Osteoarthritis

Definition

Osteoarthritis (OA) is the most common form of joint disease.

OA is not just a result of wear and tear, but is an active disorder affecting primarily the
cartilaginous structures of the joint and capable of and usually affecting all structures of
the joint.

OA is both a degenerative and inflammatory condition characterized by:

o Progressive deterioration and loss of articular cartilage
o Proliferation of new bone and soft tissue in and around involved joints
o Involvement most commonly of the hands, feet, hips, knees, and the cervical and
lumbar vertebrae.

Idiopathic (primary) OA
o No apparent predisposing factor

Secondary OA
o Predisposing factor(s), such as:

Trauma

Repetitive stress (occupation, sports)

Congenital abnormalities

Metabolic disorders [particularly calcium pyrophosphate dihydrate

deposition disease (CPPD)]

Other bone/joint diseases (e.g., rheumatoid arthritis, gouty arthritis, septic

arthritis, Pagets disease)

Erosive OA

o Term often applied to distal interphalangeal (DIP) and/or proximal

interphalangeal (PIP) OA of the hands associated with synovitis and radiographic
central erosions of the articular surface

Generalized OA
o Characterized by involvement of 3 joints or groups of joints

Epidemiology

Prevalence
o OA is the most common disease of the joints.
o >90% of persons > 40 years of age have some radiographic changes of OA in
weight-bearing joints, but only 30% are symptomatic.
o Knee OA is a leading cause of chronic disability in older persons in developed
countries.
o In the U.S., as the population ages, OA prevalence is predicted to increase further.
o Symptomatic OA of the knee (pain on most days of a recent month in a knee plus
x-ray evidence of OA in that knee) occurs in:

~12% of persons age 60 in the U.S.

6% of all adults age 30

o Symptomatic hip OA is roughly one-third as common as disease in the knee.

o Symptomatic hand OA occurs in 10% of older individuals.

Age
o Incidence of OA in women

< 45 years: 2%

4564 years: 30%

>65 years: 68%

o Incidence of OA in men

Similar to that in women, but somewhat lower in the older age groups

Sex
o Similar joint distribution of OA in men and women < 55 years of age
o Hip OA affects men more frequently than women > 55 years of age.
o OA of interphalangeal joints, thumb base, and knee (especially symptomatic knee
OA) is more common in women.

Race
o Racial differences exist in both the prevalence and pattern of joint involvement.

Chinese persons in Hong Kong have a lower incidence of hip OA than

white persons.

OA is more frequent in Native Americans than in white persons.

Interphalangeal joint OA and hip OA are much less common in South

African black persons than in white persons in the same population.

Risk Factors

Age
o Most powerful risk factor

Sex
o In persons < 55 years

Joint distribution is similar in men and women.

o In persons 55 years

Race

Hip OA is more common in men.

OA of the interphalangeal joints, thumb base, and knee is more common in

women.

o Differences may be genetic or due to differences in joint use related to lifestyle or

occupation.

Genetic factors
o Some cases of primary OA may be due to subtle congenital or developmental
defects (e.g., congenital subluxation/dislocation, acetabular dysplasia, LeggCalv-Perthes disease, or slipped capital femoral epiphysis).
o Highly heritable disease

The mother and sister of a woman with DIP joint OA (Heberdens nodes)
are, respectively, 2 and 3 times as likely to develop OA at these joints than
the mother and sister of an unaffected woman.

o Emerging evidence has identified a polymorphism within the growth

differentiation factor 5 gene (GDF5) that confers a high risk of OA.

Diminishes the quantity of GDF5, which normally has anabolic effects on

the synthesis of cartilage matrix

o Secondary OA can occur in association with genetic mutations for rare

syndromes.

Mutations in the COL2A1 gene have been associated with clinical

phenotypes ranging from mild spondyloepiphyseal dysplasia to severe
generalized OA.

Major joint trauma

o Anterior cruciate ligament insufficiency or meniscal damage (and meniscectomy)
may lead to knee OA.
o Avascular necrosis can lead to collapse of dead bone at the articular surface,
producing anatomic irregularities and subsequent OA.

Repetitive stress
o Vocational activities associated with jackhammer operators, cotton mill and
shipyard workers, and coal miners may lead to OA in the joints exposed to
repetitive occupational use.
o Particular sports and other activities have an increased risk of OA of specific
joints:

Knees: cycling, running, soccer, American football

Feet and ankles: soccer, football, dancing

Hands and upper extremities: boxing, gymnastics, cricket

Shoulders: baseball (primarily pitchers)

Cervical spine: wrestling

Obesity
o Risk factor for knee, hip, and hand OA

Even higher relative risk for severe knee OA

o In women, the relationship of weight to the risk of disease is linear, so that with
each increase in weight, there is a commensurate increase in risk.
o Weight loss in women lowers the risk of developing symptomatic disease.
o Obese persons have more severe symptoms from the disease.
o Most important modifiable risk factor

Congenital/developmental defects

Prior inflammatory joint disease

Metabolic/endocrine disorders

High bone mineral density

o Women with osteoporosis have a lower risk (about 50% lower) of OA than
women of similar age in the highest quartile of bone density.

Etiology

OA - General etiology

OA develops in 2 settings.
o The biomaterial properties of the articular cartilage and subchondral bone are
normal, but excessive loading of the joint causes the tissues to fail.

o The applied load is reasonable, but the material properties of the cartilage or bone
are inferior.

No mutation has been identified in the common primary (idiopathic) form of OA.

Most of the mutations identified are associated with relatively rare syndromes and are
thus classified as secondary OA.

Pain does not derive from damaged cartilage, which is aneural, but from supporting
structures, including the synovium, joint capsule, ligaments, muscles, and subchondral
bone.

Conditions associated with secondary OA

Trauma
o Fractures, such as trimalleolar fracture
o Cruciate ligament insufficiency
o Meniscus damage

Congenital or developmental
o Legg-Calv-Perthes disease (necrosis of the capitalar epiphysis of the femur)
o Congenital hip dislocation
o Slipped epiphysis
o Unequal lower-extremity length
o Valgus/varus deformities
o Hypermobility syndromes
o Epiphyseal dysplasia
o Spondyloepiphyseal dysplasia
o Osteonychondystrophy

Metabolic

o Ochronosis (alkaptonuria)
o Hemochromatosis
o Wilson disease
o Gaucher disease

Endocrine
o Acromegaly
o Hyperparathyroidism
o Diabetes mellitus
o Hypothyroidism

Calcium deposition disease

o CPPD
o Apatite arthropathy

Other bone and joint diseases

o Fracture
o Avascular necrosis
o Infection
o Gout
o Rheumatoid arthritis
o Other inflammatory arthritides
o Paget disease
o Osteoporosis
o Osteochondritis

Neuropathic (Charcot joints)

Endemic
o Kashin-Beck disease (joint destruction with childhood onset, seen in China)
o Mseleni (osteoarthropathy with onset in childhood, seen in South Africa)

Miscellaneous
o Frostbite
o Caisson disease (decompression sickness)
o Hemoglobinopathies

Associated Conditions

See Etiology - Conditions associated with secondary OA

Harrison's Practice
Osteoarthritis
Symptoms & Signs
General signs and symptoms

Commonly an asymmetric oligo- or polyarthritis

Can be a chronic monoarthritis

Systemic manifestations are not a feature of primary OA.

Joint pain
o

May affect 1 joints

Often described as a deep ache localized to the involved joint

Commonly worsened by use and relieved by rest

Nocturnal pain interfering with sleep occurs in advanced hip OA.

May become persistent as disease progresses

Joint stiffness after periods of inactivity (e.g., sleep or automobile ride)

o

May become a prominent feature

Usually lasts < 20 minutes (unlike the longer periods of stiffness that
can occur in inflammatory arthritis of any cause)

Synovitis may be present.

o

Synovial effusions, if present, are usually not large in smaller joints but
can be more significant in the knee.

In early stages, synovial inflammation may be absent.

Warmth and erythema are uncommon findings.

Loss of joint movement or functional limitation

Joint instability
o

May lead to stretching of the joint capsule

Muscle spasm

Joint deformity

Joint/bony crepitus (the sensation of bone rubbing against bone, evoked by

joint movement) is characteristic.

Localized tenderness

Firm or "bony" swellings of the joint margins, e.g., Heberdens nodes (DIP
joints) or Bouchards nodes (PIP joints)

Periarticular muscle wasting

o

Common

May play a major role in symptoms and in disability

Disability in patients with knee OA is more strongly associated

with quadriceps muscle weakness than with joint pain or
radiographic severity.

Objective neurologic abnormalities may be seen with spine involvement.

Varus or valgus deformities of the knees (Figure 1)

OA at specific sites
Interphalangeal joints

Idiopathic OA
o

Heberdens nodes (bony enlargement of the DIP joint) are the most
common form of idiopathic OA (Figure 2).

Bouchards nodes: similar process at PIP joints

These nodes often develop gradually with little or no discomfort; there

is usually no significant interference with function.

May present acutely with pain, redness, and swelling; sometimes

triggered by minor trauma

Gelatinous dorsal cysts may develop at insertion of digital extensor

tendon into base of the distal phalanx.

Erosive OA
o

DIP and/or PIP joints are most prominently affected.

Deformity and functional impairment may be severe.

Synovitis is common.

Generalized OA
o

Characterized by involvement of 3 joints or groups of joints (DIP and

PIP joints are counted as 1 group each.)

Heberdens and Bouchards nodes are prominent.

"Flare-ups" of inflammation may be marked by soft-tissue swelling,

redness, and warmth.

Thumb base (first carpal metacarpal joint)

Second most frequent area of involvement in OA

o

Often the first site that is sufficiently symptomatic to bring the patient
to seek medical attention

Swelling, tenderness, and crepitus on movement of joint and loss of motion

and strength are common.

"Squared" appearance

Pain with pinch leads to adduction of the thumb and contracture of the first
web space.
o

Compensatory hyperextension of the first metacarpophalangeal joint

Swan-neck deformity of the thumb

Metacarpophalangeal joint

Involvement is rare.

Hip

Pain typically felt in inguinal area, but may be in the buttock or proximal thigh

Less commonly, may present as knee pain

Pain can be evoked by putting the involved hip through its range of motion.
o

Flexion may be painless initially, but internal rotation will exacerbate

pain.

Loss of internal rotation occurs early, followed by loss of extension,

adduction, and flexion.

Knee

Bony hypertrophy (osteophytes) and tenderness may be palpated.

Effusions are generally small.

Bony crepitus with joint movement

Buckling may occur.

Medial compartment OA may result in a varus (bow-leg) deformity.

Lateral compartment OA may produce a valgus (knock-knee) deformity.

Pain with manual compression of the patella against the femur during
quadriceps contraction ("shrug" sign) may indicate patellofemoral OA.

Spine

Localized pain and musculoskeletal stiffness

Cervical and lumbar spines affected far more often than thoracic spine
o

Of the thoracic vertebrae, T8 is most commonly involved.

Radicular pain and motor weakness may occur in presence of:

o

Nerve root compression by an osteophyte blocking a neural foramen

Prolapse of a degenerated disk

Subluxation of an apophyseal joint

Frequently asymptomatic

Feet

Hallux valgus: displacement of the great toe toward the other toes

Hallux rigidus: loss of motion of the joint connecting the great toe to the
metatarsal

Contracted toes: hammer/cock-up toes

Other single sites

Glenohumeral, acromioclavicular, tibiotalar, sacroiliac, temporomandibular

joints

Differential Diagnosis

Osteonecrosis
o

Death of a segment of bone, usually caused by ischemia

Rheumatoid arthritis
o

Joint involvement is usually symmetric and polyarticular, with arthritis

in wrists and metacarpophalangeal joints (sites not usually involved in
OA).

Constitutional features are common (e.g., prolonged morning stiffness,

fatigue, weight loss, or fever).

Soft-tissue rheumatism
o

Anserine bursitis at the knee

Trochanteric bursitis at the hip

Psoriatic arthritis

Other spondyloarthropathies

Systemic lupus erythematosus

o

Joint involvement can have the appearance of deformity without

erosions

Septic arthritis

Crystal-induced arthritides
o

Gout

Pseudogout (CPPD disease)

Radiculopathy

Polymyalgia rheumatica

Referral of pain from another joint

o

25% of patients with hip disease have pain referred to the knee.

Entrapment neuropathy

Vascular disease (claudication)

Chondromalacia patellae

Syndrome of patellofemoral pain

Teenagers and young adults, commonly in females

Anterior knee pain and a positive shrug sign

Usually not a precursor of OA

Diffuse idiopathic skeletal hyperostosis

Marked calcification and ossification of paraspinous ligaments

Diagnostic Approach

Diagnosis of OA is clinical, usually based on:

o

Typical pattern of joint involvement from clinical assessment

Radiographic features

Normal laboratory tests

Synovial fluid findings

Ensure that joint pain in patient with radiographic evidence of OA is not due
to some other cause.

Often, there is considerable disparity between the severity of radiographic

findings, severity of symptoms, and functional ability in OA.
o

For example, MRI of the knee or low back in asymptomatic or mildly

symptomatic patients may show incidental abnormalities.

Synovial joint fluid analysis is of particular value in an inflamed joint to rule

out crystal-induced arthritis such as CPPD, gout, or septic arthritis.

Laboratory Tests

No laboratory studies are diagnostic for primary OA, but they may help
identify an underlying cause of secondary OA or rule out confounding
diagnoses.

Primary OA
o

Normal erythrocyte sedimentation rate (ESR), serum chemistries, blood

counts, and urinalysis

However, ESR may be elevated with active synovitis or

generalized OA.

Rheumatoid factor, anti-CCP, antinuclear antibody, and other autoantibody

studies are negative.

Synovial fluid analysis

o

Joint fluid is straw colored, with normal viscosity.

Mild leukocytosis (< 2000 cells/L), with a predominance of

mononuclear cells

Crystals are absent.

Gram stain and cultures are negative for infection.

Imaging

Radiography
o

X-rays are indicated to evaluate chronic hand and hip pain thought to
be due to OA, because the diagnosis is often unclear without
confirming radiographs.

For knee pain, x-rays should be obtained if symptoms or signs are not
typical of OA or if knee pain persists after effective treatment.

In OA, radiographic findings correlate poorly with the presence and

severity of pain.

May be normal at first

Joint space narrowing, subchondral bone sclerosis, subchondral cysts,

and osteophytes as disease progresses

Tibiofemoral joint space narrowing has been considered a

radiographic surrogate for articular cartilage thinning.

Joint space narrowing alone does not accurately indicate status

of the articular cartilage in early OA without radiographic
evidence of bony changes (e.g., subchondral sclerosis or cysts,
osteophytes).

Osteophytosis in the absence of other radiographic signs of OA

may be due to aging rather than OA.

A change in the contour of the joint, due to bony remodeling, and

subluxation may be seen.

Bony "sclerosis" from appositional bone growth in the subchondral

region

The abraded bone under a cartilage ulcer may take on the appearance
of ivory (eburnation).

Osteophytes (spurs) from growth of cartilage and bone

Erosive OA
o

More destructive than typical OA

Radiographic evidence of collapse of subchondral plate is

characteristic.

Central erosions of the articular surface seen in erosive interphalangeal

arthritis (non-nodal)

MRI
o

Erosions are distinct from those of rheumatoid and psoriatic arthritis,

as they occur subchondrally along the central portion of the joint
surface.

Increasingly used to study disease[1]

Better visualization within OA joints

Evaluates cartilage loss

May over-diagnose (i.e., may show substantial disease that is

disproportionate to any complaints the patient may have)

Ultrasonography
o

Has not been sufficiently validated to justify routine clinical use for
diagnosis of OA or monitoring disease progression

Diagnostic Procedures

Joint aspiration for synovial joint fluid analysis

o

Useful to rule out CPPD, gout, or septic arthritis

See Laboratory Tests for details.

Classification

Idiopathic OA: No underlying cause is apparent.

o

Localized

Generalized: characterized by involvement of 3 joints or groups of

joints

Secondary OA: A predisposing or underlying factor is present.

o

See Etiology for conditions associated with secondary OA.