Clinical Manifestations and Diagnosis of Osteoarthritis

Clinical manifestations and diagnosis of osteoarthritis - UpToDate 11:15, 16/11/2021
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Clinical manifestations and diagnosis of osteoarthritis

Authors: Michael Doherty, MA, MD, FRCP, FHEA, Abhishek Abhishek, MBBS, MD, FRCP, PhD
Section Editor: David Hunter, MD, PhD
Deputy Editor: Monica Ramirez Curtis, MD, MPH
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Oct 2021. | This topic last updated: Sep 24, 2021.
INTRODUCTION
Osteoarthritis (OA) is the commonest form of arthritis and possesses marked variability of
disease expression. Although most patients present with joint pain and functional
limitations [1], the age of disease onset, sequence of joint involvement, and disease
progression vary from person to person. OA ranges from an asymptomatic, incidental
finding on clinical or radiologic examination to a progressive disabling disorder eventually
culminating in "joint failure."
The clinical features and approach to the diagnosis of OA will be reviewed here. The
pathogenesis, epidemiology, and treatment of OA are discussed separately. (See
"Pathogenesis of osteoarthritis" and "Epidemiology and risk factors for osteoarthritis".)
CLINICAL MANIFESTATIONS
The primary symptoms of osteoarthritis (OA) are joint pain, stiffness, and locomotor
restriction. Symptoms usually present in just one or a few joints in a middle-aged or older
person. Other manifestations in patients with OA include sequelae such as muscle
weakness, poor balance [2], and comorbidities such as fibromyalgia [3-6].
Symptoms and signs — The following symptoms and signs may be observed in patients
with OA:
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● Pain – Pain in OA is worse with joint use (usage-related pain) and relieved by rest. It
is the most frequent symptom and may progress through three stages [7]:
• Stage 1 – Predictable, sharp pain usually brought on by a mechanical insult that

eventually limits high-impact activities with relatively modest effect on function.
• Stage 2 – Pain becomes more constant and starts to affect daily activities. There
may be unpredictable episodes of stiffness.
• Stage 3 – Constant dull/aching pain punctuated by episodes of often

unpredictable, intense, exhausting pain that results in severe limitations in
function.
However, not all patients go through such distinct stages, and pain progression may
be arrested at any stage, and even go away (especially with hand OA).
Pain is generally worse in the late afternoon and early evening but can also be worse
in the morning soon after waking up [8]. There may also be night pain in severe OA
that can interfere with sleep. In some people, the pain has a burning (neuropathic)
quality, is widespread around the joint, and is associated with paresthesia [7]; such
features also suggest comorbid fibromyalgia. Painful periarticular soft-tissue lesions
may coexist, especially with large-joint OA [9]. Periarticular soft-tissue lesions cause
localized pain away from the joint line, whereas OA-related pain more commonly is
most severe over the joint line, except for proximal joints like the hip or the shoulder
that may have the maximal pain distal to the originating joint.
Risk factors for pain development and persistence in OA include anxiety and
depression, nonrestorative sleep (reduced delta sleep), pain elsewhere, and
catastrophizing trait or state. These all cause central pain sensitization with reduced
descending pain inhibition.
● Tenderness – Joint-line tenderness suggests articular pathology, while tenderness

away from the joint line suggests periarticular soft-tissue pathology.
● Limitation of motion – Reduced range of motion (equal for both active and passive
movement) mainly results from marginal osteophytes and capsular thickening, but
synovial hyperplasia and effusion may also contribute.
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● Bony swelling – Bony swelling reflects remodeling of the bone and cartilage on
either side of the joint and marginal osteophytes, and may be evident in small (eg,
finger interphalangeal, first metatarsophalangeal [MTP]) and large (eg, knee) joints.
● Joint deformity – Deformity is a sign of advanced joint damage. Common examples

include squaring and subluxation of the thumb base in first carpometacarpal (CMC)
OA and genu varum in people with advanced tibiofemoral OA.
● Instability – Giving way or buckling is a common symptom in knee OA. Occasionally

people may stumble and fall, but usually it is a feeling of apprehension and lack of
confidence to weight-bear rather than literally "giving way." It is predominantly a
sign of muscle weakness with subsequent altered patellar tracking (with lateral
patellar subluxation) but may also associate with true joint instability. Similar
symptoms are frequently reported by patients with thumb-base OA.
Joint distribution — Many of the characteristic clinical manifestations of OA are related to

the involvement of particular joints. OA can be categorized into localized or generalized
forms of the disease.
Single- or multiple-joint osteoarthritis — OA has a predilection for the knees, hips,

finger interphalangeal joints, first CMC joints, first MTP joints, and apophyseal (facet)
joints of the lower cervical and lower lumbar spine ( figure 1) [10].
OA less commonly affects the elbow, wrist, shoulder (ie, the glenohumeral joint), and
ankle. When the elbow, shoulder (especially the acromioclavicular joint), and
metacarpophalangeal (MCP) joints (eg, the "Missouri metacarpal syndrome") are affected,
occupations that involve overuse of the upper limbs should be suspected. The symptoms
at these joints are similar to those of OA at other joints ( table 1); however, joint
involvement is more often unilateral.
Generalized osteoarthritis — Generalized OA implies a polyarticular subset of OA

typically involving the distal interphalangeal (DIP) joints, thumb bases (first CMC joints and
trapezioscaphoid joints) ( figure 2), first MTP joints, lower cervical and lumbar facet
joints, knees, and hips [11]. It is characterized by slow accumulation of multiple joint
involvement over several years. Symptoms usually commence in the hands around middle
age and subsequently affect the knees and other joints over the next few decades. The
clinical marker for generalized OA is the presence of multiple Heberden nodes, which are

posterolateral hard swellings of the DIP joints ( picture 1) [11]. Heberden nodes are
often accompanied by less well-defined posterolateral swellings of the proximal
interphalangeal (PIP) joints referred to as Bouchard nodes ( picture 2). Generalized OA
may occur in the absence of nodes, so called non-nodal generalized OA, which is more
common in men (compared with nodal generalized OA, which is more common in women)
[12,13]. There is no universal definition for the number of joints affected before someone
can be classified as having generalized OA, but guidance from the American College of
Rheumatology (ACR) and the European Alliance of Associations for Rheumatology (EULAR;
formerly known as European League Against Rheumatism) suggests that generalized OA
is present if there is OA at either the spinal or hand joints, respectively, and in at least two
other joint regions [14,15].
Imaging — The diagnosis of OA is a clinical one based on characteristic signs and

symptoms described above. When the diagnosis is unclear or important alternative
diagnoses need to be considered, several imaging modalities can be used to assess the
presence and severity of OA. Our approach to imaging for OA is generally consistent with
guidelines developed by professional organizations [16].
● Radiography – Conventional radiography is the most widely used imaging modality

in OA and allows for detection of characteristic features of OA including marginal
osteophytes, localized joint space narrowing, subchondral sclerosis, and cysts
[17,18]. Radiographs can also be used to measure joint space narrowing, which is
sometimes used as a surrogate measure of cartilage loss. However, radiographic
changes in OA are insensitive, particularly with early disease, and often correlate
poorly with symptoms [19-21]. Also, radiographic OA is a common incidental
asymptomatic finding in older people.
● Magnetic resonance imaging – Magnetic resonance imaging (MRI) is not necessary

for most patients with symptoms suggestive of OA and/or typical radiographic
features. However, MRI can identify OA at earlier stages of disease before
radiographic changes become apparent. These changes include cartilage defects
and bone marrow lesions. MRI can also be used to assess pathology in other
structures of the joint not visualized by radiography such as effusions, synovium,
and ligaments.
The sensitivity of MRI is less than that of clinical and radiographic techniques in the

diagnosis of OA, and there is no indication for using MRI in routine clinical practice
for diagnosing OA. In a large meta-analysis, the overall sensitivity and specificity of
MRI for detecting OA were reported as 61 and 82 percent, respectively, based on
pooled data from studies that used different reference standards (eg, histology,
direct visualization with arthroscopy, radiography) [22]. MRI may have a greater role
in ruling out OA. As an example, a person with a symptomatic partial thickness
meniscal tear may be incorrectly diagnosed as OA, and an MRI of the knee may
reveal the true pathology. A Delphi panel has developed MRI definitions of structural
OA at the tibiofemoral and patellofemoral joints [23]. However, these definitions
should not be used for a clinical diagnosis of OA, disease staging, or to detect early
OA. The structural changes of OA visible on MRI are commonly present in
asymptomatic noninjured joints and typically precede clinical features of OA [24,25].
The sensitivity and specificity of individual MRI features for the clinical diagnosis of
OA is not well understood.
● Ultrasonography – Ultrasonography is another imaging modality that can identify

OA-associated structural changes and is useful for detecting synovial inflammation,
effusion, and osteophytosis. Limitations of ultrasound include that it is operator-
dependent and cannot be used to assess deeper articular structures and
subchondral bone.
Synovial fluid — Synovial fluid from OA joints is usually noninflammatory or mildly

inflammatory with less than 2000 white blood cells/mm3, predominantly mononuclear
cells. Inflammatory effusion in OA may occur in the presence of calcium pyrophosphate
(CPP) crystals (see 'Osteoarthritis with calcium pyrophosphate deposition' below). A
detailed discussion on synovial fluid analysis is presented elsewhere. (See "Synovial fluid
analysis".)
Osteoarthritis with calcium pyrophosphate deposition — CPP crystals may be present

in as many as 30 to 60 percent of unselected OA patients [26]. Most patients with OA and
CPP deposition (CPPD) are older than 60 years, and common target sites are the knees,
radiocarpal joints, second and third MCP joints, shoulder, and elbow joints [27,28]. The
presence of CPPD may modify OA symptoms at that site, especially with longer early
morning stiffness and more signs of synovitis. The symptoms may be acute with marked
pain, swelling, and tenderness, at its worst within 6 to 24 hours, typically lasting from a
few days to one to two weeks (acute CPP crystal arthritis, previously called "acute

pseudogout"); intermittent; or low-grade and persistent (chronic CPP crystal inflammatory

arthritis) [29]. Joint swelling, warmth, and tenderness may be more common and more
pronounced than in OA without CPPD ( picture 3). Joint effusions are common and may
be hemorrhagic or turbid on aspiration. Large joint effusions may leak into the
surrounding soft tissues and lead to localized pain, swelling, and extensive bruising,
especially at the shoulder and knee. Symptoms are mostly restricted to one or a few joints
at a time, but polyarticular involvement can occur, especially involving knees, wrists, and
MCP joints, that superficially may mimic RA.
Although studies give conflicting results, it is likely that OA with CPPD is not any more
rapidly progressive than OA alone [30-32], and patients with end-stage knee OA with CPPD
do not have any more difficulty with activities than those with end-stage knee OA alone
[32]. However, a few patients with CPPD do appear to develop rapidly progressive
destructive arthropathy at the knees, shoulders, or hips. (See "Clinical manifestations and
diagnosis of calcium pyrophosphate crystal deposition (CPPD) disease", section on
'Osteoarthritis with CPPD'.)
CHARACTERISTICS OF SPECIFIC JOINT INVOLVEMENT
Many of the characteristic clinical manifestations of osteoarthritis (OA) are related to the
involvement of particular joints. As described above, OA has a predilection for the hand,
knee, hip, and spine, and less commonly affects the shoulder, elbow, wrist, and ankle.
Hand — Symptoms are usually bilateral, and joint involvement is usually approximately
symmetrical [15,33]. Typical symptoms affect just one or a few joints at a time [15].
Symptoms can be intermittent and target characteristic sites, ie, distal interphalangeal
(DIP) joints, thumb bases, proximal interphalangeal (PIP) joints, and second and third
metacarpophalangeal (MCP) joints, in descending order of frequency [15]. Individuals
without pain may still report an "aching" or stiffness in the hands [33]. Symptoms may
worsen in approximately half of patients over the next six years, and the predictors of
adverse clinical outcomes include a high level of baseline functional impairment and a
greater number of painful joints, with no consistent correlation between clinical
symptoms and radiographic progression [34].
Nodal osteoarthritis — Heberden and/or Bouchard nodes plus underlying

interphalangeal OA constitute nodal OA [15]. Affected people are frequently women, often

with a strong familial predisposition. Symptoms usually start in middle age, typically
around menopause, with a stuttering onset of pain, tenderness, and stiffness of one or a
few finger interphalangeal joints. At the start, there may be intermittent or persistent
warmth and soft-tissue swelling, but over a period of a few years the involved
interphalangeal joints usually become less painful, and signs of inflammation subside,
leaving behind firm-hard bony swellings on the posterolateral aspect of the
interphalangeal joints, termed Heberden and Bouchard' nodes ( picture 1 and
picture 2). Heberden nodes sometimes coalesce to form a single dorsal bar (
picture 1). Over a period of several years, new interphalangeal joints go through the
same process in a "mono-arthritis multiplex" fashion. In addition to nodes, affected
interphalangeal joints may show restriction in movement and lateral deviation (radial or
ulnar, with most deviations pointing towards the middle finger). Lateral deviation of
interphalangeal joints, without instability, is a characteristic feature of nodal OA (
picture 2). Nodes most frequently occur at the index and middle fingers [33]. Fully
evolved nodes usually are not painful but may be a cosmetic problem.
Thumb-base OA generally affects older postmenopausal women. Individuals with thumb-

base OA (OA of the first carpometacarpal and/or scaphotrapeziotrapezoid [STT] joint) have
localized deep thenar, radial wrist, or thumb-base pain, exacerbated on joint use. There
may also be distal radiation into the thumb and, to a lesser extent, proximally. Activities
that involve pinching (opposition of the thumb to a finger) are generally most painful. A
subjective grinding sensation on movement may be present. There may be radial
subluxation and adduction at the thumb base, giving it a swollen "squared" appearance (
picture 4) [15,33]. Localized tenderness may be present and passive thumb
circumduction may be painful. Unlike interphalangeal joint OA, thumb-base OA
sometimes associates with persistent symptoms and functional impairment (occasionally
requiring surgery). Thumb-base OA may also occur on its own without nodal
interphalangeal OA.
At the MCP joints, OA mainly targets the second and third MCP joints, most often causing
bony enlargement without signs of synovitis. As described above, relatively isolated MCP
joint OA sometimes occurs in older men who have had physically demanding occupations
("Missouri metacarpal syndrome") [35]. (See 'Single- or multiple-joint osteoarthritis'
above.)
Erosive osteoarthritis — Erosive OA is an uncommon and particularly aggressive subset

of hand OA. It presents with a subacute or insidious onset of pain, stiffness, soft-tissue
swelling, and sometimes paresthesiae affecting multiple interphalangeal joints (ie,
synchronous polyarticular onset) [15,36]. Compared with nodal hand OA, pain,
tenderness, and inflammation (warmth, soft-tissue swelling, sometimes erythema) are
more marked and prolonged [36,37], and erosive OA is not associated with generalized
OA (OA). Erosive OA targets just interphalangeal joints (the DIP joints more frequently
than PIP joints) and usually spares the thumb bases and MCP joints ( picture 5) [15,37].
Lateral instability at the interphalangeal joints is an occasional but characteristic finding (
picture 6), and spontaneous interphalangeal joint fusion may also occur (joint fusion is
not a feature of OA). Rarely, there may be an opera glass deformity [37], and Heberden
and/or Bouchard nodes may coexist [38].
Erosive OA has worse outcome in terms of symptom persistence and functional

impairment than nonerosive hand OA [15]. Although erosive OA as a clinical entity is rare,
radiographic subchondral erosions are present in just one or a few joints in up to 8.5
percent of patients with symptomatic hand OA [39].
Knee — The knee is an important target site for OA and worldwide is the commonest
single cause of lower-limb disability in adults over age 50. Knee OA is usually bilateral,
although one side may be more severely affected. The patellofemoral joint and/or the
medial tibiofemoral joint are most commonly affected, and isolated lateral tibiofemoral
joint OA is relatively rare.
Pain location may indicate the affected knee compartment. Pain may be anteromedial or
more generalized on the medial side in medial-compartment tibiofemoral joint OA or
anterior in patellofemoral joint OA [40]. Pain from patellofemoral joint OA is exacerbated
by prolonged sitting, standing up from a low chair, and climbing stairs or inclines (coming
down often being more painful than going up). More widespread anterior knee pain with
distal radiation suggests moderate to severe knee OA [41], and persistent pain at night
that interrupts sleep or rest occurs in advanced OA [42]. Knee OA usually does not cause
posterior knee pain unless there is a complicating popliteal (Baker's) cyst. The patients
also report a feeling of "giving way" (especially with patellofemoral joint OA and/or
quadriceps weakness) and instability, both of which can associate with falls [42].
Examination reveals typical findings ( table 1), and possibly deformities (eg, fixed flexion
and/or varus, less commonly valgus), quadriceps weakness and wasting, and hip abductor

and other muscle weakness may be present ( picture 7) [42-44]. Knee effusion is
common, though usually mild or modest, and increases in prevalence with the severity of
knee OA [45].
Hip — Hip OA presents with pain, aching, stiffness, and restricted movement. Pain due to
hip OA is usually felt deep in the anterior groin but may involve the anteromedial or upper
lateral thigh and occasionally the buttocks. Distal radiation is not uncommon, and some
individuals present with distal thigh and/or knee pain without any proximal symptoms.
However, unlike pain originating from the knee, such hip-referred pain is usually more
generalized and may be improved by rubbing the painful area. Pain is exacerbated
particularly by rising from a seated position and during the initial phases of ambulation
[46]. Unlike knee OA, hip OA is frequently unilateral [47]. Both active and passive hip
movements are equally painful [46]. Internal rotation with the hip flexed is frequently the
earliest and most affected movement ( picture 8) [46]. The typical end-stage deformity
of hip OA is external rotation, adduction, and fixed flexion ( picture 9). Wasting of thigh
muscles, a positive Trendelenburg test ( figure 3), and shortening of the affected
extremity may also be present [46].
In some patients, especially older women, hip OA can be rapidly progressive, with a
subacute onset of joint pain which progresses to joint destruction and instability in just a
few months. Such rapidly progressive destructive arthropathy has been associated with
basic calcium phosphate (mainly hydroxyapatite) crystals and is termed apatite-associated
destructive arthropathy (ADA) [48-50]. Shoulders ("Milwaukee shoulder") [51] and knees
are other target sites. Muscle wasting, deformities, and moderate to large joint effusions
with "noninflammatory" (viscous, occasionally hemorrhagic, low cell count) synovial fluid
are common in rapidly progressive large-joint OA.
Facet joint — Facet joint OA usually coexists with intervertebral disc degeneration, often
loosely termed "spondylosis." It is difficult to isolate symptoms specifically to facet joint
OA. However, lumbar facet joint OA leads to localized lumbar pain, which may radiate
unilaterally or bilaterally to the buttocks, groin, and thighs, typically ending above the
knees [52]. Symptoms are typically worse in the morning and during periods of activity
and are increased by stress, exercise, lumbar spine extension, rotary motions, and when
standing or sitting [52]. Similarly, cervical facet joint OA may present with ipsilateral neck
pain, which does not radiate beyond the shoulder and is aggravated by neck rotation or
lateral flexion [53]. The clinical manifestations of neck and back pain are discussed in

detail separately. (See "Evaluation of low back pain in adults" and "Acute lumbosacral
radiculopathy: Pathophysiology, clinical features, and diagnosis" and "Evaluation of the
adult patient with neck pain" and "Evaluation of the adult patient with neck pain", section
on 'Cervical facet osteoarthritis'.)
First metatarsophalangeal joint — First metatarsophalangeal (MTP) joint OA is usually

bilateral, and when symptomatic, leads to localized big-toe pain on standing and during
ambulation (especially during the "toe-off" stage of gait). Bony enlargement of the first
MTP joint is a common finding. Hallux valgus deformity (when the distal end of big toe
points towards the midline of the foot), hallux rigidus (or restricted flexion, and extension
at the first MTP joint), and cross-over toes are common deformities. Bony enlargement at
the first MTP joint and hallux valgus frequently lead to the development of a complicating
bursa with additional fibrous tissue reaction on the medial aspect of the first MTP joint
("bunion"). This may get inflamed, for example by rubbing against any footwear.
Apart from the first MTP joint, OA also commonly targets the talonavicular joint in the
midfoot (aggravated by pes planus) and also the subtalar and tibiotalar joints in the
hindfoot.
Shoulder — The glenohumeral joint is not a major target site for OA, but, because of its
overall high prevalence, OA is the commonest cause of glenohumeral arthritis in the
community [54]. Glenohumeral OA predominates in older adults aged over 70 and is more
common in women. Local risk factors include previous direct injury or dislocation,
humeral head or neck fracture, and large rotator cuff tears.
Patients with glenohumeral OA usually present with gradual development, over months
or years, of anterior shoulder and upper arm pain, mild morning and inactivity stiffness,
and restricted movement. The pain is predominantly usage-related, initially and most
severely affecting abduction/elevation and external rotation, but eventually potentially
affecting all movements. Night pain and persistent discomfort at rest may also occur. The
site of maximum pain is usually referred to the outer aspect of the upper arm close to the
deltoid insertion, but pain may be experienced over a wide area including the whole
deltoid contour down the radial aspect of the forearm to the elbow (rarely even to the
wrist). The pain is often eased by rubbing or squeezing the site of maximum discomfort (a
characteristic of distally referred, rather than locally originated, pain).
Examination findings may include: local glenohumeral anterior joint line tenderness; pain
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and restriction, mainly of external rotation and abduction but eventually all other
movements (findings are similar on both active and passive movement); coarse crepitus
felt maximally over the anterior joint line; and weakness and eventual wasting of all
muscles acting over the joint, including the deltoid (causing sharper bony angulation or
"squaring" of the shoulder), and rotator cuff muscles.
Patients with frozen shoulder (adhesive capsulitis) may present with similar pain and
restriction to those of patients with glenohumeral OA. However, the onset of symptoms in
frozen shoulder is subacute (over just days to weeks), and patients with shoulder OA are
typically older than those with adhesive capsulitis. (See "Frozen shoulder (adhesive
capsulitis)" and "Evaluation of the adult with shoulder complaints".)
DIFFERENTIAL DIAGNOSIS
The differential diagnosis for osteoarthritis (OA) depends largely on the location of the
affected site as well as the presence of absence of additional systemic symptoms. We
present several alternative diagnoses that may be considered in the appropriate clinical
context. However, most disorders can usually be easily distinguished from OA.
● Rheumatoid arthritis – OA in the middle-aged or older adult patient is most

commonly confused with rheumatoid arthritis (RA) when it involves the hand joints.
However, the different patterns of clinical involvement will usually lead to the correct
diagnosis ( table 2) (see "Diagnosis and differential diagnosis of rheumatoid
arthritis"). The following are examples:
• Nodal OA of the hands typically affects the distal interphalangeal (DIP) joints and
is frequently associated with the highly characteristic Heberden nodes (
picture 1). By contrast, RA typically targets the metacarpophalangeal (MCP)
and proximal interphalangeal (PIP) joints, and Heberden nodes are absent. The
carpometacarpal (CMC) joint of the thumb is typically involved in OA, rather than
the PIP joint in RA. Swelling of the joints is hard and bony in OA; by comparison,
soft, warm, and tender joint swelling is typical of RA.
• Stiffness of the joint is a very common feature of RA, but it is a relatively rare
feature of OA. Furthermore, the stiffness of RA is characteristically worse after
resting the joint (eg, morning stiffness), while the stiffness of OA (if present) is

typically worse after any effort and is often described as evening stiffness. Early
morning or inactivity-related stiffness lasts for at least 30 minutes in RA, while
early morning or inactivity-related stiffness lasts for only a few minutes in people
with OA.
• OA is characterized radiographically by narrowing of the joint space due to

cartilage loss and osteophytes due to bone remodeling, but not periarticular
erosions ( image 1). Sea-gull (central subchondral) erosions are present in joints
with erosive OA ( image 2). However, many patients with longstanding RA may
develop secondary OA.
• OA is classically associated with the absence of rheumatoid factor (RF) and

antibodies to cyclic citrullinated peptide (CCP). OA is associated with normal levels
of acute phase reactants. However, RF may be present, usually in low titer,
consistent with the patient's (older) age. In addition, the erythrocyte
sedimentation rate (ESR) and serum C-reactive protein (CRP) concentration may
be somewhat elevated, usually secondary to a comorbidity.
● Psoriatic arthritis – Psoriatic arthritis targets the DIP joints of the hands, which can
be observed in hand OA. However, unlike hand OA, psoriatic arthritis may target just
one finger, often as dactylitis, and characteristic nail changes are usually present.
(See "Clinical manifestations and diagnosis of psoriatic arthritis".)
● Crystalline arthritis – Crystalline arthritis (gout and acute calcium pyrophosphate

[CPP] crystal arthritis [previously called acute pseudogout]) can become chronic and
even assume a polyarticular distribution involving the fingers, wrists, knees, and
other large joints. The diagnosis is established by the finding of urate or CPP crystals,
respectively, in synovial fluids. The presence of tophi on physical examination and
the characteristic appearance of punched-out juxta-articular gouty erosions are also
useful in distinguishing OA from gout ( image 3). CPP crystal deposition (CPPD)
disease can be diagnosed if there is radiographic articular chondrocalcinosis (
image 4). (See "Clinical manifestations and diagnosis of gout" and "Clinical
manifestations and diagnosis of calcium pyrophosphate crystal deposition (CPPD)
disease".)
● Hemochromatosis – The arthropathy of iron overload may be confused with hand

OA. However, unlike hand OA, hemochromatosis targets the MCP joints and wrists,

and predominates in men. The characteristic radiologic findings of hemochromatosis

are squared-off bone ends and hook-like osteophytes in the MCP joints, particularly
the second and third MCP joints ( image 5). Chondrocalcinosis may also be
present. (See "Arthritis and bone disease associated with hereditary
hemochromatosis".)
● Infectious arthritis – OA of a single joint is usually associated with mild symptoms

and a noninflammatory synovial fluid (white blood cell count <2000 cells/mm3) but
can also present as an acutely painful synovitis that may mimic infection [55]. The
diagnosis of infectious arthritis is suspected from joint pain that progresses from day
to day with inflammatory signs (eg, effusion, increased warmth, erythema), and is
established by culturing the pathogen from the synovial fluid or from the blood.
Patients with septic arthritis may or may not appear toxic on examination,
depending upon the stage of their infection, the presence of medications that can
mask infection (eg, glucocorticoids), and other clinical variables. Peripheral blood
leukocytosis with a left shift is common but not invariably present. (See "Septic
arthritis in adults".)
● Other soft-tissue abnormalities – Other soft-tissue abnormalities around a single

joint may mimic OA. As an example, pain from hip OA must be distinguished from
labral impingement and/or tear, avascular necrosis of the femoral head, and
developmental hip dysplasia (anterior groin pain); greater trochanter pain syndrome
(trochanteric bursitis or tendinitis, enthesitis of gluteus medius, lateral thigh pain);
and lumbar radiculopathy, sacroiliac joint dysfunction, and hip extensor or rotator
muscle strain (posterior pelvic pain) [56]. (See "Approach to the adult with
unspecified hip pain".)
DIAGNOSIS
Osteoarthritis (OA) may be diagnosed without the use of radiography and/or laboratory
investigations in the presence of typical symptoms and signs in the at-risk age group
[1,19,20].
Clinical diagnosis — Peripheral joint OA may be diagnosed confidently on clinical

grounds alone if the following are present:

● Persistent usage-related joint pain in one or few joints

● Age ≥45 years
● Morning stiffness ≤30 minutes [1]
The presence of other clinical features of OA add to the diagnostic certainty ( table 1)
[1]. This approach to a clinical diagnosis is supported by the fact that radiographically
assessed structural changes may be present in the absence of symptoms and vice versa
[19,20].
It is important to differentiate "structural" or "radiologic" changes of OA (eg, cartilage loss

and/or osteophytes) visible on imaging and without any symptoms, from a diagnosis of
clinical OA. The clinical syndrome of OA is defined by the presence of symptoms and/or
signs. If these are typical for OA, imaging tests need not be undertaken. However, the
absence of structural changes of OA on sensitive imaging (eg, MRI) suggests an alternate
diagnosis for the cause of symptoms. (See 'Characteristics of specific joint involvement'
above and 'Imaging' above.)
When to consider additional testing — Appropriate imaging and laboratory

investigations should be carried out in:
● Younger individuals with joint symptoms/signs of OA
● Presence of atypical symptoms and signs such as an unusual site of involvement,

symptoms and signs of joint inflammation, marked rest and/or night pain, and
rapidly progressive pain
● Presence of weight loss or constitutional symptoms
● Those with knee pain and true "locking," which suggests additional mechanical
derangement
Additional laboratory testing may include an erythrocyte sedimentation rate (ESR) or C-

reactive protein (CRP). Inflammatory markers are normal in OA and may be useful in
excluding other diagnoses. In patients with hand arthralgias and a mix of inflammatory
and mechanical joint symptoms, rheumatoid factor (RF) and anti-cyclic citrullinated
peptide (CCP) antibodies may be checked to evaluate possible rheumatoid arthritis (RA).
(See "Diagnosis and differential diagnosis of rheumatoid arthritis".)

Radiographic examination may be used to support a diagnosis of OA but is not a routine

test to consider as a means to explain clinical symptoms. Patients with a robust diagnosis
of OA on clinical grounds may have normal plain radiographs, and vice versa. Also, knee
pain on most days of a month can precede radiographic changes of OA by several years
[57]. Radiographic examination may have a role in defining the prognosis of patients with
symptomatic OA [58]. However, patients should be examined carefully to exclude any
other cause of joint pain, such as periarticular soft-tissue lesions (see "Overview of soft
tissue rheumatic disorders"). When there is still diagnostic uncertainty regarding the
cause of joint pain, advanced imaging with magnetic resonance imaging (MRI) or
ultrasonography may also be helpful. (See 'Imaging' above.)
Synovial fluid examination is not routinely required to support a diagnosis of OA. (See
'Synovial fluid' above.)
CLASSIFICATION CRITERIA
Osteoarthritis (OA) can be classified according to the joints affected, age of onset,
radiographic appearance ("hypertrophic" versus "atrophic"), presumed etiology (eg,
"secondary post-traumatic" OA), and rate of progression. Several classification systems
have been proposed, each with its own strengths and weaknesses.
Common problems with classification criteria include:
● Frequent overlap, with lack of clear separation between "subsets." As an example,

subchondral changes of "erosive OA" are not uncommon in just a few
interphalangeal joints in nodal OA.
● Common coexistence of separate subsets, or evolution from one form of arthritis to

another within an individual (eg, a patient with nodal-generalized OA may
subsequently develop calcium pyrophosphate crystal deposition [CPPD] at the knees,
and rapidly progressive "atrophic" glenohumeral OA)
The American College of Rheumatology (ACR) classification of OA is the most widely used
classification system [14] but has several limitations, including artificial separation of
nodal and erosive (non-nodal) OA as two distinct subsets of hand OA; and inclusion of
intervertebral disc degeneration and Forestier disease as a subset of spinal OA, even

though OA is pathologically confined to synovial joints. The guideline development group

has recognized that these distinctions are arbitrary and have yet to be validated [14,27].
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and

regions around the world are provided separately. (See "Society guideline links:
Osteoarthritis".)
SUMMARY
● The primary symptoms of osteoarthritis (OA) are joint pain, stiffness, and locomotor
restriction. They usually present in just one or a few joints in a middle-aged or older
person. (See 'Clinical manifestations' above.)
● Many of the characteristic clinical manifestations of OA are related to the

involvement of particular joints. OA has a predilection for the knees, hips, finger
interphalangeal joints, first carpometacarpal (CMC) joints, first metatarsophalangeal
(MTP) joints, and apophyseal (facet) joints of the lower cervical and lower lumbar
spine ( figure 1). (See 'Characteristics of specific joint involvement' above and
'Single- or multiple-joint osteoarthritis' above.)
● Generalized OA implies a polyarticular subset of OA involving the distal

interphalangeal (DIP) joints, thumb bases (first CMC joints and trapezioscaphoid
joints), first MTP joints, lower cervical and lumbar facet joints, knees, and hips. (See
'Generalized osteoarthritis' above.)
● Peripheral joint OA may be diagnosed confidently on clinical grounds alone if the

following are present (see 'Clinical diagnosis' above):
• Persistent usage-related joint pain in one or few joints

• Age ≥45 years
• Morning stiffness ≤30 minutes
The presence of other clinical features of OA add to the diagnostic certainty (

table 1). This approach to a clinical diagnosis is supported by the fact that

radiographically assessed structural changes may be present in the absence of

symptoms and vice versa.
● Appropriate imaging and laboratory investigations are reserved for patients

presenting with atypical symptoms and signs such an unusual site of involvement,
symptoms and signs of joint inflammation, marked rest and/or night pain, and
rapidly progressive pain. (See 'When to consider additional testing' above.)
● The differential diagnosis for OA depends largely on the location of the affected site
as well as the presence of absence of additional systemic symptoms. The differential
diagnosis includes rheumatoid arthritis (RA), psoriatic arthritis, crystalline arthritis
(gout or calcium pyrophosphate crystal deposition [CPPD] disease),
hemochromatosis, infectious arthritis, and other soft-tissue abnormalities. (See
'Differential diagnosis' above.)
ACKNOWLEDGMENT
The UpToDate editorial staff acknowledges Kenneth Kalunian, MD, who contributed to an
earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 105723 Version 15.0

GRAPHICS
Joints affected in osteoarthritis
Target symptomatic joints for OA.
OA: osteoarthritis.
Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter D,
Kawaguchi H. 2012. Osteoarthritis Research Society International.
(http://primer.oarsi.org).
Graphic 105815 Version 1.0

Principal manifestations of osteoarthritis
Patient characteristics
Age of onset >40 years*
Symptoms
Pain Affects one or a few joints at a time

Insidious onset - slow progression over years
Variable intensity
May be intermittent
Increased by joint use and relieved by rest
Night pain in severe osteoarthritis
Stiffness Short-lived (<30 minutes) and early morning-

or inactivity-related
Swelling Some (eg, nodal osteoarthritis) patients

present with swelling and/or deformity
Constitutional symptoms Absent
Physical exam findings
Appearance Swelling (bony overgrowth ± fluid/synovial

hypertrophy)
Attitude
Deformity
Muscle wasting (global - all muscles acting
over the joint)
Palpation Absence of warmth

Swelling (effusion if present is usually small
and cool)
Joint line tenderness
Periarticular tenderness (especially knee, hip)
Range of motion Crepitus (knee, thumb bases)

Reduced range of movement
Weak local muscles
OA: osteoarthritis.

* Major joint injury and certain rare conditions may predispose to OA before the age of 40 years.
Adapted from: OARSI Primer (http://primer.oarsi.org).

Bones of the hand and wrist
Palmar view of the wrist and hand bones.
Reproduced with permission from: Anatomical Chart Company. Copyright © 2008 Wolters Kluwer
Health.

Heberden's nodes
Heberden's nodes, appearing as discrete postero-lateral swellings (index finger) or as a dorsal bar (middle
finger) over the DIP joints.
DIP: distal interphalangeal.
Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter D, Kawaguchi H. 2012. Osteoarthritis Research
Society International. (http://primer.oarsi.org).

Patient with hand osteoarthritis
Heberden's nodes (thumb, middle, ring, and little finger DIP joints),
Bouchard's nodes (index finger PIP joint), and lateral radial/ulnar
deviation (index PIP joint, ring DIP joint) in the left hand of a person
with nodal OA.

DIP: distal interphalangeal; PIP: proximal interphalangeal; OA:

osteoarthritis.
Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter
D, Kawaguchi H. 2012. Osteoarthritis Research Society International.

Knee effusion
Knee effusions are usually not marked in OA. This person had a
large effusion expanding the suprapatellar pouch, with positive
balloon sign (fluctuance) and patellar tap, and OA with CPPD.
OA: osteoarthritis; CPPD: calcium pyrophosphate crystal deposition.

Thumb-base osteoarthritis
Thumb-base OA: prominence and "squaring" of the thumb base, due to osteophyte formation and
subluxation at the first CMC joint.
OA: osteoarthritis; CMC: carpometacarpal.
Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter D, Kawaguchi H. 2012. Osteoarthritis Research
Society International. (http://primer.oarsi.org).

Erosive osteoarthritis of the hand
Erosive hand OA with marked radial deviation and fixed flexion

deformity in the left middle PIP joint, radial deviation with restriction
in the index PIP joint, and bony swelling of both fingers. Note
the absence of Heberden's nodes.
OA: osteoarthritis; PIP: proximal interphalangeal.

Erosive osteoarthritis
Marked radial/ulnar instability in a patient with erosive OA. Such

instability does not usually occur with common hand OA.
OA: osteoarthritis.

Patient with unilateral knee osteoarthritis
Unilateral knee OA: swollen left knee with varus and fixed flexion deformity in a 63-year-old man with a
prior history of knee trauma. On palpation, there was marked crepitus, restricted flexion, bony swelling,
and a small effusion. The cruciates were intact, but there was minor varus/valgus instability on stress
testing.
OA: osteoarthritis.
Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter D, Kawaguchi H. 2012. Osteoarthritis
Research Society International. (http://primer.oarsi.org).

Findings on hip examination in patient with osteoarthritis
Patient with right hip OA, showing painful restriction with internal rotation in
flexion. This is the "tight-pack" position for the hip (when the capsule is at its
tightest) and is the first movement to be affected.
OA: osteoarthritis.

Reproduced with permission from: OARSI Online Primer. Edited by Henrotin Y, Hunter D, Kawaguchi
H. 2012. Osteoarthritis Research Society International. (http://primer.oarsi.org).

Findings in patient with right hip osteoarthritis
Patient with right hip OA, showing fixed flexion and external rotation
deformity.
OA: osteoarthritis.

Trendelenburg test
Normally, the pelvis stays level when a patient stands on one leg.
When standing on the affected leg, the pelvis tilts downward toward
the unaffected side (as pictured in the abnormal patient above)
because of gluteal muscle weakness on the affected side (right side
in abnormal patient above).

Clinical distinction between rheumatoid arthritis and osteoarthritis
Feature Rheumatoid arthritis Osteoarthritis

Primary joints Metacarpophalangeal Distal interphalangeal
affected
Proximal interphalangeal Carpometacarpal
Heberden's Absent Frequently present

nodes
Joint Soft, warm, and tender Hard and bony

characteristics
Stiffness Worse after resting (eg, If present, worse after effort, may be described
morning stiffness) as evening stiffness
Laboratory Positive rheumatoid factor Rheumatoid factor-negative

findings
Positive anti-CCP antibody Anti-CCP antibody-negative
Elevated ESR and CRP Normal ESR and CRP
CCP: cyclic citrullinated peptide; ESR: erythrocyte sedimentation rate; CRP: C-reactive protein.

Osteoarthritis of the distal interphalangeal (DIP)

joints
This plain film demonstrates complete loss of the articular cartilage

at all four DIP joints, large osteophytes, and ankylosis of the DIP
joint of the middle finger.
Courtesy of Bruce C Anderson, MD.

Erosive hand osteoarthritis
Plain radiograph of the hand demonstrating features consistent with erosive

osteoarthritis (OA) of the hand. There is a central subchondral erosion and
pseudo-widening at the proximal interphalangeal (PIP) joint of the fourth finger,
and bony proliferation at the diaphysis. The distal interphalangeal (DIP) joint of

the fifth finger has a central erosion. The DIPs of the fifth and index fingers also
show subluxation, disorganization, and radial deviation. There is marked
narrowing and subluxation of the first carpometacarpal (CMC) joint, which is
sometimes a key feature of erosive hand OA.
Courtesy of Michael Doherty, MD, and Abhishek Abhishek, MD.

Gouty arthritis
Plain radiograph of the hand demonstrating features consistent

with gout. There are juxta-articular punched-out erosions and
intraosseous cystic lesions, most prominent at the index proximal
interphalangeal (PIP) joint and distal ulna. There is cartilage loss at
the little finger PIP joint and soft tissue swelling due to a
subcutaneous tophus at the index finger PIP joint. Vascular
calcification of forearm vessels is also evident.
Image courtesy of Dr. Ian Gaywood, Consultant Rheumatologist, Nottingham

University Hospitals NHS Trust.

Osteoarthritis and CPPD
Plain radiograph of the hand demonstrating features of osteoarthritis (OA) and

calcium pyrophosphate deposition (CPPD). There is cartilage loss, osteophytosis, and
bony remodeling at all finger distal interphalangeal (DIP) joints and radial deviation
of middle, ring, and little finger DIP joints; joint space narrowing, osteophytosis, and

cysts at the second metacarpophalangeal (MCP) joint; and thumb-base OA (mainly

narrowing and sclerosis of first carpometacarpal [CMC] and scapho-trapezioid
joints). There is also scapho-lunate dissociation (which is reported to associate with
CPPD) and chondrocalcinosis in the triangular cartilage.
Courtesy of Michael Doherty, MD, and Abhishek Abhishek, MD.

Hand arthritis in hemochromatosis
Serial radiographs, five years apart, of the metacarpophalangeal

joints in a patient with hereditary hemochromatosis. The second
film shows loss of joint space at the metacarpophalangeal
articulations, cyst formation, and a hook-like osteophyte on the
radial aspect of the metacarpal head of the middle finger.
Courtesy of John S Axford, BSc, MD, FRCP.

Contributor Disclosures
Michael Doherty, MA, MD, FRCP, FHEA Nothing to disclose Abhishek Abhishek, MBBS, MD, FRCP,
PhD Grant/Research/Clinical Trial Support: ACR/EULAR [CPPD]. Consultant/Advisory Boards: Inflazome
[Gout]; NGM Biopharmaceuticals [Crystal arthritis]. David Hunter, MD, PhD Consultant/Advisory
Boards: Pfizer/Lilly [Osteoarthritis]; Novartis [Osteoarthritis]; BioBone [Osteoarthritis]; Kolon
[Osteoarthritis]; TLCBio [Osteoarthritis]. Monica Ramirez Curtis, MD, MPH Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these
are addressed by vetting through a multi-level review process, and through requirements for
references to be provided to support the content. Appropriately referenced content is required of all
authors and must conform to UpToDate standards of evidence.
Conflict of interest policy

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Clinical manifestations and diagnosis of osteoarthritis - UpToDate 11:15, 16/11/2021

Official reprint from UpToDate®

https://www.uptodate.com/contents/clinical-manifestations-and-…h_result&selectedTitle=1~150&usage_type=default&display_rank=1 Trang 1 trong số 47

• Stage 1 – Predictable, sharp pain usually brought on by a mechanical insult that

• Stage 3 – Constant dull/aching pain punctuated by episodes of often

● Tenderness – Joint-line tenderness suggests articular pathology, while tenderness

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● Joint deformity – Deformity is a sign of advanced joint damage. Common examples

● Instability – Giving way or buckling is a common symptom in knee OA. Occasionally

Joint distribution — Many of the characteristic clinical manifestations of OA are related to

Single- or multiple-joint osteoarthritis — OA has a predilection for the knees, hips,

Generalized osteoarthritis — Generalized OA implies a polyarticular subset of OA

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Imaging — The diagnosis of OA is a clinical one based on characteristic signs and

● Radiography – Conventional radiography is the most widely used imaging modality

● Magnetic resonance imaging – Magnetic resonance imaging (MRI) is not necessary

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● Ultrasonography – Ultrasonography is another imaging modality that can identify

Synovial fluid — Synovial fluid from OA joints is usually noninflammatory or mildly

Osteoarthritis with calcium pyrophosphate deposition — CPP crystals may be present

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pseudogout"); intermittent; or low-grade and persistent (chronic CPP crystal inflammatory

CHARACTERISTICS OF SPECIFIC JOINT INVOLVEMENT

Nodal osteoarthritis — Heberden and/or Bouchard nodes plus underlying

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Thumb-base OA generally affects older postmenopausal women. Individuals with thumb-

Erosive osteoarthritis — Erosive OA is an uncommon and particularly aggressive subset

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Erosive OA has worse outcome in terms of symptom persistence and functional

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First metatarsophalangeal joint — First metatarsophalangeal (MTP) joint OA is usually

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● Rheumatoid arthritis – OA in the middle-aged or older adult patient is most

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• OA is characterized radiographically by narrowing of the joint space due to

• OA is classically associated with the absence of rheumatoid factor (RF) and

● Crystalline arthritis – Crystalline arthritis (gout and acute calcium pyrophosphate

● Hemochromatosis – The arthropathy of iron overload may be confused with hand

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and predominates in men. The characteristic radiologic findings of hemochromatosis

● Infectious arthritis – OA of a single joint is usually associated with mild symptoms

● Other soft-tissue abnormalities – Other soft-tissue abnormalities around a single

Clinical diagnosis — Peripheral joint OA may be diagnosed confidently on clinical

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● Persistent usage-related joint pain in one or few joints

It is important to differentiate "structural" or "radiologic" changes of OA (eg, cartilage loss

When to consider additional testing — Appropriate imaging and laboratory

● Younger individuals with joint symptoms/signs of OA

● Presence of atypical symptoms and signs such as an unusual site of involvement,

● Presence of weight loss or constitutional symptoms

Additional laboratory testing may include an erythrocyte sedimentation rate (ESR) or C-

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Radiographic examination may be used to support a diagnosis of OA but is not a routine

Common problems with classification criteria include:

● Frequent overlap, with lack of clear separation between "subsets." As an example,

● Common coexistence of separate subsets, or evolution from one form of arthritis to

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though OA is pathologically confined to synovial joints. The guideline development group

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and

● Many of the characteristic clinical manifestations of OA are related to the

● Generalized OA implies a polyarticular subset of OA involving the distal