osteoarthritis n : chronic breakdown of cartilage in the joints; the most common form of arthritis occurring usually after middle age [syn: degenerative arthritis, degenerative joint disease]

English

Etymology

osteo- + arthritis

Noun

osteoarthritis (plural osteoarthritides)

1. A form of arthritis, affecting mainly older people, caused by chronic degeneration of the cartilage and synovial membrane of the joints, leading to pain and stiffness.

Derived terms

• osteoarthritic

See also

• rheumatoid arthritis

Osteoarthritis (OA, also known as degenerative arthritis, degenerative joint disease), is a clinical syndrome 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.

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 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 the knee joint.

Causes

Although it commonly arises from trauma, osteoarthritis often affects multiple members of the same family, suggesting that there is hereditary susceptibility 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 . 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

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. 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. Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis. Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis.

Primary

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.

Secondary

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 (human)) 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.
• 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

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 .

Related pathologies whose names may be confused with osteoarthritis 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.

Treatment

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.

Conservative care

No matter the severity or location of OA, conservative measures such as weight control, appropriate rest and exercise, and the use of mechanical support devices are usually beneficial. In OA of the knees, knee braces, a cane, or a walker can be helpful 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. Heat — often moist heat — eases inflammation and swelling, and may improve circulation, which has a healing effect on the local area. Weight loss can relieve joint stress and may delay progression . 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.

Medical treatment

Medical treatment includes 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. Clinical trials employing tissue-engineering methods have demonstrated regeneration of cartilage in damaged knees, including those that had progressed to osteoarthritis. Further, in January 2007, Johns Hopkins University was offering to license a technology of this kind, listing several clinical competitors in its market analysis.

Dietary

Supplements which may be useful for treating OA include:

Glucosamine

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. However, a large study suggests that glucosamine is not effective in treating OA of the knee. A subsequent meta-analysis that includes this trial concluded that glucosamine hydrochloride is not effective and that the effect of glucosamine sulfate is uncertain.

Chondroitin

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.

The Osteoarthritis Research Society International is in support of the use of chondroitin sulfate for OA.

Other supplements

• Omega-3 fatty acid,a vitamin supplement comprised of important oils derived from fish.

• Boswellia, an herbal supplement known in Ayurvedic medicine. It is widely available in health food stores and online.

• Bromelain, a protease enzymes extracted from the plant family Bromeliaceae, blocks some proinflammatory metabolites.

• Antioxidants, including vitamins C and E in both foods and supplements, provide pain relief from OA.

• 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.

• Ginger (rhizome) extract - has improved knee symptoms moderately.

• Selenium deficiency has been correlated with a higher risk and severity of OA.

• vitamins B9 (folate) and B12 (cobalamin) taken in large doses has been thought to reduce OA hand pain in one very small, non-quantitative study of 25 people. The results of which are extremely vague at best. The risk from large doses would suggest that this is not a safe treatment.

• Vitamin D deficiency has been reported in patients with OA, and supplementation with Vitamin D3 is recommended for pain relief.

• 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.

Other nutritional changes shown to aid in the treatment of OA include decreasing saturated fat intake and using a low energy diet to decrease body fat. Lifestyle change may be needed for effective symptomatic relief, especially for knee OA.

Complications

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.

Specific medications

Paracetamol

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

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, diarrhea, and peptic ulcer. Diclofenac has also been found to cause damage to the articular cartilage.

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.

Corticosteroids

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.

Narcotics

For moderate to severe pain, narcotic pain relievers such as tramadol, and eventually opioids (hydrocodone, oxycodone or morphine) may be necessary.

Topical

"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.

Surgery

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:

Acupuncture

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".

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.http://www.jr2.ox.ac.uk/bandolier/booth/alternat/lasarth.html

Prolotherapy

Prolotherapy (proliferative therapy) 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%.

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, varus or valgus knee deformity.
• Hips: Night pain, presence of femoral osteophytes, and subchondral sclerosis in females.
• Hands: Older age.

References

See also

• Back pain
• Chronic pain
• Osteoimmunology
• Prolotherapy
• Partial knee replacement

External links

• American College of Rheumatology Factsheet on OA
• Osteoarthritis The Arthritis Foundation
• Arthritis Care major UK charity
• WebMDHealth: Osteoarthritis Basics at WebMD
• MedlinePlus: Osteoarthritis at National Institutes of Health
• Osteoarthritis Clinical Trials Resource at oatrial.com
• Overview at University of Maryland
• Focuses on living with arthritis with links to support groups in 16 different countries at paremanifesto.org
• BBC Coverage of Autologous Chondrocyte graft in UK
• UK Health Charity covers Autologous Chondrocyte grafts