('''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
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
Ligament s 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 Physician s, and half of all
NSAID (Non-Steroidal Anti-Inflammatory Drugs)
Prescription s. It is estimated that 80% of the population will have
Radiograph ic 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.
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
Muscle s and
Tendon s. 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 Node s (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
Bunion s, rendering them red or swollen.
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 Emotional ly and Psychological ly.
OA often affects multiple members of the same family, suggesting that there is a
Hereditary basis for this condition. A number of studies have shown that the 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.
Diagnosis is normally done through
X-ray s. This is possible because loss of cartilage, subchondral ("below cartilage")
Sclerosis , subchondral
Cyst s, 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.
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 Pack s after exercise, can help relieve pain and inflammation, as do
Relaxation Technique s. 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
Glycosaminoglycan s, 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.
Both 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. Data pertaining to the use of supplements for OA include:
- McAlindon ''et al'' believe that dietary Antioxidant s, 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 ).
- Low levels of Selenium have been correlated with a higher risk and severity of OA {Link without Title} .
- Supplementation with Omega-3 Fatty Acid s 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 ).
- Collagen hydrolysate (a gelatine 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.
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 (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
Prostaglandin s, which play a central role in inflammation and pain. However, these drugs are rather taxing on the
Gastrointestinal Tract , and may cause
Stomach upset,
Cramp ing
Diarrhoea , and
Peptic Ulcer .
Another type of NSAID,
COX-2 Selective Inhibitor s (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 loath to use
Steroid s 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.
Cream s and
Lotion s, 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 Injection s or similar local
Anaesthetic s, 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
Opioid s (
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. Its benefits are modest {Link without Title} .
- 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:
- 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.
