Osteoarthritis

Osteoarthritis (OA, also known as degenerative arthritis or degenerative joint disease, and sometimes referred to as "arthrosis" or "osteoarthrosis"), is a condition in which low-grade inflammation results in pain in the joints, caused by wearing of the cartilagethat 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 ligamentsmay 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 radiographicevidence of OA by age 65, although only 60% of those will be symptomatic(Green 2001). Treatment is with NSAIDs, local glucocorticoidinjections, and in severe cases, with joint replacementsurgery. There is no cure for OA, as it is impossible for the cartilage to grow back.

Signs and symptoms

The main symptom is chronic pain, causing loss of mobilityand often stiffness. "Pain" is generally described as a sharp ache, or a burning sensation in the associated musclesand tendons. OA can cause a crackling noise (called "crepitus") when the affected joint is moved or touched, and patients may experience muscle spasmand 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 hipsand 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 nodesand/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 proteincomposition 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 emotionallyand psychologically.

• Secondary OA: This type is caused by other diseases or conditions such as:
  • obesity. Obesity puts added weight on the joints, especially the knees.
  • diabetes
  • repeated trauma. Certain sports, such as weightlifting, or even football, put undue pressure on the knee joints.
  • hormonaldisorders
  • osteoporosis
  • surgeryto the joint structures
  • congenital hip luxation(which is geneticallydetermined)
  • inflammatory diseases (such as Perthes' disease), and all chronic forms of arthritis (e.g. rheumatoid arthritisand gout). In gout, uric acidcrystals cause the cartilage to degenerate at a faster pace.
  • People with abnormally-formed jointsare more vulnerable to OA, as added stress is specifically placed on the joints whenever they move.
  • Ligamentousdeterioration or instability may be a factor.

OA often affects multiple members of the same family, suggesting that there is a hereditarybasis for this condition. A number of studies have shown that the there is a greater prevalence of the disease between siblings, and especially 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.

Diagnosis

Diagnosisis 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), arthrocentesisand 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 restand 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 walkercan be a helpful aid for walking and support. Regular exercise, if possible, in the form of walkingor swimming, is encouraged. Applying local heat before, and cold packsafter 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 physiotherapistgo 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 biosynthesisof a moleculecalled glycosaminoglycanswhich 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 supplementshowing 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. Data pertaining to the use of supplements for OA are as follows:

• McAlindon et al believe that dietary antioxidants, including vitamins Cand Ein both foods and supplements, provide pain relief. (McAlindon TE, 1996).
• Vitamin Ddeficiencyhas been reported in patients with OA, and supplementation with Vitamin D3is 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).
• Low levels of seleniumhave been correlated with a higher risk and severity of OA [1].
• Supplementation with omega-3fatty acidsfrom fish oilreduces both the "degradative and inflammatory aspects of chondrocytemetabolism." (Curtis CL, 2002)
• The rhizomegingerextract has improved knee symptoms moderately (Altman RD, 1991).

Nutritional changes which have been shown to promote the treatment of OA include elevated saturated fatintake (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 medicationregime for most cases, a mild pain relievermay be sufficiently 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, ibuprofenand 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 stomachupset, crampingdiarrhoea, and peptic ulcer.

Another type of NSAID, COX-2 selective inhibitors(such as celecoxib, and the withdrawn rofecoxiband 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 acetaminophendoes 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 loath to use steroidsin the treatment of OA as their effect is modest and the adverse effects may outweigh the benefits.

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.

Creamsand 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 injectionsor similar local anaesthetics, and glucocorticoids (such as hydrocortisone). Corticosteroids (cortisone and similar agents) may temporarily reduce the pain.

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, narcoticpain relievers such as tramadol, and eventually opioids(hydrocodone, oxycodoneor morphine) may be necessary; these should be reserved for very severe cases, and are rarely medically necessary for chronic pain.

Other approaches

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. Its benefits are modest[2].
• 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.

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:

• Knees: High body mass index, varusor valgus kneedeformity.
• Hips: Night pain, presence of femoralosteophytes, and subchondral sclerosis in females.
• Hands: Older age.

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

• WebMDHealth: Osteoarthritis Basics
• MedicineNet.com: Osteoarthritis
• MedlinePlus: Osteoarthritis
• University of Maryland
• Osteoarthritisby Leah Kiviat, M.D., University of Washington Department of Radiology
• Spine-health.com: Understanding Osteoarthritis of the Spine
• ArthritisMD(Physician submitted articles) - research based arthritis articles by physiciansbg:???????

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This article is licensed under the GNU Free Documentation License.
It uses material from the http://en.wikipedia.org/wiki/Osteoarthritis Wikipedia article Osteoarthritis.