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Diagnosis and Clinical Presentation of Osteoarthritis

      Keywords

      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.
      • Rest pain, night pain, and deformity suggest severe OA.
      • Painful periarticular soft tissue disorders frequently coexist with knee, hip, and first metatarsophalangeal OA.
      • 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.
      • 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.
      • Lane N.E.
      • Brandt K.
      • Hawker G.
      • et al.
      OARSI-FDA initiative: defining the disease state of osteoarthritis.
      OA may be localized to 1 joint, to a few joints, or be generalized.
      • Lane N.E.
      • Brandt K.
      • Hawker G.
      • et al.
      OARSI-FDA initiative: defining the disease state of osteoarthritis.
      It is the commonest arthropathy, and presents with joint pain, locomotor restriction, and varying degrees of functional impairment.
      National Institute for Health and Clinical Excellence.
      • Abhishek A.
      • Doherty M.
      Disease diagnosis and clinical presentation.
      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).
      • Lane N.E.
      • Brandt K.
      • Hawker G.
      • et al.
      OARSI-FDA initiative: defining the disease state of osteoarthritis.
      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).
      • Abhishek A.
      • Doherty M.
      Disease diagnosis and clinical presentation.
      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.
      Table 1Principal manifestations of OA
      Adapted from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011.
      Symptoms
      Joint painUsually 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
      StiffnessShort-lived (<30 min) early morning stiffness
      Short-lived inactivity-related stiffness (gelling)
      SwellingSome (eg, nodal OA) patients present with swelling and/or deformity
      Age>40 y
      Major joint injury and certain rare conditions may predispose to OA before the age of 40 years.
      Constitutional symptoms (eg, weight loss, sweats, fever)Absent
      Signs
      AppearanceSwelling (usually bony ± fluid/soft tissue)
      Resting position (attitude)
      Deformity
      Muscle wasting (global: all muscles acting over the joint)
      FeelAbsence of warmth
      Swelling: bony or effusion
      Effusion if present is usually small and cool
      Joint-line tenderness
      Periarticular tenderness (especially knee, hip)
      MovementCoarse crepitus
      Audible crepitus may be a symptom of knee OA.
      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.
      b Audible crepitus may be a symptom of knee OA.
      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,
      • Yusuf E.
      • Kortekaas M.C.
      • Watt I.
      • et al.
      Do knee abnormalities visualised on MRI explain knee pain in knee osteoarthritis? A systematic review.
      • Goddard N.J.
      • Gosling P.T.
      Intra-articular fluid pressure and pain in osteoarthritis of the hip.
      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).
      • Hawker G.A.
      • Stewart L.
      • French M.R.
      • et al.
      Understanding the pain experience in hip and knee osteoarthritis–an OARSI/OMERACT initiative.
      However, pain progression may be arrested at any stage, and not all patients go through 3 distinct stages.
      Table 2Stages of pain in OA
      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.
      • Allen K.D.
      • Coffman C.J.
      • Golightly Y.M.
      • et al.
      Daily pain variations among patients with hand, hip, and knee osteoarthritis.
      It then worsens in the late afternoon/early evening to again reduce later in the evening.
      • Allen K.D.
      • Coffman C.J.
      • Golightly Y.M.
      • et al.
      Daily pain variations among patients with hand, hip, and knee osteoarthritis.
      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.
      • Hawker G.A.
      • Stewart L.
      • French M.R.
      • et al.
      Understanding the pain experience in hip and knee osteoarthritis–an OARSI/OMERACT initiative.
      Such features also suggest comorbid fibromyalgia, another common pain syndrome in older people.
      Painful periarticular soft tissue lesions may coexist with large joint OA
      • Hill C.L.
      • Gale D.R.
      • Chaisson C.E.
      • et al.
      Periarticular lesions detected on magnetic resonance imaging: prevalence in knees with and without symptoms.
      (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.
      • Altman R.
      • Asch E.
      • Bloch D.
      • et al.
      Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association.
      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).
      • Ike R.
      • O'Rourke K.S.
      Compartment-directed physical examination of the knee can predict articular cartilage abnormalities disclosed by needle arthroscopy.
      Transmitted crepitus (felt on the adjacent periarticular bone) suggests a full-thickness cartilage defect on the affected side.
      • Ike R.
      • O'Rourke K.S.
      Compartment-directed physical examination of the knee can predict articular cartilage abnormalities disclosed by needle arthroscopy.
      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.
      • Sale J.E.
      • Gignac M.
      • Hawker G.
      The relationship between disease symptoms, life events, coping and treatment, and depression among older adults with osteoarthritis.
      • Abad V.C.
      • Sarinas P.S.
      • Guilleminault C.
      Sleep and rheumatologic disorders.
      • Imamura M.
      • Imamura S.T.
      • Kaziyama H.H.
      • et al.
      Impact of nervous system hyperalgesia on pain, disability, and quality of life in patients with knee osteoarthritis: a controlled analysis.
      • Edwards R.R.
      • Bingham 3rd, C.O.
      • Bathon J.
      • et al.
      Catastrophizing and pain in arthritis, fibromyalgia, and other rheumatic diseases.
      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.
      • Suri P.
      • Morgenroth D.C.
      • Kwoh C.K.
      • et al.
      Low back pain and other musculoskeletal pain comorbidities in individuals with symptomatic osteoarthritis of the knee: data from the osteoarthritis initiative.
      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.
      • Hurley M.V.
      • Scott D.L.
      • Rees J.
      • et al.
      Sensorimotor changes and functional performance in patients with knee osteoarthritis.
      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.
      • Petrie K.J.
      • Jago L.A.
      • Devcich D.A.
      The role of illness perceptions in patients with medical conditions.
      Risk factors for poor prognosis in OA
      • 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.
      National Institute for Health and Clinical Excellence.
      • Zhang W.
      • Doherty M.
      • Peat G.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      Peripheral joint OA may be diagnosed confidently on clinical grounds alone if there is:
      • Persistent usage-related joint pain in 1 or a few joints
      • Age ≥45 years
      • Only brief morning stiffness (≤30 minutes).
        National Institute for Health and Clinical Excellence.
      Other features listed in Table 1 add to the diagnostic certainty.
      National Institute for Health and Clinical Excellence.
      This approach to a clinical diagnosis of OA is supported by the poor correlation between radiographically assessed structural changes and symptoms in OA.
      • Bedson J.
      • Croft P.R.
      The discordance between clinical and radiographic knee osteoarthritis: a systematic search and summary of the literature.
      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.
      • Altman R.
      • Asch E.
      • Bloch D.
      • et al.
      Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.
      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.
      • Peat G.
      • Thomas E.
      • Duncan R.
      • et al.
      Clinical classification criteria for knee osteoarthritis: performance in the general population and primary care.
      However, appropriate imaging and laboratory assessments should be performed:
      • In younger individuals (ie, <45 years in age) in the absence of preceding major joint trauma,
      • 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,
      • If there is weight loss or constitutional upset,
      • 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.
      • Thorstensson C.A.
      • Andersson M.L.
      • Jonsson H.
      • et al.
      Natural course of knee osteoarthritis in middle-aged subjects with knee pain: 12-year follow-up using clinical and radiographic criteria.
      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.
      • Wolfe F.
      • Lane N.E.
      The longterm outcome of osteoarthritis: rates and predictors of joint space narrowing in symptomatic patients with knee osteoarthritis.
      Global OA severity had a similar but smaller role.
      • Wolfe F.
      • Lane N.E.
      The longterm outcome of osteoarthritis: rates and predictors of joint space narrowing in symptomatic patients with knee osteoarthritis.
      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,
      • Picavet H.S.
      • Hazes J.M.
      Prevalence of self reported musculoskeletal diseases is high.
      whereas coexistent knee chondrocalcinosis (a marker of CPPD) and knee OA occur in 2.4% of patients older than 40 years.
      • Zhang W.
      • Neame R.
      • Doherty S.
      • et al.
      Relative risk of knee chondrocalcinosis in siblings of index cases with pyrophosphate arthropathy.
      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).
      • van Saase J.L.
      • van Romunde L.K.
      • Cats A.
      • et al.
      Epidemiology of osteoarthritis: Zoetermeer survey. Comparison of radiological osteoarthritis in a Dutch population with that in 10 other populations.
      Figure thumbnail gr1
      Fig. 1Joints targeted by OA.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)

      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
      • Altman R.
      • Asch E.
      • Bloch D.
      • et al.
      Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association.
      and that is possibly better suited for clinical use (Box 2).
      Simplified clinical approach to identifying OA subsets
      • 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)
      • 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
        • 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
        • g.
          Apatite-associated destructive arthritis: old age, rapid progression; targets hips, knees, and shoulders
      • 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

      GOA

      Although it was recognized earlier, Kellgren and Moore
      • Kellgren J.H.
      • Moore R.
      Generalized osteoarthritis and Heberden's nodes.
      described a polyarticular subset of OA particularly involving the distal IPJs (DIPJs), thumb bases (first CMCJs and trapezioscaphoid joints), first MTPJs, facet joints, knees, and hips, and coined the term GOA for this subset. GOA is characterized by a slow accumulation of multiple joint involvement (compared with RA, which usually affects multiple joints synchronously). Symptoms usually commence in the hand joints around middle age and affect the knees and other joints over the next few decades. The clinical marker for GOA is the presence of multiple Heberden nodes, which are posterolateral hard swellings of the DIPJs, associated with underlying OA.
      • Kellgren J.H.
      • Moore R.
      Generalized osteoarthritis and Heberden's nodes.
      Heberden nodes are often accompanied by less well-defined posterolateral swellings of the proximal IPJs (PIPJs): so-called Bouchard nodes. A form of GOA showing identical joint targeting was subsequently identified in patients without Heberden nodes,
      • Kellgren J.H.
      • Lawrence J.S.
      • Bier F.
      Genetic factors in generalized osteo-arthrosis.
      which led to GOA being classified as nodal and non-nodal forms,
      • Kellgren J.H.
      • Lawrence J.S.
      • Bier F.
      Genetic factors in generalized osteo-arthrosis.
      the former being more common in women, and the latter mainly occurring in men.
      • Lawrence J.S.
      Generalized osteoarthrosis in a population sample.
      There is no universal definition of the number of joints that must be affected before an individual can be diagnosed as having GOA. However, guidance from ACR and The European League Against Rheumatism suggests that GOA is present if there is OA at the spine or hand, and in at least 2 other joint regions.
      • Altman R.
      • Asch E.
      • Bloch D.
      • et al.
      Development of criteria for the classification and reporting of osteoarthritis. Classification of osteoarthritis of the knee. Diagnostic and Therapeutic Criteria Committee of the American Rheumatism Association.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.

      Clinical features at the main symptomatic sites

      Hands

      Hand OA is usually bilaterally symmetric.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.
      Symptoms affect just 1 or a few joints at a time.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      Symptoms are often intermittent and occur at the target sites, namely DIPJs (∼50%), thumb bases (∼35%), PIPJs (∼20%), and MCPJs (∼10%), in descending order of frequency.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      • Dahaghin S.
      • Bierma-Zeinstra S.M.
      • Ginai A.Z.
      • et al.
      Prevalence and pattern of radiographic hand osteoarthritis and association with pain and disability (the Rotterdam Study).
      Individuals without pain may report a dull ache or stiffness.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.
      The symptoms of hand OA deteriorate in half the patients over the next 6 years.
      • Bijsterbosch J.
      • Watt I.
      • Meulenbelt I.
      • et al.
      Clinical and radiographic disease course of hand osteoarthritis and determinants of outcome after 6 years.
      The predictors of a worse clinical outcome include a high level of functional impairment at baseline and a greater number of painful joints, with no correlation between clinical change and radiographic progression.
      • Bijsterbosch J.
      • Watt I.
      • Meulenbelt I.
      • et al.
      Clinical and radiographic disease course of hand osteoarthritis and determinants of outcome after 6 years.

      Nodal OA

      Heberden and/or Bouchard nodes plus underlying IPJ OA (defined clinically and/or radiologically) constitutes nodal OA.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      It affects women more frequently than men, and familial predisposition is recognized. Symptoms usually start in middle age, often around the menopause, with pain, tenderness, and stiffness of 1 or a few DIPJs in the hands. There may be warmth and soft tissue swelling at the start. Over a period of months or years, involved IPJs usually become less painful and signs of inflammation subside, leaving behind firm to hard bony swellings on the posterolateral aspect of the IPJs, termed Heberden (DIPJ) and Bouchard (PIPJ) nodes (Fig. 2). Over the next decade or so, other IPJs go through the same process, in a monoarthritis multiplex manner. Established DIPJ (or PIPJ) nodes sometimes coalesce to form a single dorsal bar (see Fig. 2). In addition to bony swelling, the affected IPJs commonly deviate laterally (radial or ulnar, with most deviations pointing toward the middle finger) and have reduced range of movement. Lateral deviation at the IPJs without IPJ instability is a characteristic feature of nodal OA (Fig. 3). Nodal OA is most common at the index and middle fingers.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.
      Fully evolved nodes are not painful, and usually associate with a good long-term functional outcome. However, some patients are concerned by the cosmetic aspect of these deformities.
      Figure thumbnail gr2
      Fig. 2(A) Heberden nodes appearing as discrete posterolateral swelling over the DIPJs, and (B) coalescing to form a single dorsal bar.
      Figure thumbnail gr3
      Fig. 3Heberden nodes and lateral deviation of IPJs in nodal OA.
      The thumb base, comprising the first CMCJ and trapezioscaphoid joint, is another target site for OA. Thumb base OA presents with pain on joint use at the thumb base area with some distal and proximal radiation. There may be radial subluxation of the metacarpal base or adduction at the thumb base, giving it a swollen, squared appearance (Fig. 4).
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand.
      Unlike IPJ OA, thumb base OA associates with persistent symptoms and with greater functional impairment (occasionally requiring surgery), so the prognosis is generally worse.
      Figure thumbnail gr4
      Fig. 4Thumb base OA: squaring of the thumb base, caused by osteophytosis and subluxation at the first carpometacarpal joint.
      OA mainly targets the second, third, and first MCPJs, in descending order of frequency, often causing bony enlargement without signs or symptoms of synovitis.
      • Dahaghin S.
      • Bierma-Zeinstra S.M.
      • Ginai A.Z.
      • et al.
      Prevalence and pattern of radiographic hand osteoarthritis and association with pain and disability (the Rotterdam Study).
      Isolated MCPJ OA sometimes occurs in elderly people who have had physically demanding occupations (Missouri arthritis).
      • Williams W.V.
      • Cope R.
      • Gaunt W.D.
      • et al.
      Metacarpophalangeal arthropathy associated with manual labor (Missouri metacarpal syndrome). Clinical radiographic, and pathologic characteristics of an unusual degeneration process.
      Widespread MCPJ changes, especially with wrist arthropathy or chondrocalcinosis, suggest the possibility of hemochromatosis.

      Erosive OA

      Erosive OA is an aggressive subset of hand OA. It presents with subacute or insidious onset of pain, stiffness, soft tissue swelling, and sometimes paresthesia affecting multiple IPJs (synchronous polyarticular onset).
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      • Punzi L.
      • Ramonda R.
      • Sfriso P.
      Erosive osteoarthritis.
      Pain, tenderness, inflammation (warmth, soft tissue swelling, sometimes erythema) are more marked and prolonged compared with nodal hand OA
      • Punzi L.
      • Ramonda R.
      • Sfriso P.
      Erosive osteoarthritis.
      • Punzi L.
      • Frigato M.
      • Frallonardo P.
      • et al.
      Inflammatory osteoarthritis of the hand.
      and there is no association with GOA. Erosive OA usually spares the thumb base and MCPJs
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      and targets DIPJs more commonly than PIPJs (Fig. 5).
      • Punzi L.
      • Frigato M.
      • Frallonardo P.
      • et al.
      Inflammatory osteoarthritis of the hand.
      Lateral instability and ankylosis at the IPJs are uncommon but characteristic clinical findings in erosive OA (Fig. 6). There may rarely be an opera-glass deformity,
      • Punzi L.
      • Frigato M.
      • Frallonardo P.
      • et al.
      Inflammatory osteoarthritis of the hand.
      and Heberden, and/or Bouchard nodes may coexist.
      • Bijsterbosch J.
      • Watt I.
      • Meulenbelt I.
      • et al.
      Clinical burden of erosive hand osteoarthritis and its relationship to nodes.
      Erosive OA is defined radiographically by subchondral erosion, cortical destruction, marked bone and cartilage attrition, and subsequent reparative change that may include bony ankylosis. It has a worse outcome in terms of symptom persistence and functional impairment than nonerosive hand OA.
      • Zhang W.
      • Doherty M.
      • Leeb B.F.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      Although erosive OA as a clinical entity is rare, radiographic erosions are present in 1 or a few joints in up to 8.5% of patients with symptomatic hand OA.
      • Cavasin F.
      • Punzi L.
      • Ramonda R.
      • et al.
      The differential diagnosis for hand OA is wide, and includes:
      • Psoriatic arthritis: targets DIPJs or affects just 1 ray
      • RA: targets wrists, MCPJs, PIPJs
      • Gout: may be superimposed on preexisting hand OA
      • Hemochromatosis: mainly targets MCPJs, and wrists
        • Zhang W.
        • Doherty M.
        • Leeb B.F.
        • et al.
        EULAR evidence-based recommendations for the diagnosis of hand osteoarthritis: report of a task force of ESCISIT.
      Figure thumbnail gr5
      Fig. 5Erosive OA: marked radial deviation and fixed flexion deformity in the left middle PIPJ, radial deviation with restriction in the index PIPJ, and bony swelling of both fingers. Note the absence of Heberden nodes.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)
      Figure thumbnail gr6
      Fig. 6Erosive OA: marked radial/ulnar instability. Such instability does not usually occur with the common hand OA.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)

      OA at Other Upper Limb Joints

      OA may be present in the other upper limb joints, especially in the presence of occupational risk factors. For example, people with mechanically demanding jobs can develop elbow, shoulder, wrist, and acromioclavicular joint OA. Shoulder (glenohumeral joint) OA may also be a consequence of, or associate with, rotator cuff tear. The symptom at these joints is as for OA in other joints (see Table 1) and is most commonly unilateral.

      Knee

      The knee is an important target site for OA. Knee OA alone is the commonest cause of lower limb disability in elderly people. It is usually bilateral, although symptoms may be more pronounced on 1 side. Unilateral knee OA is more common in young men, and is often caused by prior knee injury or surgery. Most patients with knee OA have medial compartment tibiofemoral joint (TFJ) OA, PFJ OA, or a combination of both.
      • Duncan R.C.
      • Hay E.M.
      • Saklatvala J.
      • et al.
      Prevalence of radiographic osteoarthritis–it all depends on your point of view.
      • Ledingham J.
      • Regan M.
      • Jones A.
      • et al.
      Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital.
      Knee joint pain is felt anteriorly and the location and pattern of pain indicate the affected compartment(s). Pain is anteromedial in medial compartment TFJ OA, and anterior and behind the patella in PFJ OA.
      • Creamer P.
      • Lethbridge-Cejku M.
      • Hochberg M.C.
      Where does it hurt? Pain localization in osteoarthritis of the knee.
      Pain from PFJ OA is typically worsened by prolonged sitting, standing up from low chairs, and climbing stairs or inclines (coming down often being more painful than going up). Generalized knee pain with distal radiation suggests moderate to severe knee OA.
      • Wood L.R.
      • Peat G.
      • Thomas E.
      • et al.
      Knee osteoarthritis in community-dwelling older adults: are there characteristic patterns of pain location?.
      Persistent rest and night pain occur in advanced OA.
      • Zhang W.
      • Doherty M.
      • Peat G.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis.
      Knee OA symptoms usually do not cause posterior knee pain unless there is a complicating popliteal (Baker) cyst. Apart from pain, there may be a feeling of giving way (especially with PFJ OA and/or quadriceps weakness) and instability, both of which associate with falls.
      • Zhang W.
      • Doherty M.
      • Peat G.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis.
      On examination, the findings are typical of OA (see Table 1). Tibiofemoral joint-line tenderness is felt anteriorly, on either side of the patella tendon with the knee flexed. Pain on patellofemoral compression, deformity (fixed flexion and/or varus; less commonly valgus deformity on weight bearing), quadriceps wasting and weakness, and hip muscle weakness may be present (Fig. 7).
      • Zhang W.
      • Doherty M.
      • Peat G.
      • et al.
      EULAR evidence-based recommendations for the diagnosis of knee osteoarthritis.
      • Slemenda C.
      • Brandt K.D.
      • Heilman D.K.
      • et al.
      Quadriceps weakness and osteoarthritis of the knee.
      • Hinman R.S.
      • Hunt M.A.
      • Creaby M.W.
      • et al.
      Hip muscle weakness in individuals with medial knee osteoarthritis.
      Knee effusion is common, and increases in prevalence with the severity of knee OA. For example, in a study, 36% of patients with symptomatic knee OA (Kellgren and Lawrence [K&L] score ≥2) had a clinical knee effusion, whereas only 16% of symptomatic preradiographic knee OA (magnetic resonance imaging cartilage score ≥2, and K&L score ≤2) had clinically detectable knee effusion.
      • Cibere J.
      • Zhang H.
      • Thorne A.
      • et al.
      Association of clinical findings with pre-radiographic and radiographic knee osteoarthritis in a population-based study.
      Figure thumbnail gr7
      Fig. 7Unilateral knee OA: swollen left knee with varus and fixed flexion deformities in a 63-year-old man with a history of knee trauma. On palpation there was marked crepitus, restricted flexion, bony swelling, and a small effusion. The cruciates were intact but there was minor varus/valgus instability on stress testing.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)
      Several painful periarticular soft tissue disorders coexist with knee OA and require careful assessment (Table 3).
      • Hill C.L.
      • Gale D.R.
      • Chaisson C.E.
      • et al.
      Periarticular lesions detected on magnetic resonance imaging: prevalence in knees with and without symptoms.
      • O'Reilly S.
      • Doherty M.
      Signs, symptoms, and laboratory tests.
      • Rothstein C.P.
      • Laorr A.
      • Helms C.A.
      • et al.
      Semimembranosus-tibial collateral ligament bursitis: MR imaging findings.
      Table 3Common periarticular lesions that coexist with knee OA
      Soft Tissue DisorderSigns and Symptoms
      Anserine bursitisInferomedial knee pain, localized soft tissue swelling (rarely), tenderness over the upper medial tibia
      Semimembranosus-tibial collateral ligament bursitisMedial knee pain, tenderness closer to the joint line than in anserine bursitis
      Medial collateral ligament (inferior insertion) enthesopathyMedial knee pain, localized tenderness, and pain on stressing the medial ligament (valgus strain with knee unlocked)
      Tender medial fat padMedial knee pain, tenderness over either the inferior or superior fat pad below or above the joint line
      Iliotibial tract (band) syndromeLateral distal thigh and knee pain, and tenderness maximal over the lateral femoral condyle

      Hip

      Hip OA presents with pain, stiffness, and restricted movement. Pain caused by hip OA is usually maximal deep in the anterior groin, but may spread to the anteromedial or upper lateral thigh, and occasionally the buttocks. Distal radiation is common, and pain may predominate at the knee. Some people present with knee pain without any proximal pain; unlike knee-originated pain, such hip-referred pain is usually more generalized, involves the distal thigh, and may be improved by rubbing. Pain in hip OA is exacerbated by rising from a seated position, and during initial or midambulation.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      It may be difficult to differentiate hip OA pain from referred spinal pain or concomitant knee OA,
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      and intra-articular local anesthetic injection may be required to resolve any diagnostic uncertainty.
      • Crawford R.W.
      • Gie G.A.
      • Ling R.S.
      • et al.
      Diagnostic value of intra-articular anaesthetic in primary osteoarthritis of the hip.
      Unlike knee OA, hip OA is often unilateral.
      • Gofton J.P.
      Studies in osteoarthritis of the hip. I. Classification.
      Both active and passive hip movements may be painful.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      Internal rotation with the hip flexed is frequently the earliest movement to be restricted, but movements may be globally restricted in severe disease (Fig. 8).
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      The typical end-stage deformity in hip OA is external rotation, adduction, and fixed flexion (Fig. 9). Wasting of thigh muscles, positive Trendelenburg test, antalgic gait, and shortening of the affected extremity may also be present.
      • Altman R.
      • Alarcon G.
      • Appelrouth D.
      • et al.
      The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hip.
      However, such end-stage hip OA should be rare in modern clinical practice.
      Figure thumbnail gr8
      Fig. 8Patient with right hip OA showing fixed flexion and external rotation deformity.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)
      Figure thumbnail gr9
      Fig. 9Patient with hip OA, showing painful restriction in internal rotation in flexion: the tight-pack position for the hip and the first movement to be affected.
      (Reproduced from Abhishek A, Doherty M. Disease diagnosis and clinical presentation. In: Henrotin Y, Hunter DJ, Kawaguchi H, editors. OARSI Online Primer. OARSI; 2011; with permission.)
      Hip OA may be subclassified largely according to radiographic features, specifically
      • Ledingham J.
      • Dawson S.
      • Preston B.
      • et al.
      Radiographic patterns and associations of osteoarthritis of the hip.
      • Lanyon P.
      • Muir K.
      • Doherty S.
      • et al.
      Influence of radiographic phenotype on risk of hip osteoarthritis within families.
      :
      • 1.
        Pattern of radiographic femoral head migration
        • a.
          Superior: most usual pattern (especially in men), likely to be unilateral at presentation and to progress more rapidly
        • b.
          Axial (along the axis of the femoral neck): progresses more slowly
        • c.
          Medial: mainly in women, likely to be bilateral and associate with Heberden nodes
      • 2.
        Bone response to joint space loss
        • a.
          Atrophic: characterized by marked bone attrition and minimal osteophytosis, common in elderly, associated with chondrocalcinosis
        • b.
          Hypertrophic: characterized by florid osteophytosis
      In some patients, especially elderly women, hip OA can be rapidly progressive with a subacute onset of symptoms that progresses to joint destruction and instability in a matter of months rather than years. The radiographs may show paradoxic widening of joint space (although this is reduced or absent if standing or stressed films are taken), marked bone attrition, destruction of the femoral head, and paucity of osteophytosis (atrophic OA).
      • Della Torre P.
      • Picuti G.
      • Di Filippo P.
      Rapidly progressive osteoarthritis of the hip.
      Such rapidly progressive destructive arthropathy has been associated with BCP (mainly hydroxyapatite) crystals, and termed apatite-associated destructive arthropathy (AADA).
      • Dieppe P.A.
      • Crocker P.
      • Huskisson E.C.
      • et al.
      Apatite deposition disease. A new arthropathy.
      • Dieppe P.A.
      • Doherty M.
      • Macfarlane D.G.
      • et al.
      Apatite associated destructive arthritis.
      • Nuki G.
      Apatite associated arthritis.
      Shoulders (Milwaukee shoulder)
      • McCarty D.J.
      • Halverson P.B.
      • Carrera G.F.
      • et al.
      “Milwaukee shoulder”–association of microspheroids containing hydroxyapatite crystals, active collagenase, and neutral protease with rotator cuff defects. I. Clinical aspects.
      and knees are other target sites for AADA. Muscle wasting, deformities, and moderate to large joint effusions with noninflammatory (viscous, occasionally hemorrhagic, low cell count) synovial fluid are common.
      Several other disorders may lead to pain around the hip region.
      • Williams B.S.
      • Cohen S.P.
      Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment.
      For example, anterior groin pain may be caused by osteonecrosis (avascular necrosis) of the femoral head.
      • Williams B.S.
      • Cohen S.P.
      Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment.
      With this, pain is initially usually night predominant, well localized, unrelated to usage and progressive, becoming worse on usage and more widespread once the femoral bone and overlying cartilage collapse to result in arthropathy. Posterior hip and buttock pain may be caused by lumbar radiculopathy, iliolumbar ligament syndrome, sacroiliac joint pain, and hip extensor or rotator muscle strain.
      • Williams B.S.
      • Cohen S.P.
      Greater trochanteric pain syndrome: a review of anatomy, diagnosis and treatment.
      Other periarticular disorders that may coexist with hip OA are listed in Table 4.
      Table 4Common periarticular lesions near the hip
      Soft Tissue DisorderSigns and Symptoms
      Trochanteric bursitis/gluteus medius tendinitis
      Most common.
      Lateral hip pain, worse on lying on that side at night and reproduced by pressure over the greater trochanter region
      Iliopsoas bursitisAnterior groin pain ± swelling. Frequently associates with other arthropathies
      Ischiogluteal bursitisPain over the ischia, aggravated by local pressure brought on by sitting and lying. Local tenderness present
      Adductor tendinitisMedial groin pain aggravated by passive hip abduction and resisted active adduction
      a Most common.

      Facet Joint OA

      It is often difficult to attribute symptoms to facet joint OA because it commonly coexists with intervertebral disk degeneration. However, lumbar facet joint OA is thought to lead to localized lumbar pain, which may radiate unilaterally or bilaterally to the buttocks, groins, and thighs, typically ending above the knees.
      • Kalichman L.
      • Hunter D.J.
      Lumbar facet joint osteoarthritis: a review.
      Symptoms are worse in the morning and during periods of inactivity, and are increased by stress, exercise, lumbar spine extension, rotary motions, and when standing or sitting.
      • Kalichman L.
      • Hunter D.J.
      Lumbar facet joint osteoarthritis: a review.
      Lying flat and flexion of the lumbar spine lead to pain relief.
      • Kalichman L.
      • Hunter D.J.
      Lumbar facet joint osteoarthritis: a review.
      Cervical facet joint OA similarly may present with ipsilateral neck pain that does not radiate beyond the shoulder, and is worsened by neck rotation or extension.
      • van Eerd M.
      • Patijn J.
      • Lataster A.
      • et al.
      5. Cervical facet pain.
      The osteophytes in facet joint OA may also impinge on nerve roots and lead to radiculopathy.

      First MTPJ OA

      First MTPJ OA is usually bilateral, and when symptomatic, causes localized big toe pain mainly on standing and during ambulation. Bony enlargement of the first MTPJ may be present (Fig. 11). Hallux valgus (distal end of big toe points toward the midline of the foot), hallux rigidus (restricted flexion, and extension at the first MTPJ), and crossover toes are the other common deformities. Bony enlargement at the first MTPJ and hallux valgus frequently lead to the development of a complicating bursa with additional fibrous tissue reaction on the medial aspect of the first MTPJ (bunion; Fig. 10). This joint may get inflamed (eg, by rubbing against footwear) and cause medial big toe pain. Apart from the first MTPJ, OA also commonly targets the talonavicular joint in the midfoot (aggravated by pes planus; see Fig. 11), and sometimes the ankle and subtalar joints in the hindfoot (especially in those with previous trauma).
      Figure thumbnail gr10
      Fig. 10First MTPJ OA with hallux valgus and an inflamed overlying superficial bursa (“bunion”).
      Figure thumbnail gr11
      Fig. 11Midfoot OA aggravated by pes planus. Note coexistent hallux valgus, suggesting first MTPJ OA.

      OA with CPPD

      OA with CPPD commonly occurs at the knee, radiocarpal joint, second to third MCPJs, shoulder joint, and elbow joint. Patients with OA plus CPPD are usually older than 60 years.
      • Dieppe P.A.
      • Alexander G.J.
      • Jones H.E.
      • et al.
      Pyrophosphate arthropathy: a clinical and radiological study of 105 cases.
      • Felson D.T.
      • Anderson J.J.
      • Naimark A.
      • et al.
      The prevalence of chondrocalcinosis in the elderly and its association with knee osteoarthritis: the Framingham Study.
      More than a quarter of patients with knee OA who require hospital referral, and more than half of those undergoing total knee replacement for OA, have CPPD.
      • Ledingham J.
      • Regan M.
      • Jones A.
      • et al.
      Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital.
      • Viriyavejkul P.
      • Wilairatana V.
      • Tanavalee A.
      • et al.
      Comparison of characteristics of patients with and without calcium pyrophosphate dihydrate crystal deposition disease who underwent total knee replacement surgery for osteoarthritis.
      The presence of CPPD may modify OA symptoms,
      • Ledingham J.
      • Regan M.
      • Jones A.
      • et al.
      Radiographic patterns and associations of osteoarthritis of the knee in patients referred to hospital.
      • Pattrick M.
      • Hamilton E.
      • Wilson R.
      • et al.
      Association of radiographic changes of osteoarthritis, symptoms, and synovial fluid particles in 300 knees.
      presumably because CPP crystals are hard, negatively charged particles that can exert both proinflammatory and adverse mechanical effects.
      • Liu Y.Z.
      • Jackson A.P.
      • Cosgrove S.D.
      Contribution of calcium-containing crystals to cartilage degradation and synovial inflammation in osteoarthritis.
      Compared with OA without CPPD, there may be a longer duration of early morning stiffness and more common and pronounced acute, intermittent, or low-grade and persistent synovitis (Fig. 12). Joint effusions are common, and may be hemorrhagic or turbid on aspiration. Large effusions, mainly at the knee or the shoulder, may leak into the surrounding soft tissues and lead to localized pain, swelling, and extensive bruising. Although studies give conflicting results, it is likely that OA with CPPD is not more rapidly progressive than OA alone.
      • Viriyavejkul P.
      • Wilairatana V.
      • Tanavalee A.
      • et al.
      Comparison of characteristics of patients with and without calcium pyrophosphate dihydrate crystal deposition disease who underwent total knee replacement surgery for osteoarthritis.
      • Ledingham J.
      • Regan M.
      • Jones A.
      • et al.
      Factors affecting radiographic progression of knee osteoarthritis.
      • Neogi T.
      • Nevitt M.
      • Niu J.
      • et al.
      Lack of association between chondrocalcinosis and increased risk of cartilage loss in knees with osteoarthritis: results of two prospective longitudinal magnetic resonance imaging studies.
      However, there are anecdotal reports of patients with CPPD developing rapidly progressive destructive arthropathy at knees, shoulders, or hips. Some patients with OA with CPPD may have polyarticular arthropathy involving the knees, wrists, and the MCPJs that superficially mimics RA.
      Figure thumbnail gr12
      Fig. 12Knee effusions are usually not marked in OA. This person with OA plus CPPD had a large left knee effusion expanding the suprapatellar pouch, giving a positive balloon sign (fluctuance) on palpation.

      Clinical features influence the management of OA

      Because OA has a diverse clinical presentation, it is important to target the therapeutic intervention to the patient, and to the symptoms. Patient education, appropriate advice concerning exercise and activity (ideally with physiotherapy and/or occupational therapy input), avoidance of adverse biomechanical factors, and adjunctive analgesia, are core to the management of OA. Oral paracetamol and topical analgesics (nonsteroidal antiinflamatory drugs, capsaicin) are recommended analgesics to try first, mainly based on their safety, but subsequent choice of analgesic depends on the clinical feature. For example, patients with pain and nonrestorative sleep may benefit from amitriptyline, nortriptyline, or duloxetine,
      • Carville S.F.
      • Arendt-Nielsen S.
      • Bliddal H.
      • et al.
      EULAR evidence-based recommendations for the management of fibromyalgia syndrome.
      whereas patients with neuropathic features to their pain may benefit from duloxetine, pregabalin, or amitriptyline.
      Some patients who present with rapidly progressive severe OA of the knees or hips may warrant consideration for joint replacement surgery, whereas others who present with exacerbation of their joint symptoms may benefit from local intra-articular injections of corticosteroid to achieve short-term symptom control. The latter is especially true in those with thumb base, knee, and hip OA. Those with superadded acute CPP crystal arthritis may also derive rapid benefit from intra-articular corticosteroid injection and/or colchicine. In contrast, asymptomatic radiographic changes of OA in peripheral or spinal joints in the elderly require no further interventions apart from possibly modifying risk factors for the progression of OA (eg, obesity). The presence of comorbid fibromyalgia should be specifically sought and treated in patients who present with severe OA, and in those with symptomatic OA at several sites. Patients with GOA may have a worse prognosis than those without GOA, and should be targeted for risk factor modification (eg, patients with knee OA in the context of GOA are at higher risk of progression of their knee OA).
      • Chapple C.M.
      • Nicholson H.
      • Baxter G.D.
      • et al.
      Patient characteristics that predict progression of knee osteoarthritis: a systematic review of prognostic studies.

      Summary

      Usage-related pain, short-lived morning/inactivity stiffness, and locomotor restriction are the most common symptoms of OA. In patients with typical presentation at the target sites, clinical assessment alone is sufficient to allow a diagnosis of OA. Patients with OA should be assessed in a holistic manner, which should include a targeted examination for the associated comorbidities.

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