Version May 2024
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 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 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 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 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 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 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, 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 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 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].
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: Etiology, 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 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 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".)
●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 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, 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 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 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
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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