Clinical manifestations and diagnosis of osteoarthritis

Official reprint from UpToDate® www.uptodate.com

©2023 UpToDate®

Clinical manifestations and diagnosis of osteoarthritis

Authors: Michael Doherty, MA, MD, FRCP, FHEA, Abhishek Abhishek, MBBS, MD, FRCP, PhD
Section Editors: David Hunter, MD, PhD, Daichi Hayashi, MD, PhD
Deputy Editor: Karen Law, MD

Contributor Disclosures

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Aug 2023. | This topic last updated: Aug 23, 2023.

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
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OA:

● 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
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synovial hyperplasia and effusion may also contribute.

● 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 medial 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
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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].
According to the American College of Radiology Appropriateness Criteria, radiography is
considered an appropriate initial imaging modality for evaluating patients with chronic
atraumatic joint pain such as OA [19,20]. Radiographs can also be used to measure joint
space narrowing, which typically is 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 [21-24]. Also, radiographic OA is a common
incidental asymptomatic finding in older people [25]. With these caveats, radiographic
findings may be used to grade the severity of structural changes in OA. There are several
systems, of which the Kellgren and Lawrence OA severity grading system is most widely
used in research and clinical practice. In this system, the severity of OA ranges from
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grade 0 to 4 [26]:

• Grade 0 – no joint space narrowing or osteophyte (ie, normal)

• Grade 1 – doubtful joint space narrowing, possible osteophytes
• Grade 2 – definite osteophytes, possible joint space narrowing
• Grade 3 – moderate osteophytes, definite joint space narrowing, some sclerosis,
possible bone-end deformity
• Grade 4 – large osteophytes, marked joint space narrowing, severe sclerosis, definite
bone-end deformity

● 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 the disease before radiographic
changes become apparent. These changes include cartilage defects and bone marrow
lesions. MRI is indicated when there is a clinical need for assessing pathology in other
structures of the joint not visualized by radiography, such as effusions, synovium,
menisci, and ligaments, or to rule out pathologies other than OA that can be a cause of
symptoms [27,28].

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) [29].

MRI may have a greater role in ruling out OA. As an example, a person with a
symptomatic meniscal tear with meniscal extrusion may be incorrectly diagnosed as
having OA based on the presence of radiographic joint space narrowing, and an MRI of
the knee may reveal the true pathology [30]. A Delphi panel has developed MRI
definitions of structural OA at the tibiofemoral and patellofemoral joints [31]. 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 and
incidentally present in asymptomatic radiographically normal joints and typically
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precede clinical features of OA [25,32,33]. The sensitivity and specificity of individual MRI
features for the clinical diagnosis of OA is not well understood.

● Ultrasonography – Gray-scale and color Doppler ultrasonography is another imaging

modality that can identify OA-associated structural changes and is useful for detecting
specific pathologic features such as synovial inflammation, effusion, and osteophytosis (
image 1). Ultrasonography is particularly useful for assessment of OA of hand and
knee joints [34-36]. 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 [37]. 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 [38,39]. 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) [40].
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 [41-43], and patients with end-stage knee OA with CPPD do not
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have any more difficulty with activities than those with end-stage knee OA alone [43].
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'.)

Rapidly progressive osteoarthritis — Rapidly progressive OA is a very uncommon

presentation of OA [44]. It typically occurs in older females (over 70 years old) and may be
preceded by a history of trauma. Patients with post-traumatic rapidly progressive OA tend to
be younger and male. The hip and glenohumeral joints are most often affected, but the knee
may also be involved. Patients present with subacute onset of pain, typically progressing from
mild to severe over a period of several months. Patients generally have unilateral disease,
although bilateral involvement is described. There may be a substantial reduction in range of
movement and progressive loss of function that requires joint replacement surgery within
months to a few years of symptom onset. Large cool joint effusion and loss of muscle bulk
may be evident at the shoulder, and joint deformity and instability are often apparent. On
radiography, the changes are dramatic with rapidly progressive joint space narrowing and
osteolysis and with eventual widening of joint space ( image 2), which may raise the
possibility of alternate diagnoses such as avascular necrosis, septic arthritis, or neuropathic
arthropathy. Inflammatory markers are normal. However, MRI shows bone marrow edema,
and subchondral fractures may be present. Basic calcium phosphate crystals (predominantly
hydroxyapatite) have been implicated in pathogenesis of rapidly progressive OA, especially at
the shoulder ("Milwaukee shoulder" [45]), leading to the term apatite-associated destructive
arthritis (ADA) [46-48].

A possible association of rapidly progressive hip OA after intraarticular glucocorticoid

injection has also been described and is discussed separately. (See "Management of hip
osteoarthritis", section on 'Limited role of intraarticular glucocorticoids'.)

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,
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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 [15,49]. 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 [49]. 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 [50].

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 [49]. 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

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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) [15,49].
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") [51]. (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) [15,52]. Compared with nodal hand OA, pain, tenderness, and
inflammation (warmth, soft-tissue swelling, sometimes erythema) are more marked and
prolonged [52,53], 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) [15,53]. 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 [53], and Heberden and/or Bouchard nodes
may coexist [54].

Erosive OA has a 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 [55].

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
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side may be more severely affected. The patellofemoral joint ( image 3) and/or the medial
tibiofemoral joint ( image 4) 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 [56]. 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 [57], and persistent pain at night that interrupts sleep
or rest occurs in advanced OA [58]. 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 [58].

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) [58-60]. Knee effusion is common,
though usually mild or modest, and increases in prevalence with the severity of knee OA [61].

Hip — Hip OA presents with pain, aching, stiffness, and restricted movement ( image 5).
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 [62].
Unlike knee OA, hip OA is frequently unilateral [63]. Both active and passive hip movements
are equally painful [62]. Internal rotation with the hip flexed is frequently the earliest and
most affected movement ( picture 8) [62]. 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 [62].

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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 [64].
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 [64].
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 [65]. 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 [66]. 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
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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 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
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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 6). Sea-gull (central subchondral) erosions are present in joints with erosive
OA ( image 7). 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".)

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● 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 8). CPP crystal deposition (CPPD) disease can be
diagnosed if there is radiographic articular chondrocalcinosis ( image 9). (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 10). 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 [67]. 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

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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) [68]. (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
[1,21,22].

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 [21,22].

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,

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Clinical manifestations and diagnosis of osteoarthritis

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 [69].
Radiographic examination may have a role in defining the prognosis of patients with
symptomatic OA [70]. 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
musculoskeletal disorders"). When there is still diagnostic uncertainty regarding the cause of
joint pain, advanced imaging with 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, radiologic
appearance ("hypertrophic" versus "atrophic"), presumed etiology (eg, "primary" or
"secondary post-traumatic" OA), and rate of progression. Most patients with OA have
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Clinical manifestations and diagnosis of osteoarthritis

concordance between osteophytosis and joint space narrowing, with only 1.3 percent having
an atrophic phenotype (ie, severe cartilage loss in the presence of minimal or no
osteophytosis) and 0.2 percent having a hypertrophic phenotype (ie, large osteophytes
without severe joint space narrowing) at the knee, in the Framingham study [71].

Apart from radiologic appearances, presumed etiology, and rate of progression, OA

phenotypes can be defined according to the presence or absence of other factors (namely,
pain sensitization, adverse psychological profile, joint malalignment [especially at the knee],
comorbidities, obesity with metabolic abnormalities, and inflammation) [72]. These factors
are important to consider in day-to-day clinical practice as they may affect the choice of
treatments and patient outcomes. 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 [14,38].

SOCIETY GUIDELINE LINKS

Links to society and government-sponsored guidelines from selected countries and regions
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Clinical manifestations and diagnosis of osteoarthritis

around the world are provided separately. (See "Society guideline links: Osteoarthritis".)

PATIENT PERSPECTIVE TOPIC

Patient perspectives are provided for selected disorders to help clinicians better understand
the patient experience and patient concerns. These narratives may offer insights into patient
values and preferences not included in other UpToDate topics. (See "Patient perspective: Knee
osteoarthritis".)

SUMMARY

● Clinical presentation – 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.)

● Characteristics of specific joint involvement – 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 osteoarthritis – 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.)

● Diagnosis – 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 a few joints

• Age ≥45 years
• Morning stiffness ≤30 minutes
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Clinical manifestations and diagnosis of osteoarthritis

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.

● Additional testing in selected patients – 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.)

● Differential diagnosis – 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.

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