History and exam

Key diagnostic factors

common

pain

OA-related joint pain is associated with 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.

functional difficulties

Functional difficulties, such as a knee giving way or locking, can be present. This can reflect an internal derangement, such as a partial meniscal tear or a loose body within the joint.

knee, hip, hand, or spine involvement

Commonly involved joints are the knee, hip, hands, and lumbar and cervical spine.[3][75][78]

bony deformities

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

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

limited range of motion

Both active and passive range of joint movement is reduced in moderate to advanced OA, and this is usually associated with pain.

malalignment

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]

Other diagnostic factors

common

tenderness

OA can cause local tenderness over the joint line. The location of the tenderness can help differentiate OA from other local structures contributing to the pain, such as the pes anserine bursa in the knee and the greater trochanteric bursa in the hip.

crepitus

Crepitus is a palpable, and sometimes audible, creaking evident on active and passive movements of joints affected by OA.

uncommon

stiffness

Early morning stiffness is usually present for only a few minutes and, almost invariably, <30 minutes.[3][73]​​ This helps differentiate OA from other inflammatory arthritis, including rheumatoid arthritis.

One exception is inflammatory OA of the hand, which causes more prominent stiffness during the early stages.

shoulder, elbow, wrist, or ankle involvement

OA is less likely to involve joints such as the shoulder, elbows, wrists, or ankles, unless there is an underlying injury, occupational risk, or other etiology.

effusion

An effusion is fluid within the joint cavity. In OA these are usually small and lack other inflammatory signs such as warmth and redness.

In knee OA, a large effusion may reflect an underlying internal derangement such as a meniscal tear, or inflammatory arthritis such as gout or pseudogout.

antalgic gait

Patients with lower limb OA often limp because of pain (antalgic gait), but spinal OA can also cause limping secondary to weakness, back pain, or radicular pain.

Risk factors

strong

age >50 years

Aging is the strongest risk factor associated with OA.[10][15]

The effect of aging on OA seems to be more pronounced in females.[10] Incidence increases sharply around age 50 years.[9][10]

In a prospective study of women from a UK population cohort, the oldest group of women (upper tertile) was at greatest risk of OA (adjusted odds ratio 2:41).[49]

In a longitudinal study of aging, the incidence of radiographic features of hand OA in men increased with age.[50]

female sex

Women are affected more than men.[10][16][18][19] However, OA is a common disease that affects both sexes.

obesity

Being overweight or obese increases the risk of OA; the strongest association is with knee OA.[22][23]

In the Framingham study, high body mass index at baseline exam was associated with increased risk for incident OA.[51] For women in the most overweight quintile, relative risk was 2.07.[52] Among obese men participating in the Framingham study, the age-adjusted relative risk of developing OA was 1.51.[52]

genetic factors

Twin and family studies have shown that the genetic contribution to OA is about 40% to 50%.[24][25]

Certain hereditary disorders associated with OA, such as Stickler syndrome, are caused by defects in type-2 collagen, but the genetics and mechanisms in other forms of OA are poorly understood.[53][54][55]

Hand OA is common in female siblings of people affected by OA.[24] Heberden nodes are more common in females with a family history of hand OA.[56]

joint anatomy and/or malalignment

Evidence suggests that the antaomy and/or malalignment of knee or hip increases the risk of the development of OA and the subsequent progression of the disease.[26][28][31]​​​​[32][57]

physically demanding occupation/sport

OA is common in manual workers, and there is a strong association between increased physical activity and lower limb OA.[58][59][60]

Knee OA is common in miners, and hip OA is common in agricultural workers.[61] Heavy labor and activities can predispose specific joints to OA.

Evidence suggests that certain sports including running, weight-lifting, and wrestling are associated with developing OA of the knee.[62]

post trauma/injury

Previous trauma to the joint significantly increases the risk of developing OA.[23][63]​​

The prevalence of OA increases after an anterior cruciate ligament (ACL) reconstruction.[29][30][64]​​

Evidence suggests that longer chronicity of ACL tear and older age at the time of surgery positively correlates with the development of OA, and that development of OA on the ipsilateral knee is more likely than OA on the contralateral side post ACL reconstruction.[29][30]

weak

high bone mineral density

Several studies report higher bone mineral density in patients with hip and knee OA.[65][66][67]

Eight-year follow-up of the Framingham Cohort found that incident OA (defined by the appearance of osteophytes) was lowest in those with the lowest bone mineral density.[16]

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