osteoarthritis - wikipedia, the free encyclopedia.pdf
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Osteoarthritis
Classification and external resources
ICD-10 M15 (http://apps.who.int
/classifications/icd10/browse
/2010/en#/M15)-M19
(http://apps.who.int/classifications
/icd10/browse/2010/en#/M19), M47
(http://apps.who.int/classifications
/icd10/browse/2010/en#/M47)
ICD-9 715 (http://www.icd9data.com
/getICD9Code.ashx?icd9=715)
OMIM 165720 (http://omim.org/entry
/165720)
DiseasesDB 9313
(http://www.diseasesdatabase.com
/ddb9313.htm)
MedlinePlus 000423 (http://www.nlm.nih.gov
/medlineplus/ency/article
/000423.htm)
eMedicine med/1682
(http://www.emedicine.com
/med/topic1682.htm) orthoped/427
(http://www.emedicine.com/orthoped
/topic427.htm#) pmr/93
(http://www.emedicine.com
/pmr/topic93.htm#) radio/492
(http://www.emedicine.com/radio
/topic492.htm#)
OsteoarthritisFrom Wikipedia, the free encyclopedia
Osteoarthritis (OA) also known as degenerative arthritis
ordegenerative joint disease orosteoarthrosis, is a group
of mechanical abnormalities involving degradation of
oints,[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
deficitsmay 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 becomesdebilitating, 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.[4]
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MeSH D010003 (http://www.nlm.nih.gov
/cgi/mesh/2013/MB_cgi?field=uid&
term=D010003)
Bouchard's nodes and Heberden's
nodes may form in osteoarthritis
Contents
1 Signs and symptoms
2 Causes
2.1 Primary
2.2 Secondary
3 Pathophysiology
4 Diagnosis
4.1 Classification
5 Management
5.1 Lifestyle modification
5.2 Physical measures
5.3 Medication
5.4 Surgery
5.5 Alternative medicine
6 Epidemiology
7 Etymology
8 History
9 Research
10 References
11 External links
Signs and symptoms
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 associated muscles and tendons. OA can cause a crackling noise
(called "crepitus") when the affected joint is moved or touched and
people may experience muscle spasms and contractions in the tendons.
Occasionally, the joints may also be filled with fluid.[5] Some people
report increased pain associated with cold temperature, high humidity,
and/or a drop in barometric pressure, but studies have had mixed
results.[6]
OA commonly affects the hands, feet, spine, and the large weight
bearing joints, such as the hips and knees, although in theory, any jointin 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.
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Primary osteoarthritis of the left knee.
Note the osteophytes, narrowing of
the joint space (arrow), and increased
subchondral bone density (arrow).
OA is the most common cause of a joint effusion of the knee.[7]
Causes
Damage from mechanical stress with insufficient self repair by joints is believed to be the primary cause of
osteoarthritis.[8] Sources of this stress may include: misalignments of bones caused by congenital or pathogenic
causes; mechanical injury; excess body weight; loss of strength in the muscles supporting a joint; and
impairment of peripheral nerves, leading to sudden or uncoordinated movements.[8] However exercise,
including running in the absence of injury, has not been found to increase the risk.[9] Nor has cracking one's
knuckles been found to play a role.[10]
Primary
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] Although a single factor is not generally sufficient
to cause the disease, about half of the variation in susceptibility has been
assigned to genetic factors.[12]
The development of OA is correlated with a history of previous joint
injury and with obesity, especially with respect to knees.[13] Since the
correlation with obesity has been observed not only for knees but also
for non-weight bearing joints and the loss of body fat is more closely
related to symptom relief than the loss of body weight, it has been
suggested that there may be a metabolic link to body fat as opposed to
ust mechanical loading.[14]
Changes in sex hormone levels may play a role in the development ofOA as it is more prevalent among post-menopausal women than among
men of the same age.[15][16] A study of mice found natural female
hormones to be protective while injections of the male hormone
dihydrotestosterone reduced protection.[17]
Secondary
This type of OA is caused by other factors but the resulting pathology is the same as for primary OA:
AlkaptonuriaCongenital disorders of joints
Diabetes
Ehlers-Danlos Syndrome
Hemochromatosis and Wilson's disease
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 or ligaments (such as the ACL), as a result of an accident or orthopedic operations.
Ligamentous deterioration or instability may be a factor.
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Marfan syndrome
Obesity
Septic arthritis (infection of a joint)
Pathophysiology
Primary 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 thecartilage decreases[18] as a result of a reduced proteoglycan content, thus causing the cartilage to be less
resilient. The water content of healthy cartilage is finely balanced by compressive force driving water out &
swelling pressure drawing water in.[19]
Collagen fibres exert the compressive force, whereas the Gibbs-Donnan
effect & cartilage proteoglycans create osmotic pressure which tends to draw water in.[19] However during
onset of OA there is an increase in cartilage water content. [20][21][22][23][24] This increase occurs because whilst
there is an overall loss of proteoglycans,[21][25] it is outweighed by a loss of collagen.[19][25] 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.
Diagnosis
Diagnosis is made with reasonable certainty based on history and clinical examination.[26][27]
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.[28]
Plain films may
not correlate with the findings on physical examination or with the degree of pain.[29] Usually other imaging
techniques are not necessary to clinically diagnose OA.
In 1990, the American College of Rheumatology, using data from a multi-center study, developed a set of
criteria for the diagnosis of hand OA based on hard tissue enlargement and swelling of certain joints.[30] These
criteria were found to be 92% sensitive and 98% specific for hand OA versus other entities such as rheumatoid
arthritis and spondyloarthropathies.[31]
Related pathologies whose names may be confused with OA 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 OA which is a degenerative pathologyaffecting a high incidence of distal phalangeal joints of female patients. A polished ivory-like appearance may
also develop on the bones of the affected joints, reflecting a change called eburnation.[32]
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Damaged cartilage from
sows. (a) cartilage
erosion (b)cartilage
ulceration (c)cartilage
repair (d)osteophyte
(bone spur) formation.
Histopathology of
osteoarthrosis of a knee
joint in an elderly
female.
Histopathology of
osteoarthrosis of a knee
joint in an elderly
female.
Severe osteoarthritis
and osteopenia of the
carpal joint and 1st
carpometacarpel joint.
Classification
OA can be classified into either primary or secondary depending on whether or not there is an identifiable
underlying cause.
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 distal interphalangeal joints and has characteristic changes on x-ray.
Management
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.[33] This is due to the relative greater safety of acetaminophen.[33]
Lifestyle modification
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, improves function, reduces stiffness and fatigue, and
reduces medical usage.[34] 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. [34]
Physical measures
Moderate exercise is beneficial with respect to pain and function in those with osteoathritis of the knee and
possibly hip.[35] While some evidence supports certain physical therapies evidence for a combined program is
limited.[36] There is not enough evidence to determine the effectiveness of massage therapy.[37]
The use of orthoses (commonly referred to as splints, braces or insoles as applicable) can reduce the symptoms
of OA. In the lower limb, orthoses are used for the foot and ankle[38] and knee.[39] Knee braces may be
useful.[40] In the upper limb, splinting of the base of the thumb leads to improvements after one year.[41]
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The evidence for manual therapy is inconclusive.[42] Functional, gait, and balance training has been
recommended to address impairments of position sense, balance, and strength in individuals with lower
extremity arthritis as these can contribute to higher falls in older individuals.[43]
Medication
The analgesic paracetamol (INN; acetaminophen is the USA) is the first line treatment for OA.[33][44] For mild
to moderate symptoms effectiveness is similar to non-steroidal anti-inflammatory drugs (NSAIDs), though formore severe symptoms NSAIDs may be more effective.[33] NSAIDs such as ibuprofen while more effective in
severe cases are associated with greater side effects such as gastrointestinal bleeding.[33] Another class of
NSAIDs, COX-2 selective inhibitors (such as celecoxib) are equally effective to NSAIDs with lower rates of
adverse gastrointestinal effects but higher rates of cardiovascular disease such as myocardial infarction.[45]
They are also much more expensive. Oral steroids are not recommended in the treatment of OA because of their
modest benefit and high rate of adverse effects.[citation needed]
There are several NSAIDs available for topical use including diclofenac. They have fewer systemic side-effects
and at least some therapeutic effect.[46] A Cochrane review concluded that opioid analgesics such as morphine
and fentanyl reduce pain, but this benefit is outweighed by frequent adverse events and thus they should notroutinely be used.[47] Topical capsaicin is controversial with a 2011 review[48] finding effectiveness and a 2009
review not.[46]
Injection of glucocorticoids (such as hydrocortisone) leads to short term pain relief that may last between a few
weeks and a few months.[49] Joint injections of hyaluronic acid have not been found to lead to significant
improvement.[46][50] Hyaluronic acid injects have been associated with significant harm.[50]
Surgery
If disability is significant and more conservative management is ineffective, joint replacement surgery orresurfacing may be recommended. Evidence supports joint replacement for both knees and hips.[51] For the
knee it improves both pain and functioning.[52] Arthroscopic surgical intervention for OA of the knee however
has been found to be no better than placebo at relieving symptoms.[53]
Alternative medicine
Dietary supplements
Many dietary supplements are sold as treatments for OA and some of them have been found to be effective.
Phytodolor,[48] SAMe,[54] and SKI 306X (a Chinese herbal mixture)[55] may be effective in improving pain,
and there is some evidence to support the use of cat's claw as an anti-inflammatory.[56] There is tentative
evidence to support avocado/soybean unsaponifiables,[57]Boswellia serrata extracts (frankincense),[58][59]
MSM[48] and rose hip.[48]
The effectiveness of glucosamine is controversial.[60][61] A 2010 meta-analysis found that it is no better than
placebo.[62] Some older reviews conclude that glucosamine sulfate was an effective treatment[63][64] while
some others have found it ineffective.[65] A difference may exist between glucosamine sulfate and glucosamine
hydrochloride, with glucosamine sulfate showing a benefit and glucosamine hydrochloride not.[66] The
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Disability-adjusted life year for OA
per 100,000 inhabitants in 2004.[74]
no data
200
200220
220240
240260
260280
280300
300320
320340
340360
360380
380400
400
Osteoarthritis Research Society International recommends that glucosamine be discontinued if no effect is
observed after six months[67] and the National Institute of Clinical Excellence no longer recommends its use.[68
If there is a benefit it is at best slight.[69]
There is little evidence supporting benefits for some supplements, including: the Ayurvedic herbal preparations
with brand names Articulin F and Eazmov, collagen, devils claw, Duhuo Jisheng Wan (a Chinese herbal
preparation), fish liver oil, ginger, the herbal preparation Gitadyl, glucosamine, hyaluronic acid, omega-3 fatty
acids, the brand-name product Reumalax, stinging nettle, turmeric, vitamins A, C, and E in combination,
vitamin E alone, vitamin K and willow bark. There is insufficient evidence to make a recommendation about
the safety and efficacy of these treatments.[48][56] Chondroitin is not recommended as a treatment for OA.[70]
Manual therapies
While acupuncture leads to a statistically significant improvement in pain relief, 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.[71] Acupuncture does not seem to
produce long-term benefits.[72] While electrostimulation techniques such as TENS have been used for twenty
years to treat osteoarthritis in the knee, there is no conclusive evidence to show that it reduces pain ordisability.[73]
Epidemiology
Globally approximately 250 million people have osteoarthritis of the
knee (3.6% of the population).[75]
OA 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.[76] In the United States,hospitalizations for OA increased from 322,000 in 1993 to 735,000 in
2006.[77]
Globally OA causes moderate to severe disability in 43.4 million people
as of 2004.[78]
Etymology
OA is derived from the Greek word part osteo-, meaning "of the bone",
combined with arthritis: arthr-, meaning "joint", and -itis, the meaningof which has come to be associated with inflammation. The -itis of OA
could be considered misleading as inflammation is not a conspicuous feature. Some clinicians refer to this
condition as osteoarthosis to signify the lack of inflammatory response.
History
Evidence for OA found in the fossil record is studied by paleopathologists, specialists in ancient disease and
injury. OA has been reported in fossils of the large carnivorous dinosaurAllosaurus fragilis.[79]
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Research
There are ongoing efforts to determine if there are agents that modify outcomes in OA. Sprifermin is one
candidate drug. There is also tentative evidence that strontium ranelate may decrease degeneration in OA and
improve outcomes.[80][81]
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External links
American College of Rheumatology Factsheet on OA (http://www.rheumatology.org/practice/clinical
/patients/diseases_and_conditions/osteoarthritis.asp)Osteoarthritis (http://www.arthritis.org/disease-center.php?disease_id=32) The Arthritis Foundation
Treatment Guidelines. (http://www.oarsi.org/index2.cfm?section=Publications_and_Newsroom&
content=OAGuidelines) Osteoarthritis Research Society International. Recommendations for the
management of hip and knee osteoarthritis. Part II OARSI Recommendations for Management of Hip &
Knee OA 2007. Part III Changes in Evidence 2010.
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