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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. 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.
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 your knee joint. 
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. 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.
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:
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 .
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.
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. 
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.
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. 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.
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.
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. Reducing sugar, processed foods, fatty foods and nightshade vegetables in the diet has helped many. According to Dr. John McDougall, 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. A randomized controlled trial comparing acetaminophen to 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, 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.
There are various other modalities in use for osteoarthritis:
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..
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:
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
|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|
|Dorsopathies||Kyphosis - 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 disorders||muscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva) Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia|
|Osteopathies||disorders 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
|Chondropathies||Juvenile 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)|