Osteoarthritis (OA), the commonest arthropathy, targets the knees, hips, finger interphalangeal joints, thumb bases, first metatarsophalangeal joints, and spinal facet joints, and displays marked heterogeneity of clinical presentation. Signs of OA include coarse crepitus, bony enlargement, reduced range of movement, and joint-line tenderness. Muscle wasting and joint deformity occur with severe OA. Painful periarticular disorders often coexist with OA. Inflammation is absent or only modest, although mild-moderate effusions are common at the knee. The diagnosis of OA may be made without recourse to radiographic or laboratory investigations in the at-risk age group with typical symptoms and signs.
Key points
- •
Osteoarthritis (OA) has a marked variability of clinical presentation and prognosis.
- •
OA targets specific joints (eg, knees, hips, finger IPJs, thumb bases, first metatarsophalangeal joints, and spinal facet joints).
- •
Frequent symptoms and signs include usage-related joint pain, morning-related or inactivity-related stiffness of short duration, locomotor restriction, coarse crepitus, bony enlargement, and joint-line tenderness.
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Rest pain, night pain, and deformity suggest severe OA.
- •
Painful periarticular soft tissue disorders frequently coexist with knee, hip, and first metatarsophalangeal OA.
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The diagnosis of OA may be reached without any laboratory or radiographic investigations in the at-risk population in the presence of typical signs and symptoms.
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Associated calcium pyrophosphate and basic calcium phosphate crystal deposition is common, especially in the elderly, and may be associated with inflammatory symptoms and signs.
Introduction
Osteoarthritis (OA) is a condition of synovial joints that represents failed repair of joint damage that results from stresses that may be initiated by an abnormality in any of the synovial joint tissues. OA may be localized to 1 joint, to a few joints, or be generalized. It is the commonest arthropathy, and presents with joint pain, locomotor restriction, and varying degrees of functional impairment. It has a marked variability of phenotypic expression. The age of onset, pattern of joint involvement, and rate of progression vary from person to person and from site to site. For example, OA may be an asymptomatic incidental finding on clinical or radiographic examination, or be a progressive, painful, and disabling disorder at different joints in the same person. Thus there is an imperfect overlap between the disease OA (structural changes visualized on imaging) and the illness OA (patients’ reported symptoms). This article describes the clinical features of OA with an emphasis on symptoms and signs at the key target sites.
Introduction
Osteoarthritis (OA) is a condition of synovial joints that represents failed repair of joint damage that results from stresses that may be initiated by an abnormality in any of the synovial joint tissues. OA may be localized to 1 joint, to a few joints, or be generalized. It is the commonest arthropathy, and presents with joint pain, locomotor restriction, and varying degrees of functional impairment. It has a marked variability of phenotypic expression. The age of onset, pattern of joint involvement, and rate of progression vary from person to person and from site to site. For example, OA may be an asymptomatic incidental finding on clinical or radiographic examination, or be a progressive, painful, and disabling disorder at different joints in the same person. Thus there is an imperfect overlap between the disease OA (structural changes visualized on imaging) and the illness OA (patients’ reported symptoms). This article describes the clinical features of OA with an emphasis on symptoms and signs at the key target sites.
Clinical features
Pain, stiffness, and locomotor restriction are the main symptoms of OA ( Table 1 ). Other symptoms include crepitus, joint deformity, or joint swelling (caused by bony remodeling, excessive osteophytosis, or joint subluxation). These symptoms typically begin in just 1 or a few joints in a person of middle or older age.
| Symptoms | |
| Joint pain | Usually affects 1 to few joints at a time |
| Insidious onset: slow progression over months to years | |
| Variable intensity throughout the day and the week | |
| May be intermittent and relapsing | |
| Increased by joint use and impact | |
| Relieved by rest | |
| Night pain may occur in severe OA | |
| Stiffness | Short-lived (<30 min) early morning stiffness |
| Short-lived inactivity-related stiffness (gelling) | |
| Swelling | Some (eg, nodal OA) patients present with swelling and/or deformity |
| Age | >40 y a |
| Constitutional symptoms (eg, weight loss, sweats, fever) | Absent |
| Signs | |
| Appearance | Swelling (usually bony ± fluid/soft tissue) |
| Resting position (attitude) | |
| Deformity | |
| Muscle wasting (global: all muscles acting over the joint) | |
| Feel | Absence of warmth |
| Swelling: bony or effusion | |
| Effusion if present is usually small and cool | |
| Joint-line tenderness | |
| Periarticular tenderness (especially knee, hip) | |
| Movement | Coarse crepitus b |
| Reduced range of movement | |
| Weak local muscles | |
a Major joint injury and certain rare conditions may predispose to OA before the age of 40 years.
Pain worse with joint use and relieved by rest (usage or mechanical pain) is often the most troublesome symptom. The origin of pain in OA is not completely understood. Pain may arise from the nociceptive fibers and mechanoreceptors in the synovium, subchondral bone, periosteum, capsule, tendons, or ligaments. Pain in large joint OA (eg, knee or hip) is also thought to arise from bone marrow lesions, and synovitis/effusion by stimulation of nociceptive fibers and intra-articular hypertension, respectively, and a similar mechanism may also operate in the small joints. However, hyaline cartilage is aneural, and is not a source of pain in OA. Whatever its source, both central and peripheral sensitization perpetuate and amplify pain in OA. Pain generally progresses through 3 stages ( Table 2 ). However, pain progression may be arrested at any stage, and not all patients go through 3 distinct stages.
| Stage 1 (Early) | Predictable sharp pain, usually brought on by a mechanical insult that eventually limits high-impact activities. There may only be a minimal effect on function. |
| Stage 2 (Mild-moderate) | Pain becomes a more regular feature, and begins to affect daily activities. There may be unpredictable episodes of stiffness. |
| Stage 3 (Advanced) | Constant dull/aching pain, punctuated by short episodes of often unpredictable intense, exhausting pain that results in severe functional limitations. |
Temporal and seasonal variations in OA pain have been reported as for other arthropathies. Pain in OA is reported to be worst on waking up in the morning, with an improvement in the next 2 hours. It then worsens in the late afternoon/early evening to again reduce later in the evening. However, night pain can be present in OA, which interferes with sleep and leads to fatigue, lack of well-being, and increased pain sensitivity. Such nonusage night pain is thought to arise largely from the subchondral bone. In some people, the pain has a burning (neuropathic) quality, is widespread around the joint, and associates with tenderness and paresthesiae. Such features also suggest comorbid fibromyalgia, another common pain syndrome in older people.
Painful periarticular soft tissue lesions may coexist with large joint OA (eg, pes-anserine bursitis, greater trochanter pain syndrome) and it may be difficult to identify the cause of the pain. One solution to this problem is to ask the patient to point to the most painful area and then to map out the area that feels uncomfortable. Periarticular soft tissue lesions cause localized pain away from the joint line, whereas OA pain more commonly is most severe over the joint line except for proximal joints (hip, shoulder), which may have the maximal site of pain distal to the originating joint (radiated pain).
Stiffness is also common in OA. Stiffness may be thought of as a difficulty or discomfort during movement caused by a perceived inflexibility of the joint. Stiffness is usually most noticeable early in the morning, but may also occur later in the day, typically after periods of inactivity. Early morning stiffness is present both in classic inflammatory arthritis (eg, rheumatoid arthritis [RA]), and in OA. It can be considered an inflammatory symptom when prolonged and present for at least 30 minutes before maximal improvement. The morning stiffness in OA is typically short lived (usually a few minutes, but in general <30 minutes). Short-lived stiffness (gelling) may also be brought on by inactivity. In patients with OA, both morning and inactivity-related stiffness quickly improve and resolve with joint use, whereas the joint pain subsequently worsens with continued use.
Locomotor restriction and the resulting functional impairment depend on the site and severity of OA. For example, first carpometacarpal joint (CMCJ) OA may cause difficulty in gripping, whereas knee or hip OA may impair the ability to get up from a chair and walk. The resulting participation restriction depends on the individual’s daily activities and occupational/recreational requirements.
The main physical signs of OA are coarse crepitus, joint-line tenderness, bony swelling, deformity, and reduced range of movement.
Crepitus is a coarse crunching sensation or sound caused by friction between damaged articular cartilage and/or the bone. It may be more prominent during active movement than during passive movement during physical examination. It is often present throughout the range of movement. Crepitus may be exacerbated by stressing the joint surfaces (eg, patellofemoral joint [PFJ] crepitus is increased by applying downward pressure on the patella with the examining hand during knee flexion). Transmitted crepitus (felt on the adjacent periarticular bone) suggests a full-thickness cartilage defect on the affected side.
Tenderness in and around the joint is common in OA. Joint-line tenderness suggests an articular disorder, whereas tenderness away from the joint line suggests a periarticular soft tissue disorder. Both joint-line and periarticular tenderness may be present simultaneously because of a high frequency of periarticular soft tissue disorders near joints with OA. Reduced range of movement (equal for both active and passive movements) mainly results from marginal osteophytosis and capsular thickening, but synovial hyperplasia and effusion also contribute. Fixed flexion deformities (the inability to fully extend the joint) occurs at the knees, hips, or elbows in advanced severe OA. Bony swelling, which may be evident in both small (eg, IPJ, first metatarsophalangeal) and large (eg, knee) joint OA, occurs because of a combination of bony remodeling, marginal osteophytosis, and joint subluxation. Deformity and instability are signs of marked joint damage. Muscle wasting suggests advanced OA.
Holistic assessment
Patients with OA should be assessed in a targeted manner for depression, sleep deprivation, hyperalgesia, central sensitization, and catastrophization. Each of these has the potential to increase the pain severity. An attempt must similarly be made to assess the presence of joint pain at other sites as it increases pain severity at the index joint. Mobility assessment and neuromuscular examination should be performed for patients with suspected hip or knee OA because these both associate with muscle weakness, impaired joint position sense, and falls. The risk of falls may be further increased by postural hypotension, visual or vestibular impairment, and polypharmacy, which are common in the elderly. Fibromyalgia is another common comorbidity in the elderly and should be considered and sought (by examination for widespread hyperalgesic tender sites) in anyone presenting with musculoskeletal pain, especially if they report nonrestorative or nonrefreshing sleep. Adverse risk factors ( Box 1 ) should be sought and considered in the management plan. In addition, illness perceptions regarding joint pain and OA should be explored and discussed with the patient because these may influence treatment adherence and outcome.
Age
Obesity
Knee malalignment (varus-valgus), hindfoot malalignment
Lower limb length inequality (≥1–2 cm)
Presence of OA in multiple joints (eg, generalized OA [GOA])
Excess or no joint use
Muscle wasting and weakness
Joint laxity
Poor mental health, lack of self-efficacy, and poor social support (for worsening symptoms only)
Role of investigations
OA is a clinical diagnosis. It may be diagnosed without recourse to laboratory or radiographic investigations in the presence of typical symptoms and signs in the at-risk age group. Peripheral joint OA may be diagnosed confidently on clinical grounds alone if there is:
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Persistent usage-related joint pain in 1 or a few joints
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Age ≥45 years
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Only brief morning stiffness (≤30 minutes).
Other features listed in Table 1 add to the diagnostic certainty. This approach to a clinical diagnosis of OA is supported by the poor correlation between radiographically assessed structural changes and symptoms in OA. The American College of Rheumatology (ACR) clinical classification criteria for knee, hip, and hand OA have a high sensitivity, and at least a moderate to high specificity for discriminating OA from other rheumatic conditions in a hospital setting. However, the ACR criteria are not diagnostic, and failure to meet the classification criteria does not exclude OA. They also have a low sensitivity and specificity for classifying mild-moderate OA in the community setting. However, appropriate imaging and laboratory assessments should be performed:
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In younger individuals (ie, <45 years in age) in the absence of preceding major joint trauma,
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If symptoms and signs are atypical; for example, not usual target sites for OA, symptoms and signs of significant joint inflammation, marked rest and/or night pain, rapidly progressive pain,
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If there is weight loss or constitutional upset,
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If there is true locking at the knee, which suggests additional mechanical derangement.
Inflammatory markers (C-reactive protein, erythrocyte sedimentation rate, plasma viscosity) are normal or only minimally increased in OA, and may be useful in excluding other diagnoses. Radiographic examination may be used to support a clinical diagnosis of OA. However, patients with a clinically robust diagnosis of OA may have normal radiographs, and vice versa. Thus, radiographic examination should not be used to establish a diagnosis of OA by itself, and neither should a normal plain radiograph be used to refute a clinical diagnosis of OA; 86% of middle-aged community-dwelling residents (mean age 45 years) with knee pain for more than 3 months develop radiographic knee OA over the next 12 years, suggesting that knee pain may be the first sign of OA. However, such patients should be examined carefully to exclude any other cause of joint pain, such as periarticular soft tissue lesions, before arriving at a diagnosis of OA and more sensitive examination of the joint (eg, ultrasound or magnetic resonance imaging) may be warranted. However, radiographic examination may have a role in defining the prognosis of patients with OA. In a prospective study of more than 1507 patients with knee OA, those with more severe joint space narrowing at baseline progressed more rapidly to complete joint space loss over time than those with no joint space narrowing at baseline. Global OA severity had a similar but smaller role. In summary, OA may be diagnosed on clinical grounds alone in the at-risk population, with radiographs being used more for prognostic than diagnostic purposes.
Synovial fluid examination is not routinely required to support a diagnosis of OA. However, joint aspiration and synovial fluid analysis are indicated if there is a suspicion of coexistent crystal deposition. Both monosodium urate and calcium pyrophosphate (CPP) crystal deposition (CPPD) associate with OA and may cause acute synovitis or more chronic inflammation in OA joints. Community-based studies suggest that coexistent self-reported gout and OA of the knee and hip occur in 1.1% and 0.8% of patients older than 25 years, respectively, whereas coexistent knee chondrocalcinosis (a marker of CPPD) and knee OA occur in 2.4% of patients older than 40 years. Basic calcium phosphate (BCP) crystal deposition is also common in OA but requires sophisticated techniques (eg, scanning electron microscopy) for accurate identification, and its presence is not sought routinely.
Distribution of joints affected by OA
OA can affect any synovial joint. However, it targets the knees, hips, first CMCJs, finger IPJs, first metatarsophalangeal (bunion) joints (first metatarsophalangeal joints [MTPJs]) and apophyseal (facet) joints of the lower cervical and lower lumbar spine ( Fig. 1 ).
Classification
OA can be classified according to the number of affected joints, presumed cause, age of onset, radiographic appearance (hypertrophic vs atrophic), presence of calcium crystals, and rate of progression. Several classification systems have been proposed. Each has its own strengths and weaknesses. We present a simplified system adapted from the original ACR classification and that is possibly better suited for clinical use ( Box 2 ).
- 1.
Number of joints involved
- a.
Localized: 1–2 joint regions involved only (specify location)
- b.
GOA: ≥3 joint regions involved, with spine/hands being one of the regions affected (nodal GOA if nodes present)
- a.
- 2.
Classic or atypical OA (atypical OA: unusual distribution, young age of onset [<45 years], rapid progression)
Causes of atypical OA include:
- a.
Prior trauma (common): mainly monoarticular or oligoarticular OA, young onset, often with a clear history of injury
- b.
Dysplasia:
- i.
Localized (eg, hip): childhood or young adult onset
- ii.
Polyarticular (eg, spondyloepiphysial dysplasia): young onset, short stature, morphologic features, and a positive family history may be present
- i.
- c.
Childhood arthropathy or derangement: eg, juvenile idiopathic arthritis, Perthes disease and slipped femoral epiphysis of hip, septic arthritis
- d.
Metabolic or endocrine diseases: eg, hemochromatosis, which mainly targets metacarpophalangeal joints (MCPJs), wrists, hips, and may be of young onset, mainly in men; acromegaly, which has typical signs of OA with little restriction in movements, hypermobility
- e.
Late avascular necrosis: predominantly hips, shoulders, and knees, more rapid progression, risk factors present (eg, steroid use)
- f.
Neuropathic joints: rapid clinical progression, marked joint disorganization
- i.
Hindfoot, midfoot: diabetes mellitus
- ii.
Shoulders, elbows, wrists: syringomyelia
- i.
- g.
Apatite-associated destructive arthritis: old age, rapid progression; targets hips, knees, and shoulders
- a.
- 3.
Clinical joint inflammation: usually absent; if present, consider:
- a.
Crystal deposition: CPPD and gout (OA encourages deposition of both crystal types)
- b.
Coexistent inflammatory arthritis: eg, RA, seronegative spondyloarthropathy
- c.
Erosive OA: targets hand IPJs
- a.
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