Osteoarthritis (OA, also known as degenerative arthritis, degenerative joint disease), is a group of diseases and mechanical abnormalities involving degradation of joints, including articular cartilage and the subchondral bone next to it. Clinical manifestations of OA may include joint pain, tenderness, stiffness, creaking, locking of joints, and sometimes local inflammation. In OA, a variety of potential forces—hereditary, developmental, metabolic, and mechanical—may initiate processes leading to loss of cartilage — a strong protein matrix that lubricates and cushions the joints. As the body struggles to contain ongoing damage, immune and regrowth processes can accelerate damage. When bone surfaces become less well protected by cartilage, subchondral bone may be exposed and damaged, with regrowth leading to a proliferation of ivory-like, dense, reactive bone in central areas of cartilage loss, a process called eburnation. The patient increasingly experiences pain upon weight bearing, including walking and standing. As a result of decreased movement because of the pain, regional muscles may atrophy, and ligaments may become more lax. OA is the most common form of arthritis, and the leading cause of chronic disability in the United States.
“Osteoarthritis” is derived from the Greek word “osteo”, meaning “of the bone”, “arthro”, meaning “joint”, and “itis”, meaning inflammation, although the “itis” of osteo arthritis is somewhat of a misnomer — inflammation is not a conspicuous feature of the disease. Osteoarthritis is not to be confused with rheumatoid arthritis, an autoimmune disease with joint inflammation as a main feature. A common misconception is that OA is due solely to wear and tear, since OA typically is not present in younger people. However, while age is correlated with OA incidence, this correlation may illustrate that OA is a process that takes time to develop — or that repair and regeneration that may keep pace with damage in the joints of younger people do slow with age. There is usually an underlying cause for OA, in which case it is described as secondary OA. If no underlying cause can be identified it is described as primary OA. “Degenerative arthritis” is often used as a synonym for OA, but the latter involves both degenerative and regenerative changes.
OA affects about 8 million people in the United Kingdom and nearly 27 million people in the United States, where it accounts 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 US population will have radiographic evidence of OA by age 65, although only 60% of those will show symptoms. In the United States, hospitalizations for osteoarthritis soared from about 322,000 in 1993 to 735,000 in 2006.
OA affects about eight million people in the United Kingdom, and about 27 million people in the United States, where it accounts 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 US population will have radiographic evidence of OA by age 65, although only 60% of those will be symptomatic. Some investigators believe that mechanical stress on joints underlies all osteoarthritis, with many and varied sources of mechanical stress, including misalignments of bones caused by congenital or pathogenic causes; mechanical injury; being overweight; loss of strength in muscles supporting joints; and impairment of peripheral nerves, leading to sudden or uncoordinated movements that overstress joints.
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 as a result of 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 but the resulting pathology is the same as for primary OA:
The main symptom is acute pain, causing loss of ability and often stiffness. “Pain” is generally described as a sharp ache, or a burning sensation in the associate 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 and cold 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. Some people notice these physical changes before they experience any pain.
OA is the most common cause of joint effusion, sometimes called water on the knee in lay terms, an accumulation of excess fluid in or around the knee joint.
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 no laboratory or pathological definition of osteoarthritis, and therefore no accepted laboratory tests to diagnose it. Diagnosis can often be made with reasonable certainty by clinical examination. Confirmation can be done through x-rays. This is possible because loss of cartilage, subchondral (“below cartilage”) sclerosis, subchondral cysts from synovial fluid entering small microfractures under pressure, narrowing of the joint space between the articulating bones, and bone spur formation (osteophytes) – from increased bone turnover in this condition, show up clearly on x-rays. Plain films, however, often do not correlate well with the findings of physical examination of the affected joints. Usually other imaging techniques are not necessary to clinically diagnose osteoarthritis.
In 1990, the American 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 of OA consists of exercise, manual therapy, lifestyle modification, medication and other interventions to alleviate pain.
No matter the severity or location of OA, conservative measures such as weight control, appropriate rest, exercise, and the use of mechanical support devices can be beneficial. In OA of the knees, knee braces can be helpful. A cane, or a walker can reduce pressure on involved leg joints which can be helpful for walking and support. Regular exercise such as walking or swimming, or other low impact activities are encouraged. Applying local heat before, and/or cold packs after exercise, can help relieve pain, as can relaxation techniques. Weight loss can relieve joint stress and may delay progression although research supporting this is equivocal.
Proper advice and guidance by health care providers such as chiropractors, physical therapists, occupational therapists, and medical doctors is important in OA management, enabling people with this condition to improve their quality of life.
Functional, gait, and balance training has been recommended to address impairments of proprioception, balance, and strength in individuals with lower extremity arthritis. These deficits can contribute to higher fall risk in older individuals.
Patient education has been shown to be helpful in the self-management of patients with arthritis in decreasing pain, improving function, reducing stiffness and fatigue, and reducing medical usage. A meta-analysis has shown patient education can provide on average 20% more pain relief when compared to NSAIDs alone in patients with hip OA or rheumatoid arthritis.
Moderate exercise leads to improved functioning and decreased pain in people with osteoarthritis of the knee.
Adequate joint motion and elasticity of periarticular tissues are necessary for cartilage nutrition and health, protection of joint structures from damaging impact loads, function, and comfort in daily activities. Exercise to regain or maintain motion and flexibility by low-intensity, controlled movements that do not cause increased pain. Muscle weakness around an osteoarthritic joint is a common finding. Progressive resistive/strengthening exercises load muscles in a graduated manner to allow for strengthening while limiting tissue injury.
Splinting of the thumb for OA of the base of the thumb leads to improvements after one year.
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.
Paracetamol (Tylenol/acetaminophen), is commonly used to treat the pain from OA, and was recommended in 16 of 16 guidelines evaluated in a 2007 review of existing guidelines. 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, paracetamol at a dose of 4 grams per day can increase liver function tests. In 2006, however, a Cochrane review found a small benefit (effect size of 0.13) from paracetamol, suggesting questionable clinical significance. There is equivocal evidence for gastrointestinal bleeding or renal (kidney) damage with long-term use of 4 g/day. NSAIDs appear to be more potent, but pose greater risk of side-effects.
In more severe cases, non-steroidal anti-inflammatory drugs (NSAID) reduce both the pain and inflammation; they all act by inhibiting the formation of prostaglandins, which play a central role in inflammation and pain. However, it should be noted that this class of drugs is not without risk for adverse events including increased gastrointestinal bleeding. Most prominent drugs in the class include diclofenac, ibuprofen, naproxen and ketoprofen. High oral drug doses are often required. However, diclofenac has been found to cause damage to the articular cartilage. Even more importantly all systemic NSAIDs are rather taxing on the gastrointestinal tract, and may cause stomach upset, cramping, diarrhea, and peptic ulcer. Such systemic adverse side effects are normally not observed when using NSAIDs topically, that is, on the skin around the target area. The typically weak and/or short-lived therapeutic effect of such topical treatments may be improved by using the drug in more modern formulations, including or ketoprofen associated with the Transfersome carriers or diclofenac in DMSO solution.
Another type of NSAID, COX-2 selective inhibitors (such as celecoxib, and the withdrawn rofecoxib and valdecoxib) are often used but are no more effective than the other NSAIDs. These latter NSAIDs carry an elevated risk for cardiovascular disease, and some have now been withdrawn from the market.
Oral steroids are not recommended in the treatment of OA because of their modest benefit and high rate of adverse effects. However intra – articular corticosteroid temporarily improve symptoms as discussed below.
For moderate to severe pain a opioid analgesic such as morphine or codeine may be necessary.
There are several NSAIDs available for topical use (e.g. diclofenac, ibuprofen, and ketoprofen) with little, if any, systemic side-effects and at least some therapeutic effect. The more modern NSAID formulations for direct use, containing the drugs in an organic solution or the Transfersome carrier based gel, reportedly, are as effective as oral NSAIDs.
Creams and lotions, containing capsaicin, are effective in treating pain associated with OA if they are applied with sufficient frequency.
A 2005 review of injections of hyaluronic acid, known as vicosupplementation, did not find that it led to clinical improvement in OA. A subsequent 2009 study found similar results. Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months.
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. Arthroscopic surgical intervention for osteoarthritis of the knee has been found to be no better than placebo at relieving symptoms.
The majority of patients with arthritis have tried alternative treatments for their pain. Various studies have reported some benefit for many of these approaches, including acupuncture and some herbal supplements. However, the response rates tend to be low and there is concern about bias in many studies.
Though findings are tentative and preliminary, there is evidence that acupuncture can be useful in the symptomatic treatment of osteoarthritis. All studies suggested that the results were equivocal and more high-quality evidence was needed.
There is controversy about glucosamine’s effectiveness for OA of the knee. A 2005 review concluded that glucosamine may improve symptoms of OA and delay its progression. However, a subsequent large study suggests that glucosamine is not effective in treating OA of the knee, and a 2007 meta-analysis that included this trial states that glucosamine hydrochloride is not effective.. In addition, in vitro analysis of glucosamine has revealed that glucosamine inhibits cartilage cell characteristics . There is a “striking” difference between the results reported from trials involving glucosamine sulfate as compared to glucosamine hydrochloride, with glucosamine sulfate reporting an effect size of 0.44 compared to a 0.06 effect size from glucosamine hydrochloride; Osteoarthritis Research Society International recommends discontinuing glucosamine if no effect is observed after six months. There is concern that industry bias has affected the earlier trials, although a 2008 OARSI consensus review stated that this was “unsubstantiated”. No adverse effects have been observed. The European League Against Rheumatism practice guidelines recommend glucosamine.
Chondroitin sulfate has also become a widely used dietary supplement for treatment of osteoarthritis, both in combination with glucosamine and by itself. A meta-analysis of randomized controlled trials found no benefit from chondroitin, although this meta-analysis included only 3 trials, one which had “an exceptionally high placebo response” and one which was published as only an abstract.
OA affects nearly 27 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 show symptoms. In the United States, hospitalizations for osteoarthritis soared from about 322,000 in 1993 to 735,000 in 2006.
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