Approach

The most common symptoms of OA are joint pain, stiffness, and sometimes swelling. OA most commonly affects the knee, hip, small hand joints (proximal interphalangeal [PIP] and distal interphalangeal [DIP] joints), and the spine (especially lumbar and cervical regions). In other joints (e.g., the ankle and wrist), OA is rare and there is usually an underlying aetiology (e.g., crystal arthropathy, trauma).

History

More patients present in their 50s as OA is more common at this age, with a higher number of women presenting than men.[9][10][15][16][18][19][24][56]​​

Patient history may include a physically demanding job or sport, with joint pain worsening during activities or weight bearing. Joint pain should not be present at night, except in advanced OA; if the patient has joint pain during the night, a differential diagnosis should be considered.

The distribution of joint involvement is important. Some women have inflammatory OA mainly affecting the proximal interphalangeal (PIP) and distal interphalangeal (DIP) joints of the hands, which may be erythematous and swollen. The MCP joint can occasionally be affected by OA; however, if MCP symptoms are present, a differential diagnosis of calcium pyrophosphate dihydrate deposition (CPPD) disease, rheumatoid arthritis, or other secondary aetiology should be considered.[72] 

People with OA present with morning stiffness of no more than 30 minutes.[3][73]​​​​ If stiffness persists for longer than this, other diagnoses should be considered, such as rheumatoid arthritis.

Joint swelling and functional difficulties, such as a knee giving way or locking may be reported by patients. This can reflect an internal derangement, such as a partial meniscal tear or a loose body within the joint.

Physical examination

Weight and body mass index are important, as knee OA and, to a lesser degree, hip OA are common in overweight patients.[23][22]

Swelling may be observed, with bony deformities and malalignment of the affected joint.[33][48][74][32]

Bony deformities are particularly common in the hands and lead to enlargement of the PIP joints (Bouchard nodes) and DIP joints (Heberden nodes), as well as squaring at the base of the thumb (the first carpometacarpal joint).[75]

Bony malalignment is common, particularly in the knee, where OA causes both genu valgum (knock-knees) and genu varum (bow-legs).[33] In addition, a varus thrust, which is a worsening varus alignment in a weight-bearing knee, seems to further worsen the risk of progression of medial knee OA.[32]

In advanced knee OA, there may be new bone formation, causing bony swellings around the knee joint.[3][76]

It is common to palpate crepitus during the range of motion of the joint. Limited range of motion, small effusions, and joint line tenderness may be elicited. An abnormal gait can be observed.

Hip examination
Hip examination

A consultant physician demonstrates hip examination techniques, including the Trendelenburg test, the modified Thomas test, and Ober's test. These tests inspect the lateral alignment, anterior and posterior alignment, gait, active and passive movement, and internal and external rotation of the hip.

Knee examination
Knee examination

A consultant physician demonstrates knee examination techniques, inspecting the biomechanics of the knee and assessing for effusion, wasting, or hypertension. The physician performs tests for the integrity of the medial and lateral collateral ligaments, damage to the cruciate ligaments (Lackman's test, Drawer test, Pivot shift test), tests of the patella (patella apprehension test, Clarke's test), and tests of the iliotibial band (Ober's test).

Wrist examination
Wrist examination

A consultant physician demonstrates wrist examination techniques for assessing range of movement, inspecting for synovitis, wasting, squaring at the base of the thumb, and previous surgery for carpal or Guyon’s canal syndrome.

OA is essentially a clinical diagnosis

Guidelines recommend that OA is diagnosed clinically based on symptoms, patient age, and examination findings.[3][73]​​​[77]

A clinical diagnosis can be considered in a patient with a typical OA presentation:[3][73]​​​[77]

  • Activity-related joint pain

  • With either no morning joint-related stiffness or morning stiffness that lasts no longer than 30 minutes

  • >45 years of age.

Atypical features that suggest an alternative or additional diagnosis include:​[73]

  • Prolonged morning joint-related stiffness

  • History of recent trauma

  • Palpable warmth over the joint

  • Rapid worsening of symptoms

  • Concerns that may suggest infection or malignancy.

Laboratory assessment

​When an alternative or additional diagnosis of rheumatoid arthritis is suspected, inflammatory markers (C-reactive protein [CRP], erythrocyte sedimentation rate [ESR]), rheumatoid factor, and anti-cyclic citrullinated peptide (anti-CCP) antibodies may be helpful as differential tests.[3][78]​ These tests are normal in OA.

It should be noted that elevated inflammatory markers are also associated with age, increased weight, and other conditions; therefore, they should not be interpreted as definitive evidence of inflammatory conditions in the absence of other symptoms.

Imaging studies

Imaging studies are not routinely recommended for the diagnosis of OA, they should only be considered if the diagnosis is unclear or an alternative/additional diagnosis is suspected subsequent to initial investigations.[73]

Radiography

If imaging studies are required, radiography should be considered before other imaging modalities.[77][79]

Conventional radiographic diagnosis of OA includes narrowing of the joint space, osteophytes, subchondral cysts, and subarticular sclerosis.[79][80]

Radiographs may also help to exclude less common aetiologies for pain and in monitoring unexpected rapid progression or changes in symptoms that may be related to OA severity or an additional diagnosis.[77]

While radiographic evidence of OA is poorly correlated with the symptoms, one study suggested that radiological progression in early symptomatic knee OA over 5 years was related to worsening pain and function.[81]

Magnetic resonance imaging (MRI)

Although more sensitive than plain radiographs in detecting OA changes, MRI is not indicated for the diagnosis of simple OA. If needed, MRI should be ordered if spinal OA with neurological deficits is suspected, to identify and evaluate the extent and severity of spinal stenosis or nerve root entrapment.

MRI can be used to rule out other aetiologies for hip or knee pain, such as avascular necrosis or other less common conditions such as pigmented villonodular synovitis or bone tumours.[77][79]​ Although more sensitive than plain x-ray in detecting OA changes, MRI is not indicated for the diagnosis of simple OA in most joints.

Bone marrow lesions (oedema), which are associated with knee pain in OA, are readily detected using MRI.[79][82][83]​ Medial and lateral compartment bone marrow lesions confer increased risk of progression of medial and lateral tibiofemoral OA, respectively.[84]

Other imaging modalities

Ultrasound (US) and computed tomography (CT) scans can be used to make additional diagnoses. Soft tissues are best imaged by US or MRI and bone by CT or MRI.[77] In practice, CT is not widely used for the diagnosis of OA.

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