Osteoarthritis

From Freepedia

Osteoarthritis (OA, also known as arthrosis, osteoarthrosis or degenerative joint disease), 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.

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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 and/or Bouchard's nodes, 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 disease

The crucial factor in the development of OA is the wearing out and eventual disappearance of synovium, and later, all cartilage of the affected joints. OA may be divided into two types:

  • Primary OA: This type is caused by ageing. As a person ages, the water content of the cartilage increases, 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.
  • Secondary OA: This type is caused by other diseases or conditions such as obesity, diabetes, repeated trauma, hormonal disorders, osteoporosis, surgery to the joint structures, congenital hip luxation (which is genetically determined), inflammatory diseases (such as Perthes' disease), and all chronic forms of arthritis (e.g. rheumatoid arthritis and gout). Obesity puts added weight on the joints, especially the knees. In gout, uric acid crystals cause the cartilage to degenerate at a faster pace. People with abnormally-formed joints are more vulnerable to OA, as added stress is specifically placed on the joints whenever they move. Certain sports, such as weightlifting, or even football, puts undue pressure on the knee joints.

It has been found that OA occasionally inflicts multiple members of the same family, suggesting that there is a hereditary basis for this condition, but this has not been proven satisfactorily.

Diagnosis

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.

Treatment

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

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.

Dietary

Almost without exception, doctors will 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 a molecule called glycosaminoglycans which is the main ingredient of the synovial fluid (a fluid that fills the space between joints) and the 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.

The substances, glucosamine and chondroitin sulphate, have recently 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). Another isolated nutritional supplement showing promise is 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.

Standardized dietary treatment of OA is in its infancy. McAlindon et al believe that dietary antioxidants, including vitamins C and E in both foods and supplements, provide pain relief. (McAlindon TE, 1996). Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief (Arabelovic, 2005). Flynn et al showed that large dosages of oral vitamins B9 (folate) and B12 (cobalamin) significantly reduced OA hand pain, presumbably by reducing systemic inflammation (Flynn MA 1994). Supplementation with omega-3 fatty acids from fish oil reduces both the "degradative and inflammatory aspects of chondrocyte metabolism." (Curtis CL, [[[2002]]) The rhizome ginger extract has improved knee symptoms moderately (Altman RD, 1991).

Nutritional changes which have been 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).

Systemic treatment

Included in the medication regime for most cases, a mild pain reliever may be sufficient efficacious. In more severe cases, NSAIDs (non-steroid anti-inflammatory drugs) 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 — often moist heat — 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 loathe to use steroids (though effective) in the treatment of OA as their adverse effects are well known and proven.

Topical

"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).

Surgery

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.

Prognosis

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:

References

  • Green GA. Understanding NSAIDS: from aspirin to COX-2. Clin Cornerstone 2001; 3:50-59. PMID 11464731.
  • McAlindon T, Formica M, LaValley M, Lehmer M, Kabbara K. Effectiveness of glucosamine for symptoms of knee osteoarthritis: Results from an internet-based randomized double-blind controlled trial. Am J Med 2004; 117:643-9. PMID 15501201.
  • McAlindon TE, Jacques P, Zhang Y, et al. Do antioxidant micronutrients protect against the development and progression of knee osteoarthritis? Arthritis Rheum 1996; 39:648-656
  • Arabelovic S, McAlindon TE. Curr Rheumatol Rep. 2005 Mar; 7(1):29-35.
  • Flynn MA, Irvin W, Krause G. J Am Coll Nutr. 1994 Aug; 13(4):351-6.
  • Curtis CL et al. Proc Nutr Soc. 2002 Aug; 61(3):381-9.
  • Altman RD, Marcussen KC. Arthritis Rheum. 2001 Nov; 44(11):2531-8
  • Wilhemi G. Z Rheumatol. 1993 May-Jun; 52(3):174-9.
  • Christensen R. Osteoarthritis Cartilage. 2005 Jan; 13(1):20-7.
  • De Filippis L et al. Reumatismo. 2004 Jul-Sep; 56(3):169-84.
  • Mooney V. Spinal arthritis complete treatment guide Spine-health.com May 25, 2005.

External links

Retrieved from "http://en.freepedia.org/Osteoarthritis.html"


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