Last Updated: March 2001

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Diagnosis

The diagnosis of osteoarthritis (OA) is primarily based on history and physical examination. Usually, the clinical features that a patient exhibits — specifically the symptoms he complains of and the signs noted on examination — are sufficient to make the diagnosis of OA. In a patient with use-related pain in a single joint who also has bony swelling, crepitus, and reduced range of motion, the diagnosis is likely OA. However, the differential diagnosis should include rheumatoid arthritis and pseudogout. Additionally, if joints such as the elbow or shoulder are involved, the possibility of an etiology other than OA, such as a neoplastic or metabolic disorder, should be considered.

Plain radiographs of the affected joint can both help confirm a diagnosis of OA and grade its severity. Results of routine laboratory tests are normal and are, therefore, only useful in screening for associated conditions and for establishing a baseline for monitoring therapy.

American College of Rheumatology Diagnostic Criteria for OA

The heterogeneity of OA has led to attempts to establish diagnostic criteria for the disorder at the most commonly affected sites (i.e., the hand, hip, knee and; see following tables). According to the most widely used criteria — developed by the American College of Rheumatology (ACR) — the major criteria for diagnosis of OA is joint pain for most days of the month. This is contrasted to radiographic criteria, in which many patients do not report joint pain.

ACR Criteria for the Classification and Reporting of OA of the Hand

Classification criteria for OA of the hand, traditional format*

Hand pain, aching, or stiffness
      and
At least three of the following four features:
       Hard tissue enlargement of two or more of 10 selected joints
       Hard tissue enlargement of two or more DIP joints
       Fewer then three swollen MCP joints
       Deformity of at least one of the 10 selected joints

*The 10 selected joints are the second and third distal interphalangeal (DIP), the second and third proximal interphalangeal, and the first carpometacarpal joints of both hands. This classification method yields a sensitivity of 94% and a specificity of 87%.
MCP=metacarpophalangeal.
From Altman et al. [1990]; with permission.

ACR Criteria for the Classification and Reporting of OA of the Hip

Classification criteria for OA of the hip, traditional format*

Hip pain
      and
At least two of the following three features:
       ESR<20 mm/hour
       Radiographic femoral or acetabular osteophytes
       Radiographic joint space narrowing (superior, axial, and /or medial)

*This classification method yields a sensitivity of 89% and specificity of 91%.
ESR=erythrocyte sedimentation rate (Westergren).
From Altman et al. [1991]; with permission.

ACR Criteria for the Classification and Reporting of OA of the Knee

Criteria for classification of idiopathic OA of the knee

Clinical and Laboratory Clinical and Radiographic Clinical*

Knee pain plus at least five of nine:
    Age >50
    Stiffness <30 minutes
    Crepitus
    Bony tenderness
    Bony enlargement
    No palpable warmth
    ESR <40 mm/hour
    RF <1:40
    SF OA
92% sensitive
75% specific

Knee pain plus at least one of three:
    Age >50
    Stiffness <30 minutes
    Crepitus

plus
Osteophytes

91% sensitive
86% specific

Knee pain plus at least three of six:
    Age >50
    Stiffness <30 minutes
    Crepitus
    Bony tenderness
    Bony enlargement
    No palpable warmth

95% sensitive
69% specific

*Alternative for the clinical category would be four of six, which is 84% sensitive and 89% specific.
RF=rheumatoid factor; SF OA= synovial fluid signs of OA (clear, viscous, or white blood cell count <2000/mm³).
From Altman et al. [1986]; with permission.

Clinical Features

OA usually has a slow and insidious onset and affects only one or a few joints. The most important symptoms in OA are pain and limitation of motion. Although the pain is an annoyance that can curtail daily activities, the limitation of motion can translate into loss of function. OA of the hands can lead to an inability to perform daily activities. OA of the hip or knee may produce an inability to walk requiring surgery or the need to be placed in a nursing home.

The signs and symptoms of OA, such as pain and stiffness, are often localized to the symptomatic joint(s) and can be elicited by having the patient flex or extend the joint. Examination of the affected joint during passive movement allows for the assessment of joint stability and the presence of pain. Bony enlargements may exist around the joint, which may also cause pain. Limitation of joint motion and bony crepitus may also be present during examination. Signs of local inflammation with warmth and swelling, which is usually mild, and joint effusions may be seen. In contrast to rheumatoid arthritis, OA does not cause systemic signs or symptoms, such as fever, weight loss, or internal organ pathology. The lack of systemic involvement is a key distinguishing feature between these two forms of arthritis. An overview of OA signs and symptoms is provided in the following table.

The Primary Signs and Symptoms of OA

Signs Symptoms

Tenderness around joint margin and nearby structures Use-related joint pain

Crepitus (cracking or grinding sensation) Short-lived stiffness or "gelling" after periods of inactivity

Signs of mild soft tissue inflammation (cool joint effusions) Loss of joint movement/difficulty performing certain tasks

Instability (obvious, severe bone/joint destruction) Joint locking or "giving way"

Joint locking or "giving way" Feeling of instability

Firm swelling Restricted, painful movements

Data from Dequeker and Dieppe [1998].

Signs

Signs of OA include tenderness and the development of firm swellings around the joint margins. Bony enlargement of the affected joint(s) and crepitus are signs that help physicians differentiate OA from other rheumatic disorders. Crepitus may be associated with pain and is commonly felt when the affected joint (especially the knee) is moved. In advanced OA, crepitus may even be heard with walking, producing loud creaks. This noise is probably due to the roughening of the joint surface and outgrowths at the rim of the joint that interfere with normal movement. These signs of OA may be accompanied by evidence of soft-tissue inflammation, manifested as joint effusion(s).

A restricted, painful, tight joint or a loose, unstable joint may be found upon physical examination in advanced disease. Muscle atrophy may be apparent when the affected joint is compared to the same joint (unaffected joint) located on the other side of the body. Joint damage is usually accompanied by instability and, frequently, deformity of the joint.

Symptoms

Use-related joint pain, often described as a diffuse, intermittent "aching" pain starting within seconds or minutes of joint use, is often the earliest and, undoubtedly, the most important symptom of OA. It is frequently accompanied by tenderness and is exacerbated by "knocking" or "bumping" the joint against an object. Pain associated with OA usually increases with activity and is relieved with rest. However, it may continue for hours after the joint is allowed to rest. About half of all patients with OA complain of joint pain at rest and 30% experience night pain [Dequeker and Dieppe, 1998].

Many people believe that weather conditions affect their joint pain. Although there are no scientific data, it has been suggested that joint pain increases concurrently with a simultaneous fall in barometric pressure and rise in humidity, (e.g., rain). Therefore, in individuals who feel that weather influences their arthritis, the effect is probably real but the cause may be unknown.

In addition to pain, most OA patients report a sensation of "stiffness." Although stiffness may be severe, it usually lasts only a few seconds or minutes (rarely longer than 30 minutes). The most characteristic feature of this stiffness is known as the "gelling" phenomenon, which is manifested by difficulty initiating joint movement after a period of inactivity. Joint stiffness can result in difficulty moving the joint through its full range of motion or the occurrence of pain on movement [Dequeker and Dieppe, 1998].

Other common symptoms of OA include a reduction in the range of motion of the affected joint, "locking" of the joint, or the sensation that the joint has become unstable and is likely to "give way." Limitation of motion is usually associated with the following:

formation of osteophytes
severe loss of cartilage, leading to malalignment or contractures of the joint
spasms of the periarticular muscles.

Locking of the joint during motion is most likely a result of loose cartilage fragments floating within the joint capsule. Joint instability can be observed with joint motion and it may be associated with the loss of strength and function of the periarticular muscles. Periarticular muscle atrophy develops from infrequent use of a painful joint. Other muscles may be used more to compensate, which may cause pain to the unaffected side of the body. An example of this is in the case of a limp, in which the good leg is overused to spare a painful joint on the opposite side. These symptoms may result in progressive loss of joint function and eventual disability.

Pain in OA

The presence of osteophytes, the loss of normal joint structure, and the development of joint instability can all result in abnormal forces on the surrounding ligaments, capsule, and other innervated structures, resulting in pain. The pain may be localized to the affected joint or it may be referred to another area of the body. For example, a patient with OA of the hip may complain of referred pain down the thigh, running into the knee, sometimes mistakenly thought to be due to arthritis of the knee.

Sources of Pain in an OA Joint

Because pain is the most common and important symptom in OA and articular cartilage has no nerve endings, what is the source(s) of arthritic pain?

The source(s) of pain in OA must come from other areas within the joint. Sites and causes of pain, as shown in the following figure, in the OA joint include:

subchondral bone: increased vascularity and activity leads to sclerosis and cysts; increased intraosseous pressure leads to pain
joint margin: thickening of the capsule and osteophytes may cause pain
capsule and synovium: increased thickness and mild inflammation may cause pain
tendons and bursae: periarticular tendinitis and bursitis cause pain, resulting in decreased joint motion, leading to muscle wasting and weakness.

Potential Sites and Causes of Pain Generation in OA Knee

Click on image for larger version.

OA at Specific Joint Sites

Just as there is heterogeneity in the effects and manifestations of OA at one joint, there is variation in the pattern of joint OA distribution in different individuals. There is a particular predilection for OA at the DIP joints of the hand, base of the thumb, knee, hip, and intervertebral facet joints (see following figure).

Distribution of OA

Click on image for animation/larger version.

Hand OA

OA commonly affects hand joints (see figure below). The DIP joints are the most commonly affected, followed by the first carpometacarpal joint (CMC), and then the proximal interphalangeal (PIP) joints. The MCP joints and wrist joints are less often and less severely affected.

Distribution of OA in the Hand Joints

Click on image for larger version.

Hand OA usually starts with discomfort and joint aches that wax and wane over months or years. Involvement of the hand is much more common in women than in men and is associated with a strong genetic predisposition. The most striking sign of hand OA is the presence of firm swellings on the DIP joints (Heberden's nodes) and the PIP joints (Bouchard's nodes). These nodes are often tender, may be red, and may result in loss of lateral joint stability and the ability to bend the joint. Flares of disease activity are common, during which involved joints may become mildly warm, red, and tender, showing clear signs of inflammation. After a few years, the joints can become nontender, despite the remaining deformity and, as the disease progresses, the swellings can become firm and fixed and the range of joint motion diminished. Eventually, the patient may be unable to move the affected joint at all.

OA of the CMC joint is common. Although the "opposing" function of the thumb is a unique evolutionary development, the thumb may be "underdesigned" for the biomechanical stresses that are typically applied to it and may be predisposed to ligament damage, causing problems with manual dexterity. Although this joint is more prone to causing severe pain and disability than the DIP and PIP joints, it may not be easily recognized. "Squaring" of the thumb base, meaning the presence of a sharp corner instead of the usual rounded form, is a classic presentation. In addition, there is a strong association with carpal tunnel syndrome and deQuervain's tenosynovitis. OA of the thumb base may also be associated with prior hypermobility of the joint.

Knee OA

Knee OA evolves slowly, with the condition remaining relatively stable for several years. However, symptomatic "flares" with notable inflammation, lasting days or weeks may occur. Occasionally, knee OA may take a more aggressive course, resulting in severe pain, rapid destruction, and gait disturbance.

There is a strong association between obesity and knee OA. However, occupational factors and genetics may also play a role. Occupations that require a great deal of squatting or knee bending can predispose an individual to the development of OA, as can abnormalities in the structure of the knee.

The symptoms include pain on walking, stiffness of the joint, and difficulty with steps and stairs. Signs, such as muscle wasting, bony swelling, joint tenderness, crepitus, painful limitation of motion and, in some cases, an effusion can be seen. Valgus and varus joint deformities can be seen in advanced cases (see figure below).

Comparison of Valgus and Varus Deformity

Click on image for larger version.

Hip OA

The natural history of hip OA is extremely variable. Most patients experience relatively mild problems over prolonged periods, whereas a few appear to "recover" spontaneously. Yet others undergo a rapid progression of the disease that often leads to surgery. Occasionally, frank joint destruction occurs, which may lead to severe pain and disability.

Hip OA affects slightly more men than women; this is possibly due to hip loading. Other risk factors include local congenital abnormalities of the hip, such as congenital dislocation.

The most prominent symptom of hip OA is pain with walking. This pain may be referred to the buttocks, groin, thigh, or knee, complicating the diagnosis. Patients afflicted with hip OA may have difficulty bending to put on socks or shoes and may report sexual difficulties because of painful hip motion. Signs and symptoms include pain, inactivity stiffness, crepitus, and reduced range of motion.

OA at Other Sites

OA of the spine occurs in the areas where there is the most motion, such as the lower back. Pain associated with OA of the back increases with walking and may, therefore, limit walking, exercise, and recreational activities. OA of the back may need to be distinguished from a herniated disc, if there is an acute onset of the back pain. Severe osteophyte formation on the facet joints that join the vertebral bones together may impinge upon the spinal column, causing a condition called spinal stenosis. The typical patient with this problem complains about back and leg pain that is exacerbated with walking and relieved with rest.

OA can also develop in the temporomandibular joint, shoulder, elbow, and front and back of the foot. OA at each of these sites is also associated with characteristic signs and symptoms.

Imaging Modalities

Plain Radiographs or X-rays

Plain X-rays have been the primary imaging method used to confirm the diagnosis of OA, stage its severity, and follow its progression. Unfortunately, the severity of radiographic findings do not correlate well with the severity of symptoms or the presence of functional disability. Although more than 90% of people over age 40 have some radiographic evidence of osteoarthritic joint changes, only 30% have symptoms. This limits the use of radiography, both as a diagnostic tool and as a tool for ongoing assessment of disease progression.

The hallmark radiologic features for OA are shown in the following table. If joint space narrowing, subchondral sclerosis, and osteophyte formation are not present on radiographs, another diagnosis should be considered. Some of these characteristic findings are shown in the figure below.

The Hallmark Radiologic Features for OA

Joint space narrowing, which is often irregular or asymmetric

Subchondral sclerosis, which appears as an increased density in subchondral bone

Bony proliferation with the presence of osteophytes/spurs

The presence of cysts in subchondral marrow adjacent to or sometimes remote from the joint (usually seen in later cases)

Soft-tissue changes (small effusions, calcification, and soft-tissue swelling)

Data from Dequeker and Dieppe [1998].

Radiograph of OA Hands

Courtesy of Getty Images, Inc.; with permission.
Click on image for larger version.

Other Imaging Techniques

Because the plain radiograph is almost always sufficient, most of the following techniques are only used in special circumstances to aid in the diagnosis of OA. For example, these studies can be used to eliminate an infected joint (e.g., radionuclide scintigraphy) or to look for a herniated disc in the back (e.g., magnetic resonance imaging [MRI]).

Arthrography

This involves the injection of contrast media into a joint. Arthrography is a relatively time-consuming and invasive procedure, but it may be useful in detecting meniscal injury, loose bodies in the joint cavity, and other local changes in joint structure. It has been mostly replaced by MRI.

Ultrasound

Ultrasound is inexpensive and widely available, and does not expose the patient to ionizing radiation; however, its use is limited because ultrasound waves do not readily pass through bone tissue. It is particularly valuable in the imaging of soft-tissue structures and tendons associated with the joint. Although ultrasound cannot evaluate bone, it can distinguish between solid and cystic soft-tissue lesions. It is also helpful in demonstrating joint effusions behind the knee (Baker's or popliteal cyst) and to guide a needle for aspiration of fluid (arthrocentesis).

Radionuclide scintigraphy

Also known as a bone scan, this is a sensitive, but nonspecific, method of detecting OA activity. It creates images by scanning affected areas of the body with a gamma camera after a bone-seeking radiopharmaceutical is injected. Radionuclides, such as technetium-99 HDP, are attracted to areas of bone with relatively high blood flow, edema, and high bone-mineral turnover rates (abnormal joint physiology). Joints that are unusually active "light up" in the resulting images.

Scintigraphic imaging can be used to distinguish between joints with active disease and those that are altered, but inactive. Moreover, scintigraphic imaging may detect the presence of OA before these changes are detectable on X-rays. Unfortunately, this technique is very costly and time consuming, and requires the use of a radioactive material, which in turn needs special handling. Thus, it is not an appropriate technique for the routine diagnosis or management of OA.

Magnetic resonance imaging

MRI is a very expensive imaging technique that uses the behavior of atomic nuclei in a magnetic field to create images. Patients are exposed to radiowaves and a strong magnetic field, rather than X-rays or other types of radiation. This technique provides excellent reconstructed images of interior organs, and can delineate muscle, bone, blood vessels, and nerves.

MRI is limited as a diagnostic modality because of its expense. Although it is not routinely performed in patients with OA, MRI is useful when other entities — such as meniscal tears or ligament injuries — need to be eliminated because it permits the simultaneous imaging of all joint components with excellent contrast between different tissues. MRI has proven to be particularly valuable in imaging joint effusions, menisci, joint ligament, osteophytes, and defects in bone, articular cartilage, and synovial tissue. Moreover, this technique has specific advantages in diagnosing osteonecrosis, internal joint derangements, bone and joint infections, and disorders of the structures around joints (e.g., rotator cuff lesions).

Computed tomography

Computed tomography is helpful in detecting fine detail of cortical bone. It is also a relatively expensive test. Relative to MRI, it gives poor definition of soft-tissue boundaries.

Laboratory Findings

Because OA is not a systemic disease, routine laboratory tests — such as blood chemistry, blood count, and urinalysis — would be expected to be normal. These laboratory tests are only useful for screening for associated conditions or secondary causes of OA and to establish a baseline for monitoring therapy. Other laboratory tests indicative of inflammation, such as the erythrocyte sedimentation rate and C-reactive protein, are also usually normal.

Synovial fluid analysis

There are usually only a small number of white blood cells (WBCs) present in synovial joint fluid (usually <200). Synovial fluid taken from a joint affected by OA may show only a few WBCs or there might be a slight increase in the number of WBCs, usually less than 1000-2000 WBC/mm³ with less than 30% polymorphonucleocytes (PMNs), which normally appear with inflammation. Although this level of WBCs is considered to be noninflammatory, it is a relative term when compared with rheumatoid arthritis, in which WBC counts range between 10,000 and 50,000 WBC/mm³ with usually greater than 50% PMNs. The synovial fluid is usually viscous or thick, similar to normal synovial fluid, and it may contain cartilage fragments and calcium-containing crystals.

The synovial fluid of a patient with OA also contains a variety of "biochemical markers," representative of the breakdown and repair of cartilage and bone (e.g., keratan sulfate, chondroitin sulfate, hyaluronic acid, and pyridinoline crosslinks), along with cytokines and other markers of inflammation. Currently, these markers are used as research tools, and are not useful for clinical purposes. Tests for some of these markers may be developed for diagnostic and assessment purposes in the future.

References

Altman R, Alarcon G, Appelroth D, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip. Arthritis Rheum. 1991;34:505-514.

Altman R, Alarcon G, Appelroth D, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum. 1990;33:1601-1610.

Altman R, Alarcon G, Appelroth D, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the knee. Arthritis Rheum. 1986;29:1039-1049.

American College of Rheumatology. Clinical Slide Collection on the Rheumatic Diseases. Atlanta: American College of Rheumatology, 1997.

Dequeker J, Dieppe PA, eds. Disorders of bone cartilage and connective tissue. In: Klippel JH, Dieppe PA, eds. Rheumatology. 2nd ed. London: Mosby, 1998.

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