidence is weak at best that this has any connection to arthritis .
- Inflammatory diseases (such as Perthes' disease), and all chronic forms of arthritis (e.g. costochondritis, gout, and rheumatoid arthritis). In gout, uric acid crystals cause the cartilage to degenerate at a faster pace.
- Injury to joints, as a result of an accident.
- hormonal disorders.
- Ligamentous deterioration or instability may be a factor.
- Obesity. Obesity puts added weight on the joints, especially the knees.
- Osteopetrosis (High bone density).
- Sports injuries, from exercise, athletic activity, or work. For example, certain sports, such as weightlifting, running, or even football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time wear of the cartilage and eventually osteoarthritis.
- Surgery to the joint structures.
Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral ("below cartilage") sclerosis, subchondral cysts, the narrowing of the joint space between adjacent bones, and bone spur formation (osteophytes) show up clearly in x-rays. Plain films, however, often do not correlate with the findings of a physical examination in the early stages of the disease.
With or without other techniques, such as MRI (magnetic resonance imaging), arthrocentesis and arthroscopy, a careful study of the duration, location, the character of the joint symptoms, and the appearance of the joints themselves, will help the doctor to determine whether his patient suffers from OA.
Since OA is the result of irreversible worn-out cartilage, the goal of treatment is to reduce the joint pain while at the same time, improving and maintaining the function of the joint.
Coping skills and lifestyle changes
No matter what the severity, or where the OA lies, conservative measures, such as weight control, appropriate rest and exercise, and the use of mechanical support devices are usually beneficial to sufferers. In the case of OA of the knees, knee braces, a cane, or a walker can be a helpful aid for walking and support. Regular exercise, if possible, in the form of walking or swimming, is encouraged. Applying local heat before, and cold packs after exercise, can help relieve pain and inflammation, as do relaxation techniques. Weight loss can delay progression. As such, the proper advice and guidance by a physiotherapist go a long way in OA management, enabling sufferers to get back closer to their previous routine.
Dealing with chronic pain can be difficult and result in depression. Communicating with other OA sufferers is helpful, as is maintaining a positive attitude. People who take control of their treatment, communicate with their doctor, and actively manage their arthritis experience suffer less pain and function better.
Most physicians recommend the oral intake of glucosamine. Glucosamine is a natural substance found in almost all tissues in the body, and is involved in the biosynthesis of glycosaminoglycans, the main ingredient of the synovial fluid (a fluid that fills the space between joints) and cartilage. Glucosamine is not found in food sources, but is produced naturally by the body, and if for some reasons, the body does not produce it, it would probably lead to the development of OA.
Supplements which may be useful for treating OA include:
- Antioxidants, including vitamins C and E in both foods and supplements, provide pain relief from OA. (McAlindon TE, et al, 1996).
- Chondroitin sulphate improves symptoms of OA, and delays its progression (Poolsup N et al, 2005).
- Collagen hydrolysate (a gelatin product) may also prove beneficial in the relief of OA symptoms, as substantiated in a German study by Beuker F. et. al. and Seeligmuller et. al. In their 6-month placebo-controlled study of 100 elderly patients, the verum group showed significant improvement in joint mobility.
- Ginger (rhizome) extract - has improved knee symptoms moderately (Altman RD, 1991).
- Glucosamine has also been shown to improve symptoms of OA, and to delay its progression (Poolsup N et al, 2005). However, recent evidence shows that glucosamine is not effective in reversing OA of the knee (McAlindon et al 2004).
- Methylsulfonylmethane (MSM): after several reports that MSM helped arthritis in animal models, a double-blind, placebo-controlled study suggested that 1500 mg per day MSM (alone or in combination with glucosamine sulfate) was helpful in relieving symptoms of knee osteoarthritis (Usha and Naidu 2004). Kim et al. then conducted a double-blind clinical trial of MSM for treatment of patients with osteoarthritis of the knee. Twenty-five patients took 6 g/day MSM and 25 patients took a placebo for 12 weeks. Ten patients did not complete the study, and intent-to-treat analysis was performed. Patients who took MSM had significantly reduced pain and improved physical functioning, without major adverse events (Kim et al). No evidence of a more general anti-inflammatory effect was found, as there were no significant changes in two measures of systemic inflammation: C-reactive protein level and erythrocyte sedimentation rate. The authors cautioned that this short pilot study did not address the long-term safety and usefulness of MSM, but suggested that physicians should consider its use for certain osteoarthritis patients, and that long-term studies should be conducted (Kim et al. 2006).
- Omega-3 fatty acids in the form of fish oil supplements reduces both the "degradative and inflammatory aspects of chondrocyte metabolism." (Curtis CL, 2002)
- S-adenosyl methionine: small scale studies have shown it to be as effective as NSAIDs in reducing pain, although it takes about four weeks for the effect to take place.
- Selenium in low levels has been correlated with a higher risk and severity of OA, therefore selenium supplementation may reduce this risk .
- vitamins B9 (folate) and B12 (cobalamin) taken in large doses significantly reduced OA hand pain, presumbably by reducing systemic inflammation (Flynn MA 1994).
- Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief (Arabelovic, 2005).
Other nutritional changes shown to promote the treatment of OA include elevated saturated fat intake (Wilhelmi G, 1993) and elevated body fat (Christensen R, 2005). Lifestyle change may be needed for effective symptomatic relief, especially for knee OA (De Filippis L, 2004).
Included in the medication regime for most cases, a mild pain reliever may be sufficiently efficacious. In more severe cases, NSAIDs are usually prescribed which can reduce both the pain and inflammation quite effectively. These include medications such as diclofenac, ibuprofen and naproxen. High doses are often required. All NSAIDs act by inhibiting the formation of prostaglandins, which play a central role in inflammation and pain. However, these drugs are rather taxing on the gastrointestinal tract, and may cause stomach upset, cramping diarrhoea, and peptic ulcer.
Another type of NSAID, COX-2 selective inhibitors (such as celecoxib, and the withdrawn rofecoxib and valdecoxib) reduce this risk substantially. These latter NSAIDs carry an elevated risk for cardiovascular disease, and some have now been withdrawn from the market. Another medication, acetaminophen (paracetamol), is commonly used to treat the pain from OA, although unlike NSAID's acetaminophen does not treat the inflammation. Application of heat â€” often moist heat â€” eases inflammation and swelling in the joints, and can help improve circulation, which has a healing effect on the local area.
Most doctors nowadays are loath to use steroids in the treatment of OA as their effect is modest and the adverse effects may outweigh the benefits.
"Topical treatments" are treatments designed for local application and action. Some NSAIDs are available for topical use (e.g. ibuprofen) and may improve symptoms without having systemic side-effects.
Creams and lotions, containing capsaicin, are effective in treating pain associated with OA if they are applied with sufficient frequency.
Severe pain in specific joints can be treated with local lidocaine injections or similar local anaesthetics, and glucocorticoids (such as hydrocortisone). Corticosteroids (cortisone and similar agents) may temporarily reduce the pain.
If the above management is ineffective, surgery (joint replacement) may be required. Individuals with very painful OA joints may require surgery such as fragment removal, repositioning bones, or fusing bone to increase stability and reduce pain. For severe pain, narcotic pain relievers such as tramadol, and eventually opioids (hydrocodone, oxycodone or morphine) may be necessary; these should be reserved for very severe cases, and are rarely medically necessary for chronic pain.
There are various other modalities in use for osteoarthritis:
- Low level laser therapy ; this is a light wave based treatment that may reduce pain. The treatment is painless, inexpensive and without risks or side effects. Unfortunately, it may not actually have any real benefits..
- Prolotherapy (proliferative therapy); this is the injection of an irritant substance (such as dextrose) to create an acute inflammatory reaction. It is claimed to strengthen and heal damaged tissues including ligaments, tendons and cartilage as part of this reaction. The injection is painful (like corticosteroids or hyaluronic acid) and may cause an increase in pain for a few days afterwards. The only other significant risk is the rare possibility of infection.
- Radiosynoviorthesis: A radioactive isotope (a beta-ray emitter with a brief half-life) is injected into the joint to soften the tissue. Due to the involvement of radioactive material, this is an elaborate and costly procedure, but it has a success rate of around 80%.
The most common course of OA is an intermittent, progressive worsening of symptoms over time, although in some patients the disease stabilizes. Prognosis also varies depending on which joint is involved.
Factors associated with progression of OA: