| Osteoarthritis | |
|---|---|
| Classification and 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 or degenerative joint disease, is a group of mechanical abnormalities involving degradation of joints,[1] including articular cartilage and subchondral bone. Symptoms may include joint pain, tenderness, stiffness, locking, and sometimes an effusion. A variety of causes—hereditary, developmental, metabolic, and mechanical—may initiate processes leading to loss of cartilage. When bone surfaces become less well protected by cartilage, bone may be exposed and damaged. As a result of decreased movement secondary to pain, regional muscles may atrophy, and ligaments may become more lax.[2]
Treatment generally involves a combination of exercise, lifestyle modification, and analgesics. If pain becomes debilitating, joint replacement surgery may be used to improve the quality of life. OA is the most common form of arthritis,[2] and the leading cause of chronic disability in the United States.[3] It affects about 8 million people in the United Kingdom and nearly 27 million people in the United States.
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Osteoarthritis can be classified into either primary or secondary depending on whether or not there is an identifiable underlying cause.
The main symptom is 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.[4][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 better with gentle use but worse with excessive or prolonged use, 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.[6]
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; overweight; loss of strength in muscles supporting joints; and impairment of peripheral nerves, leading to sudden or uncoordinated movements that overstress joints.[7] However exercise, including running in the absence of injury, has not been found to increase one's risk of developing osteoarthritis.[8] Nor has cracking ones knuckles been found to play a role.[9]
Primary osteoarthritis 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[10] 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 what 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.
A number of studies have shown that there is a greater prevalence of the disease among siblings and especially identical twins, indicating a hereditary basis.[11] Up to 60% of OA cases are thought to result from genetic factors.
Both primary generalized nodal OA and erosive OA (EOA. also called inflammatory OA) are sub-sets of primary OA. EOA is a much less common, and more aggressive inflammatory form of OA which often affects the DIPs and has characteristic changes on X-Ray.
This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:
Diagnosis is made with reasonable certainty based on history and clinical examination.[12][13] X-rays may confirm the diagnosis. The typical changes seen on X-ray include: joint space narrowing, subchondral sclerosis (increased bone formation around the joint), subchondral cyst formation, and osteophytes.[14] Plain films may not correlate with the findings on physical examination or with the degree of pain.[15] 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 spondyloarthropathies.[16]
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.
Lifestyle modification (such as weight loss and exercise) and analgesics are the mainstay of treatment. Acetaminophen / paracetamol is used first line and NSAIDS are only recommended as add on therapy if pain relief is not sufficient.[17] This is due to the relative greater safety of acetaminophen.[17]
For most people with OA, graded exercise should be the mainstay of their self-management. Moderate exercise leads to improved functioning and decreased pain in people with osteoarthritis of the knee.[18][19]
For overweight people, weight loss may be an important factor. Patient education has been shown to be helpful in the self-management of arthritis. It decreases pain, improving function, reducing stiffness and fatigue, and reducing medical usage.[19] 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.[19]
There is sufficient evidence to indicate that physical interventions can reduce pain and improve function.[20] There is some evidence that manual therapy is more effective than exercise for the treatment of hip osteoarthritis, however this evidence could be considered to be inconclusive.[21] Functional, gait, and balance training has been recommended to address impairments of proprioception, balance, and strength in individuals with lower extremity arthritis as these can contribute to higher falls in older individuals.[22] Splinting of the thumb for OA of the base of the thumb leads to improvements after one year.[23]
Acetaminophen is the first line treatment for OA.[17][24] For mild to moderate symptoms effectiveness is similar to Non-steroidal anti-inflammatory drugs (NSAIDs), though for more severe symptoms NSAIDs may be more effective.[17] NSAIDs such as ibuprofen while more effective in severe cases are associated with greater side effects such as gastrointestinal bleeding.[17] Another class of NSAIDs, COX-2 selective inhibitors (such as celecoxib) are equally effective to NSAIDs but no safer in terms of side effects. They are however much more expensive. There are several NSAIDs available for topical use including diclofenac. They have fewer systemic side-effects and at least some therapeutic effect.[25] While opioid analgesic such as morphine and fentanyl improve pain this benefit is outweighed by frequent adverse events and thus they should not routinely be used.[26]
Oral steroids are not recommended in the treatment of OA because of their modest benefit and high rate of adverse effects. Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few weeks and a few months.[27] Topical capsaicin and joint injections of hyaluronic acid have not been found to lead to significant improvement.[25][28][29]
Tanezumab, a monoclonal antibody that binds and inhibits nerve growth factor, appears to relieve joint pain enough to improve function in people with osteoarthritis of the knee, according to research published online Sept. 29 in the New England Journal of Medicine. The FDA is reviewing the safety of tanezumab that could still emerge as an effective treatment for the pain of osteoarthritis.[30][31]
While electrostimulation techniques (NEST) have been used for twenty years to treat osteoarthritis in the knee, a Cochrane Review of studies determined that there is no evidence to show that it reduces pain or disability.[32]
If the above management is ineffective, joint replacement surgery or resurfacing may be required in advanced cases. Arthroscopic surgical intervention for osteoarthritis of the knee however has been found to be no better than placebo at relieving symptoms.[33]
Many alternative medicines are purporting to decrease pain associated with arthritis. However, there is no evidence supporting benefits for most alternative treatments including: vitamin A, C, and E, ginger, turmeric, omega-3 fatty acids, chondroitin sulfate and glucosamine. These treatments are thus not recommended.[34][35] Glucosamine was once believed to be effective[36], but a recent analysis has found that it is no better than placebo.[37] S-Adenosyl methionine may relieve pain similar to nonsteroidal anti-inflammatory drugs.[36][38]
A Cochrane review found that while acupuncture leads to a statistically significant improvement in pain, this improvement is small and may be of questionable clinical significance. Waiting list-controlled trials for peripheral joint osteoarthritis do show clinically relevant benefits, but these may be due to placebo effects.[39] Acupuncture does not seem to produce long-term benefits.[40]
Controversy surrounds glucosamine.[41] A 2010 meta-analysis has found that it is no better than placebo.[37] Some older reviews conclude that glucosamine sulfate was an effective treatment[42][43] while some others have found it ineffective.[44][45] A difference has been found between trials involving glucosamine sulfate and glucosamine hydrochloride, with glucosamine sulfate showing a benefit and glucosamine hydrochloride not. The Osteoarthritis Research Society International (OARSI) recommends that glucosamine be discontinued if no effect is observed after six months.[46]
Mud pack therapy has been suggested to temporarily relieve pain in patients with osteoarthritis of the knees. According to researchers of the Ben Gurion University of the Negev, treatment with mineral-rich mud compresses such as that of those extracted from the Dead Sea, can be used to augment conventional medical therapy in these patients.[47]
Osteoarthritis affects nearly 27 million people in the United States, accounting for 25% of visits to primary care physicians, and half of all NSAID prescriptions. It is estimated that 80% of the population have radiographic evidence of OA by age 65, although only 60% of those will have symptoms.[49] In the United States, hospitalizations for osteoarthritis increased from 322,000 in 1993 to 735,000 in 2006.[50]
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.
Evidence for osteoarthritis found in the fossil record is studied by paleopathologists, specialists in ancient disease and injury. Osteoarthritis has been reported in fossils of the large carnivorous dinosaur Allosaurus fragilis.[51]
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