My watch list  


Not Osteoarthritis
Classification & external resources
ICD-10 M15.-M19., M47.
ICD-9 715
OMIM 165720
DiseasesDB 9313
MedlinePlus 000423
eMedicine med/1682  orthoped/427 pmr/93 radio/492
MeSH D010003

Osteoarthritis (OA, also known as degenerative arthritis, degenerative joint disease), is a condition in which low-grade inflammation results in pain in the joints, caused by abnormal wearing of the cartilage that covers and acts as a cushion inside joints and destruction or decrease of synovial fluid that lubricates those 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. Keeping this in mind, other closely related pathologies include pseudo-arthrosis. This is derived from the Greek words pseudo, meaning "false", and arthrosis, meaning "joint." Radiographic diagnosis results in diagnosis of a fracture within a joint, which is not to be confused with osteoarthritis which is a degenerative pathology affecting a high incidence of distal phalangeal joints of female patients.

Many people erroneously think that OA is due to wear and tear. This common misconception is due to the fact that OA typically does not present in younger people. Abnormal loading of joints due to poor posture may increase risk for OA, but only because of the abnormal loading of the joint. If a joint is loaded normally, there should be no OA - the coefficient of friction of a normal joint is frequently described as sliding ice on ice - it will go forever.

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.[1] Treatment is with NSAIDs, local injections of glucocorticoid or hyaluronan, and in severe cases, with joint replacement surgery. There has been no cure for OA, as cartilage has not been induced to regenerate. However, if OA is caused by cartilage damage (for example as a result of an injury) Autologous Chondrocyte Implantation may be a possible treatment.[2] Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis.[3] Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, [4] listing several clinical competitors in its market analysis.


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.[5]

OA commonly affects the hands, 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. 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.

OA is the most common cause of water on the knee, an accumulation of excess fluid in or around your knee joint. [6]


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 identical twins, indicating a hereditary basis[citation needed]. Up to 60% of OA cases are thought to result from genetic factors. Researchers are also investigating the possibility of allergies, infections, or fungi as a cause. There is some evidence that allergies, whether fungal, infectious or systemically induced, may be a significant contributing factor to the appearance of osteoarthritis in a synovial sac.

Two types


This type of OA is a chronic degenerative disorder related to but not caused by aging, as there are people well into their nineties who have no clinical or functional signs of the disease. As a person ages, the water content of the cartilage decreases due to a reduced proteoglycan content, thus causing the cartilage to be less resilient. Without the protective effects of the proteoglycans, the collagen fibers of the cartilage can become susceptible to degradation and thus exacerbate the degeneration. Inflammation of the surrounding joint capsule can also occur, though often mild (compared to that which occurs in rheumatoid arthritis). This can happen as breakdown products from the cartilage are released into the synovial space, and the cells lining the joint attempt to remove them. New bone outgrowths, called "spurs" or osteophytes, can form on the margins of the joints, possibly in an attempt to improve the congruence of the articular cartilage surfaces. These bone changes, together with the inflammation, can be both painful and debilitating.


This type of OA is caused by other factors or diseases but the resulting pathology is the same as for primary OA:

  • Congenital disorders, such as:
    • Congenital hip luxation
    • People with abnormally-formed joints (e.g. hip dysplasia) are more vulnerable to OA, as added stress is specifically placed on the joints whenever they move. [However, recent studies have shown that double-jointedness may actually protect the fingers and hand from osteoarthritis.]
  • Cracking joints—the evidence is weak at best that this has any connection to arthritis.
  • Diabetes.
  • Inflammatory diseases (such as Perthes' disease), (Lyme 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.
  • A joint infection, e.g. from an injury.
  • 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, or similar injuries from exercise or work. Certain sports, such as running or football, put undue pressure on the knee joints. Injuries resulting in broken ligaments can lead to instability of the joint and over time to wear on the cartilage and eventually osteoarthritis.
  • Pregnancy
  • Alkaptonuria
  • Hemochromatosis and Wilson's disease


Diagnosis is normally done through x-rays. This is possible because loss of cartilage, subchondral ("below cartilage") sclerosis, subchondral cysts, narrowing of the joint space between the articulating bones, and bone spur formation (osteophytes) show up clearly on x-rays. Plain films, however, often do not correlate well with the findings of physical examination of the affected joints.

With or without other techniques, such as MRI (magnetic resonance imaging), arthrocentesis and arthroscopy, diagnosis can be made by a careful study of the duration, location, the character of the joint symptoms, and the appearance of the joints themselves. As yet, there are no methods available to detect OA in its early and potentially treatable stages.

In 1990, the College of Rheumatology, using data from a multi-center study, developed a set of criteria for the diagnosis of hand osteoarthritis based on hard tissue enlargement and swelling of certain joints. These criteria were found to be 92% sensitive and 98% specific for hand osteoarthritis versus other entities such as rheumatoid arthritis and spondyloarthropities [7].


Generally speaking, the process of clinically detectable osteoarthritis is irreversible, and typical treatment consists of medication or other interventions that can reduce the pain of OA and thereby improve the function of the joint.

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.

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 can relaxation techniques. Weight loss can relieve joint stress and may delay progression[citation needed]. Proper advice and guidance by a health care provider is important in OA management, enabling people with this condition to improve their quality of life.

In 2002, a randomized, blinded assessor trial was published showing a positive effect on hand function with patients who practiced home joint protection exercises (JPE). Grip strength, the primary outcome parameter, increased by 25% in the exercise group versus no improvement in the control group. Global hand function improved by 65% for those undertaking JPE. [8]

Dealing with chronic pain can be difficult and result in depression. Communicating with other patients and caregivers can be helpful, as can maintaining a positive attitude. People who take control of their treatment, communicate with their health care provider, and actively manage their arthritis experience can reduce pain and improve function.[citation needed]


Supplements which may be useful for treating OA include:


A molecule derived from glucosamine is used by the body to make some of the components of cartilage and synovial fluid. Supplemental glucosamine may improve symptoms of OA and delay its progression.[9] However, a large study suggests that glucosamine is not effective in treating OA of the knee.[10] A subsequent meta-analysis that includes this trial concluded that glucosamine hydrochloride is not effective and that the effect of glucosamine sulfate is uncertain.[11]


Along with glucosamine, chondroitin sulfate has become a widely used dietary supplement for treatment of osteoarthritis. A meta-analysis of randomized controlled trials found no benefit from chondroitin.[12]

Other supplements

  • Omega 3 Fish oils,a vitamin supplement comprised of important oils derived from fish to relieve symptoms in a natural way.
  • Boswellia, an herbal supplement known in Ayurvedic medicine. It is widely available in health food stores and online.
  • Antioxidants, including vitamins C and E in both foods and supplements, provide pain relief from OA. [13]
  • Hydrolyzed 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.[citation needed]
  • Ginger (rhizome) extract - has improved knee symptoms moderately.[14]
  • Methylsulfonylmethane (MSM): A small study by Kim et al. suggested that MSM significantly reduced pain and improved physical functioning in OA patients without major adverse events (Kim et al). The authors cautioned that although this short pilot study did not address the long-term safety and usefulness of MSM, they suggest that physicians should consider its use for certain osteoarthritis patients.[citation needed]
  • 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 deficiency has been correlated with a higher risk and severity of OA, therefore selenium supplementation may reduce this risk.[15]
  • vitamins B9 (folate) and B12 (cobalamin) taken in large doses significantly reduced OA hand pain, presumably by reducing systemic inflammation.[16]
  • Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief.[17]
  • Bone Morphogenetic Protein 6 (BMP-6) has recently been shown to have a functional role in the maintenance of joint integrity and is now being produced in an orally ingested form. [18]

Other nutritional changes shown to aid in the treatment of OA include decreasing saturated fat intake[19] and using a low energy diet to decrease body fat.[20] Lifestyle change may be needed for effective symptomatic relief, especially for knee OA.[21] Reducing sugar, processed foods, fatty foods and nightshade vegetables in the diet has helped many. According to Dr. John McDougall,[22] a low fat vegetarian diet can reduce arthritis symptoms. A macrobiotic diet has been known to reduce symptoms as well.



A mild pain reliever may be sufficiently efficacious. Acetaminophen (tylenol/paracetamol), is commonly used to treat the pain from OA, although unlike NSAIDs, acetaminophen does not treat the inflammation.[citation needed] A randomized controlled trial comparing acetaminophen to ibuprofen in x-ray-proven mild to moderate osteoarthritis of the hip or knee found equal benefit.[23] However, acetaminophen at a dose of 4 grams per day can increase liver function tests.[24]

Non-steroidal anti-inflammatory drugs

In more severe cases, non-steroidal anti-inflammatory drugs (NSAID) may reduce both the pain and inflammation. 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.

COX-2 selective inhibitors

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.


Most doctors nowadays avoid the use of steroids in the treatment of OA as their effect is modest and the adverse effects may outweigh the benefits.


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.


"Topical treatments" are treatments designed for local application and action. Some NSAIDs are available for topical use (e.g. ibuprofen and diclofenac) 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, joint replacement surgery 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.

Other approaches

There are various other modalities in use for osteoarthritis:


A meta-analysis of randomized controlled trials of acupuncture for knee osteoarthritis concluded "clinically relevant benefits, some of which may be due to placebo or expectation effects".[25]

Low level laser therapy

Low level laser therapy 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.[1].

Rotational Field Quantum Magnetic Resonance (“RFQMR”)

Rotational Field Quantum Magnetic Resonance (“RFQMR”) has been claimed to be effective for regeneration of cartilage in the knee joints. A three-year trial of this method involving 500 patients has been conducted at the Indian Airforce's Institute of Aerospace Medicine, Bangalore (India), the principal investigator being Dr V.G. Vasishta. The concept was founded by Dr.R.V.Kumar of CARD( Center for Advanced Research and Development) who researched for over 10 years before finally conducting the clinical trials. Later, other centres also started proving the facility. RFQMR Technology is claimed to utilize sub-radio and near-radio frequency electromagnetic radiation focused onto tissues to alter proton spin inside and outside cells, generating streaming voltage potentials resulting in stimulation of cartilage growth. The treatment is said to be painless and is claimed to be safe. Pre and post 3 months MRI showed significant increase in cartilage growth. The RFQMR beam is generated by an equipment known as Cytotron.


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:


  1. ^ Green GA. Understanding NSAIDS: from aspirin to COX-2. Clin Cornerstone 2001; 3:50-59. PMID 11464731.
  2. ^ Autologous Chondrocyte Implantation
  3. ^ Hollander AP, Dickinson SC, Sims TJ, et al (2006). "Maturation of tissue engineered cartilage implanted in injured and osteoarthritic human knees". Tissue Eng. 12 (7): 1787-98. doi:10.1089/ten.2006.12.1787. PMID 16889509.
  4. ^ Repairing knee joints by growing new cartilage using an injectable hydrogel
  5. ^ MedlinePlus Medical Encyclopedia: Osteoarthritis
  6. ^ Water on the knee,
  7. ^ Altman R, Alarcón G, Appelrouth D, et al (1990). "The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand". Arthritis Rheum. 33 (11): 1601-10. PMID 2242058.
  8. ^ Stamm TA, Machold KP, Smolen JS, et al (2002). "Joint protection and home hand exercises improve hand function in patients with hand osteoarthritis: a randomized controlled trial". Arthritis Rheum. 47 (1): 44-9. PMID 11932877.
  9. ^ Poolsup N, Suthisisang C, Channark P, Kittikulsuth W (2005). "Glucosamine long-term treatment and the progression of knee osteoarthritis: systematic review of randomized controlled trials". The Annals of pharmacotherapy 39 (6): 1080-7. doi:10.1345/aph.1E576. PMID 15855241.
  10. ^ 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.
  11. ^ Vlad SC, Lavalley MP, McAlindon TE, Felson DT (2007). "Glucosamine for pain in osteoarthritis: Why do trial results differ?" 56 (7): 2267-2277. doi:10.1002/art.22728. PMID 17599746.
  12. ^ Reichenbach S, Sterchi R, Scherer M, et al (2007). "Meta-analysis: chondroitin for osteoarthritis of the knee or hip". Ann. Intern. Med. 146 (8): 580-90. PMID 17438317.
  13. ^ 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
  14. ^ Altman RD, Marcussen KC. Arthritis Rheum. 2001 Nov; 44(11):2531-8
  15. ^ UNC News release -- Study links low selenium levels with higher risk of osteoarthritis. Retrieved on 2007-06-22.
  16. ^ Flynn MA, Irvin W, Krause G. J Am Coll Nutr. 1994 Aug; 13(4):351-6.
  17. ^ Arabelovic S, McAlindon TE. Curr Rheumatol Rep. 2005 Mar; 7(1):29-35.
  18. ^ K. Bobacz, R. Gurber, A Soleiman, L. Erlacher, J.S. Smolen, and W.B. Grainger, Arthritis & Rheumatism 2003 Sep; 48(9) 2501
  19. ^ Wilhelmi G. Z Rheumatol. 1993 May-Jun; 52(3):174-9. Vasishta VG et al, Rotational Field Magnetic Resonance (RFQMR) in treatment of osteoarthritis of the knee joint, Indian Journal of Aerospace Medicine, 48 (2), 2004; 1-7.
  20. ^ Christensen R. Osteoarthritis Cartilage. 2005 Jan; 13(1):20-7.
  21. ^ De Filippis L et al. Reumatismo. 2004 Jul-Sep; 56(3):169-84.
  22. ^ Hot Topics: Arthritis. Retrieved on 2007-06-22.
  23. ^ Bradley JD, Brandt KD, Katz BP, Kalasinski LA, Ryan SI (1991). "Comparison of an antiinflammatory dose of ibuprofen, an analgesic dose of ibuprofen, and acetaminophen in the treatment of patients with osteoarthritis of the knee". N. Engl. J. Med. 325 (2): 87-91. PMID 2052056.
  24. ^ Watkins PB, Kaplowitz N, Slattery JT, et al (2006). "Aminotransferase elevations in healthy adults receiving 4 grams of acetaminophen daily: a randomized controlled trial". JAMA 296 (1): 87-93. doi:10.1001/jama.296.1.87. PMID 16820551.
  25. ^ Manheimer E, Linde K, Lao L, Bouter LM, Berman BM (2007). "Meta-analysis: acupuncture for osteoarthritis of the knee". Ann. Intern. Med. 146 (12): 868-77. PMID 17577006.

See also

acquired deformities of fingers and toes (Boutonniere deformity, Bunion, Hallux rigidus, Hallux varus, Hammer toe) - other acquired deformities of limbs (Valgus deformity, Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot, Unequal leg length, Winged scapula)

patella (Luxating patella, Chondromalacia patellae)

Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte
Systemic connective
Polyarteritis nodosa - Churg-Strauss syndrome - Kawasaki disease - Hypersensitivity vasculitis - Goodpasture's syndrome - Wegener's granulomatosis - Arteritis (Takayasu's arteritis, Temporal arteritis) - Microscopic polyangiitis - Systemic lupus erythematosus (Drug-induced) - Dermatomyositis (Juvenile dermatomyositis) - Polymyositis - Scleroderma - Sjögren's syndrome - Behçet's disease - Polymyalgia rheumatica - Eosinophilic fasciitis - Hypermobility
DorsopathiesKyphosis - Lordosis - Scoliosis - Scheuermann's disease - Spondylolysis - Torticollis - Spondylolisthesis - Spondylopathies (Ankylosing spondylitis, Spondylosis, Spinal stenosis) - Schmorl's nodes - Degenerative disc disease - Coccydynia - Back pain (Radiculopathy, Neck pain, Sciatica, Low back pain)
Soft tissue disordersmuscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva)

synovium and tendon: Synovitis - Tenosynovitis (Stenosing tenosynovitis, Trigger finger, DeQuervain's syndrome)

bursitis (Olecranon, Prepatellar, Trochanteric)

fibroblastic (Dupuytren's contracture, Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis, Fasciitis, Fibromatosis)

enthesopathies (Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis)

other, NEC: Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia
Osteopathiesdisorders of bone density and structure: Osteoporosis - Osteomalacia - continuity of bone (Pseudarthrosis, Stress fracture) - Monostotic fibrous dysplasia - Skeletal fluorosis - Aneurysmal bone cyst - Hyperostosis - Osteosclerosis
Osteomyelitis - Avascular necrosis - Paget's disease of bone - Algoneurodystrophy - Osteolysis - Infantile cortical hyperostosis
ChondropathiesJuvenile osteochondrosis (Legg-Calvé-Perthes syndrome, Osgood-Schlatter disease, Köhler disease, Sever's disease) - Osteochondritis - Tietze's syndrome
See also congenital conditions (Q65-Q79, 754-756)
  This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Osteoarthritis". A list of authors is available in Wikipedia.
Your browser is not current. Microsoft Internet Explorer 6.0 does not support some functions on Chemie.DE