Osteoarthritis

• Osteoarthritis (OA) is the most common form of arthritis: a slowly progressive, whole-joint disease rather than simple "wear and tear" of cartilage.
• It is defined by the combination of focal loss of articular cartilage and new bone formation at the joint margin (osteophytes), with low-grade inflammation of the synovium.
• Pain is activity-related and brief stiffness after rest; it most often affects the knees, hips and hands.
• The clinical picture is usually enough for diagnosis in a person aged 45 or over with activity-related joint pain and morning stiffness lasting no more than 30 minutes. ^[1]
• Core management is the same everywhere: education, tailored therapeutic exercise and weight management, with simple analgesia and joint replacement reserved for severe disease.

By the end of this page you should be able to:

1. Define osteoarthritis and distinguish it from inflammatory arthritides.
2. Explain why cartilage loss and osteophyte formation occur, and how they produce symptoms.
3. Recognise the typical patterns of hand, knee and hip osteoarthritis, including Heberden and Bouchard nodes.
4. Diagnose osteoarthritis in primary care without imaging, and know when an X-ray is genuinely useful.
5. Outline a management plan that follows current NICE, OARSI and ACR guidance, including exercise, weight loss, drugs, injections and referral for joint replacement.
6. Recognise red flags that suggest something other than osteoarthritis is present.

The word "osteoarthritis" is slightly misleading: there is no marked synovial proliferation of the kind seen in rheumatoid disease, and the damage is usually focal rather than uniform. The disease affects the joint as an organ (cartilage, bone, synovium, meniscus, capsule and supporting muscle), which is why treatments aimed only at cartilage rarely succeed. Cartilage itself has no nerve supply, so the pain of OA comes from subchondral bone, the joint capsule, periosteum and inflamed synovium rather than from the smooth surface that is seen on imaging.

Osteoarthritis is usually classified in two useful ways.

• Primary (idiopathic) OA develops without a single identifiable cause, usually in later life and often in several joints. It is the common pattern in the knees, hips and hands of older adults.
• Secondary OA follows a recognised insult: prior trauma, fracture or meniscal injury, congenital or developmental deformity, inflammatory arthritis, crystal disease, avascular necrosis, Paget disease of bone or other metabolic disorder. It often appears earlier, may be unilateral, and tends to progress faster.

A further clinical distinction is by distribution:

• Localised OA affects one or a few joints.
• Generalised OA affects several joint groups, often with nodal (hand) disease.
• Nodal OA of the hands, with Heberden and Bouchard nodes.
• Erosive OA of the hands, a more inflammatory, destructive variant.
• Rapidly destructive OA, an uncommon but aggressive form, classically of the hip.

Heberden nodes are bony enlargements at the distal interphalangeal joints; Bouchard nodes are bony enlargements at the proximal interphalangeal joints. Both represent osteophytes and represent clinical markers of nodal disease. They are usually painless once formed, but can be tender during active disease. Together with base-of-thumb (first carpometacarpal) osteoarthritis, they define the hand pattern most students are asked to recognise.

Osteoarthritis is the most common form of arthritis. ACR 2019 estimated that it affects about 302 million people worldwide and that it is a leading cause of disability among older adults. ^[3] The knees, hips and hands are the most commonly affected appendicular joints. ^[3] Prevalence rises steeply with age, and the condition is usually more common and more disabling in women after mid-life, although reported ratios vary between populations and joints.

Because the disease is strongly age-related and survival is long, an "epidemic" of symptomatic OA is being driven by ageing populations and rising body weight. ^[3] Primary care therefore sees knee and hand disease most often, and orthopaedic services see end-stage hip and knee disease most often. In most regions there is no population screening programme: case-finding is clinical, triggered by joint pain in an older adult.

A single cause is rarely identified in older adults. OA is best understood as the outcome of a mismatch between the mechanical load a joint experiences and the ability of cartilage, meniscus and subchondral bone to absorb it. The table lists the factors a student should be able to discuss in an examination.

Ask about body weight, occupation, previous injury and family history whenever a patient presents with new joint pain. The strongest modifiable targets for an individual patient are body weight and muscular conditioning.

OA is a sequence, not an event. Understanding the sequence explains both the symptoms and why early imaging is unhelpful.

1. Cartilage matrix degrades. Chondrocytes shift from a resting to a repair phenotype and release matrix metalloproteinases and aggrecanases. Proteoglycan content falls, water content rises and the cartilage becomes soft and fibrillated. The change starts focally, often in a high-load area, and spreads.
2. Subchondral bone changes. Increased bone turnover thickens and stiffens the subchondral plate; bone marrow lesions appear. Because bone is pain-sensitive, this is a major source of pain.
3. Osteophytes form. Mesenchymal cells at the joint margin differentiate into bone and produce the bony spurs that are the hallmark of OA. Osteophytes can stabilise the joint but also cause mechanical block and impingement.
4. The synovium inflames. Synovial macrophages react to cartilage debris and crystals of hydroxyapatite or calcium pyrophosphate. The resulting low-grade synovitis produces effusion, stiffness and pain.
5. Soft tissues and muscle decline. Quadriceps weakness and reduced proprioception allow abnormal loading, accelerating the mechanical damage. Pain leads to disuse, which leads to more weakness.
6. Joint shape changes. Loss of cartilage and osteophyte growth alter joint geometry, producing deformity (varus or valgus knee, fixed flexion). Once deformity and bone-on-bone contact are established, the change is largely irreversible.

The key message for a student is that OA is active biology throughout: it is a failure of repair as much as a failure of resistance.

At arthroscopy or post-mortem, OA shows focal loss of articular cartilage, with a softened, fibrillated surface, the earliest changes in high-load areas. Osteophytes appear at the joint margins, the synovium may be mildly inflamed, and the subchondral bone becomes dense and sometimes cystic. Under the microscope, cartilage shows loss of proteoglycan staining, chondrocyte clustering and cell death, while subchondral bone shows thickened trabeculae and remodelling. Histology is rarely needed for the diagnosis, but excised or replaced joint material shows these changes clearly, and biopsy may be used when tumour or infection is suspected.

The patient's words usually reveal the diagnosis before the examination begins.

• Pain is the leading symptom. It is felt deep in the joint, is worse on use and weight-bearing, and eases with rest. In advanced disease the pain can be present at night or at rest.
• Stiffness occurs after periods of inactivity ("gelling") and after waking. In OA it lasts less than 30 minutes; prolonged morning stiffness points away from OA and towards an inflammatory arthritis.
• Functional loss is often the real complaint: difficulty rising from a chair, climbing stairs, kneeling, opening jars, turning keys or walking distance. Ask about specific tasks rather than "how are you".
• Swelling may be episodic and follows activity. A sudden hot, swollen joint suggests crystal arthritis, infection or an inflammatory flare rather than uncomplicated OA.
• Flares are defined as a temporary worsening of pain, swelling and stiffness that is worse than normal, may affect sleep, activity, function and psychological wellbeing, and may lead to change in therapy for at least 24 hours. ^[1]
• Crepitus may be reported as grinding, clicking or "bone on bone" during movement.
• No systemic symptoms are expected. Fever, weight loss, prolonged morning stiffness or multiple small-joint swelling are red flags.

Observe the patient walking in and rising from a chair before asking them to undress a joint. Look, feel and move each joint in turn.

• Inspection for deformity (varus or valgus angulation, flexion contracture), bony enlargement, swelling and muscle wasting. In the hand, look for Heberden nodes at the distal interphalangeal joints and Bouchard nodes at the proximal interphalangeal joints, and for swelling or pronation at the base of the thumb.
• Palpation for warmth (minimal in uncomplicated OA; marked warmth suggests inflammation or infection), joint-line tenderness, effusion and crepitus. Press each interphalangeal joint individually; many nodes are painless once formed.
• Range of movement is reduced by pain and by capsular contracture. Crepitus on movement is common. Fixed flexion deformity of the knee or hip is a marker of advanced disease.
• Muscle strength around the joint is often reduced, especially quadriceps strength in knee OA.
• Special tests for the knee include assessment of varus and valgus stability and the presence of an effusion. For the hip, the FADIR and FABER tests are useful when considering alternative pathology; forced internal rotation and flexion that reproduce groin pain suggest hip-driven pain.
• Gait may show an antalgic limp, shortened stride or trunk lean over the affected side in hip disease.

Hand. The classic pattern involves the distal interphalangeal, proximal interphalangeal and first carpometacarpal joints, often bilaterally but asymmetrically. The metacarpophalangeal joints are relatively spared, in contrast to rheumatoid arthritis. Heberden and Bouchard nodes are common, and base-of-thumb osteoarthritis causes pain on pinch and grip. The erosive variant causes more inflammatory symptoms and joint destruction.

Knee. Tibiofemoral (medial compartment predominates) and patellofemoral disease are both common. Pain is felt around or behind the kneecap, or along the joint line. Stiffness, swelling after activity, giving way and varus deformity are typical. Quadriceps wasting and a fixed flexion deformity mark severe disease.

Hip. Pain is usually groin pain, sometimes referred to the anterior thigh or knee. It is worse on walking, turning in bed and putting on shoes or socks. Internal rotation is the first movement lost. Abductor weakness and a limp are common. Hip OA can masquerade as lumbar spine or knee disease.

A single hot swollen joint, recent trauma, prolonged morning stiffness, rapid progression or deformity, fever or weight loss should make you think again. ^[1] In these cases imaging and laboratory tests, rather than a clinical diagnosis of OA, are appropriate.

Osteoarthritis is usually diagnosed clinically, but it co-exists with other conditions and mimics them. The table separates the common mimics by the feature that most reliably distinguishes them.

Figure 1F66-rizoartrosis-AL

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Long description

An AP radiograph of the right thumb of a 66-year-old woman showing trapeziometacarpal osteoarthritis with joint space narrowing, subchondral sclerosis, and osteophytes.

Osteoarthritis is a clinical diagnosis. Imaging should be used to answer a specific question, not to label the disease.

Radiographic severity is commonly graded with the Kellgren-Lawrence system, which records joint-space narrowing, osteophytes, subchondral sclerosis and deformity from no radiographic disease to severe disease. A high grade on an X-ray is not the same as a severe patient: images correlate poorly with symptoms, and treatment should follow symptoms and function rather than the film. ^[1]

The diagnostic approach is deliberately simple. NICE guidance states that OA should be diagnosed clinically without imaging in a person who is 45 or over, has activity-related joint pain and has either no morning joint-related stiffness or morning stiffness that lasts no longer than 30 minutes. ^[1] This keeps diagnosis practical and avoids unnecessary radiation. Imaging is reserved for atypical features or where an alternative or additional diagnosis is suspected. ^[1]

Severity in routine practice is judged clinically: pain intensity, limitation of everyday tasks, deformity, gait and the impact on sleep, work and mood. Numerical scoring systems (for example WOMAC, KOOS or HOOS) are useful for measuring change in trials and after arthroplasty, but NICE advises using clinical assessment rather than a numerical severity score to decide when to refer for joint replacement. ^[1]

Management of OA rests on a small set of principles that apply to every patient, from every guideline:

• The patient is the manager; the clinician is the adviser. Explain the diagnosis, its cause and its course, and correct the common myths (OA is not simply "wearing out", rest does not cure it, and activity does not wear the joint away faster).
• Treat symptoms and function, not the X-ray.
• The core treatments are therapeutic exercise and weight management (if appropriate), along with information and support. ^[1]
• Start with treatments that have the least systemic exposure or toxicity.
• Use drugs at the lowest effective dose for the shortest possible time. ^[1]
• Escalate to injections, then joint replacement, only when core and drug treatment are ineffective or unsuitable.

Therapeutic exercise is the central non-surgical treatment for osteoarthritis. Offer exercise tailored to the patient's needs (local muscle strengthening and general aerobic fitness) to everyone with OA, and consider supervised sessions. ^[1] Pain may initially increase when exercise begins; explain that regular, consistent exercise reduces pain and improves function over time and that long-term adherence magnifies the benefit. ^[1] Combining exercise with an education or behaviour-change programme in a structured treatment package helps. ^[1]

The best exercise is the one the patient will actually do. Options with good evidence include walking (often the most accessible), stationary cycling, strengthening with machines, bands or body weight, neuromuscular training for the knee and aquatic exercise. Programmes work better when supervised (often by a physiotherapist) and when combined with self-management support or weight loss. ^[3] No hierarchy of one exercise over another is implied in current guidance, and there is insufficient evidence to prescribe an exact type, dose or intensity. ^[3]

Weight management helps whenever the patient is overweight. In OA, any weight loss is likely to be beneficial, but losing 10% of body weight is likely to be better than losing 5%. ^[1] ACR 2019, summarising a dose-response relationship, notes that loss of at least 5% of body weight can be associated with changes in clinical and mechanistic outcomes, with increasing benefit at 5-10%, 10-20% and above 20% of body weight, and that weight loss works best together with exercise. ^[3] Refer for dietetic support and use shared goal-setting rather than prescribing a number.

Manual therapy should only be considered for hip or knee OA and only alongside exercise. ^[1] ACR 2019 advises against adding manual therapy to exercise alone in knee or hip OA. ^[3]

Adjuncts that may help selected patients: walking aids for lower-limb disease (walking sticks, crutches, frames and rollators), ^[1] tibiofemoral knee bracing for tibiofemoral disease, hand orthoses for first carpometacarpal OA, and patellofemoral bracing for patellofemoral disease. ^[3] Devices such as insoles, splints or supports should not be used routinely; reserve them for joint instability or abnormal loading when exercise alone is not enough. ^[1]

Approaches not to use: acupuncture or dry needling, ^[1] electrotherapy (TENS, ultrasound, interferential, laser, pulsed short-wave, neuromuscular stimulation), ^[1] arthroscopic lavage or debridement, ^[1] intra-articular hyaluronic acid (not offered; NICE advises against it, ^[1] and OARSI 2019 does not recommend it for hip or polyarticular disease ^[2]), glucosamine and strong opioids. ^[1] ACR 2019 additionally lists colchicine, fish oil, lateral or medial wedged insoles, modified shoes, massage, iontophoresis and pulsed vibration therapy as not recommended. ^[3] Capsaicin is conditionally recommended for knee OA in the ACR guideline but conditionally recommended against for hand disease. ^[3]

Drug treatment supports exercise and weight loss; it does not replace them. Every agent should be used at the lowest effective dose for the shortest possible time, alongside non-pharmacological care. ^[1]

Topical NSAIDs are the first drug for many patients. Offer a topical NSAID for knee OA and consider it for OA at other joints. ^[1] ACR 2019 strongly recommends topical NSAIDs for knee OA and conditionally for hand OA, and recommends considering them before oral NSAIDs. ^[3] Topical treatment makes particular sense in older patients, in whom systemic NSAID exposure is risky. Practical tips: apply over (not into) the joint, avoid broken skin and the eyes, and avoid heat over the area after application.

Oral NSAIDs are the initial oral drug of choice for OA whatever the joint, but only when topical treatment is ineffective or unsuitable. ^{[1] [3]} Choose the lowest-risk agent for the patient, taking into account gastrointestinal, renal, hepatic and cardiovascular toxicity, age, pregnancy, current medication and comorbidities, ^[1] and always offer a gastroprotective treatment such as a proton pump inhibitor together with the NSAID. ^[1] Doses should be as low as possible and treatment continued for as short a time as possible. ^[3] OARSI 2019 declines to recommend any oral NSAID for people with cardiovascular comorbidities or frailty. ^[2] This is an important example of guideline divergence: NICE leaves the decision to shared assessment of risk, whereas OARSI is more restrictive.

Paracetamol (acetaminophen) receives a weak or absent recommendation. Routine use is not advised because the benefit is small and unsupported by strong evidence. ^[1] ACR 2019 conditionally recommends it for short-term, episodic use in patients with few alternatives, with regular monitoring for hepatotoxicity and a maximum of 3 g daily in divided doses. ^[3] NICE limits routine opioid or weak opioid use to infrequent short-term relief when other options are contraindicated, not tolerated or ineffective. ^[1]

Duloxetine, tramadol and other agents. ACR 2019 conditionally recommends duloxetine and tramadol, and conditionally recommends against non-tramadol opioids; where an opioid is considered at all, tramadol is preferred over others. ^[3] NICE advises against offering strong opioids. ^[1] Local and regional opioid policy should guide practice.

Intra-articular injections. Intra-articular hyaluronan is not recommended. ^{[1] [2]} Consider intra-articular corticosteroid injection when other pharmacological treatments are ineffective or unsuitable, or to support therapeutic exercise, but explain that relief is short-term, usually 2 to 10 weeks. ^[1] ACR 2019 strongly recommends intra-articular glucocorticoid for knee and hip OA, considers it for hand OA, and strongly recommends ultrasound guidance for hip injection. ^[3] OARSI 2019 places intra-articular corticosteroids as level 1B/level 2 options for knee disease depending on comorbidity status, and does not recommend them for hip or polyarticular disease. ^[2] These differences between guidelines are real and should be explained to the patient. Repeat injections indefinitely are not supported by the evidence; use them sparingly, usually to settle a flare or to enable rehabilitation.

Refer (or discuss referral) when joint symptoms (pain, stiffness, reduced function or progressive deformity) substantially affect quality of life and non-surgical management is ineffective or unsuitable. ^[1] Use clinical assessment to decide, not a numerical severity score. ^[1] Do not exclude a patient from referral because of age, sex or gender, smoking, comorbidities or overweight and obesity measured by BMI; unequal exclusion on these grounds worsens outcomes and inequity. ^[1] Explain that the risk profile of surgery varies with these same factors. ^[1]

Do not offer arthroscopic lavage or debridement for OA. ^[1] It does not improve pain or function beyond placebo in this population.

Consider patient-initiated follow-up for most patients and planned follow-up where needs suggest it, taking into account treatments needing monitoring, the patient's ability to seek help, occupation, and symptom severity. ^[1] Routine imaging is not needed for follow-up or to guide non-surgical management. ^[1]

• Progressive pain and loss of function, including difficulty with stairs, rising, transfers and walking distance.
• Fixed flexion deformity, varus or valgus angulation and joint instability.
• Falls and reduced activity, leading to deconditioning and loss of independence in older adults.
• Secondary or reactive synovitis and occasional haemarthrosis.
• Side effects of treatment, particularly gastrointestinal bleeding, renal impairment, cardiovascular events and hypertension from NSAIDs; these drive much of the excess morbidity in older adults.
• Complications of surgery in those who proceed to arthroplasty, including infection, thromboembolism, dislocation and revision; these are uncommon but important.

The burden of these complications is why prevention of further joint damage and maintenance of muscle strength matter so much.

OA is a chronic, usually slowly progressive disease. Pain and function fluctuate over months and years; many patients have long stable periods. Structural progression on imaging is not the same as progression of symptoms, and many people with radiographic OA never develop significant symptoms. ^[1] Once severe fixed deformity and bone-on-bone contact are present, symptoms usually progress. Obesity, malalignment and quadriceps weakness accelerate functional decline; weight loss, exercise and adequate analgesia often produce clinically important improvement even late in the disease.

There is no established population screening programme for OA. Prevention focuses on the modifiable risks listed earlier:

• Maintain a healthy body weight from early adulthood.
• Keep physically active and strengthen the muscles around the joints; activity in general does not damage healthy joints and is protective.
• Prevent and treat joint injuries, including meniscal tears and ligament injuries, and rehabilitate thoroughly.
• Avoid prolonged kneeling, squatting and heavy loading where possible; use ergonomic aids and modify tasks.
• Manage diabetes and other metabolic disease, and keep bone health in mind in older adults.
• Encourage early presentation for joint pain so that core treatment begins before deformity and muscle loss are established.

OA that is diagnosed early is easier to manage; the disease becomes harder to control once deformity and advanced muscle wasting are present.

Pregnancy. Osteoarthritis is uncommon in women of reproductive age. During pregnancy, pain increases in women with existing disease because of weight gain and ligament laxity. Pharmacological treatment should take pregnancy into account as a risk factor, ^[1] and oral NSAIDs generally need caution, especially later in pregnancy. Use non-drug measures (exercise, physiotherapy, weight management, heat, supports) first and work with the obstetric and rheumatology teams before giving analgesics. Consider relative contraindications carefully and follow local formulary guidance.

Children. Primary OA is not a disease of childhood. Joint pain in a child or young adult should raise the possibility of secondary OA from injury, dysplasia, inflammatory arthritis, metabolic disorder or (in the case of the hip) slipped capital femoral epiphysis or Perthes disease, rather than OA itself. Early referral and investigation of a young patient with "OA" are safer than assuming the adult pattern.

Older adults. This is the most common group. Polypharmacy, frailty, renal impairment, cardiovascular disease and risk of falls shape every decision. Drug choice should emphasise topical over oral agents, the lowest effective doses and close monitoring. Exercise remains beneficial even in frailty, but programmes must be supervised and fall-safe. Consider bone health and function holistically and ensure home and community support.

• OA can usually be diagnosed clinically without imaging, so a plain radiograph is reserved for red flags or uncertainty. ^[1]
• Exercise, weight loss and education are the core of treatment and can be delivered by physiotherapists, nurses and community health workers.
• A walking stick, quadriceps strengthening and activity pacing cost little and help a lot.
• Oral NSAIDs are cheap but carry the same risks; use the lowest effective dose for the shortest time and avoid them in renal or cardiovascular disease and in frail patients. ^{[1] [2]}
• Topical NSAIDs, if available, are safer for many older patients.
• Joint replacement is effective but requires referral to a centre with surgical capacity; identify severe, end-stage cases early.
• Intra-articular steroid injection, where skills and asepsis are available, can settle a flare and allow rehabilitation.

• Osteoarthritis is a whole-joint disease of cartilage loss, subchondral bone change, osteophyte formation and low-grade synovial inflammation.
• It affects roughly 302 million people worldwide and is a leading cause of disability in older adults.
• Activity-related pain and brief stiffness under 30 minutes are typical; prolonged morning stiffness suggests inflammatory disease.
• The knees, hips and hands are the common sites; Heberden nodes are at the distal and Bouchard nodes at the proximal interphalangeal joints.
• Diagnosis is clinical in a person aged 45 or over with activity-related joint pain and short-lived morning stiffness.
• Imaging correlates poorly with symptoms; use it for red flags or diagnostic uncertainty, not to label disease.
• Core treatment for everyone is information, therapeutic exercise and weight management.
• Topical NSAIDs come before oral NSAIDs; oral NSAIDs must be combined with a proton pump inhibitor.
• Intra-articular corticosteroids give short (2 to 10 weeks) symptomatic relief; hyaluronic acid is not recommended.
• Joint replacement is indicated for severe symptoms despite non-surgical care and should not be withheld because of age, BMI, comorbidity or smoking.
• Oral or transdermal opioids, glucosamine, TENS, routine hyaluronic acid and arthroscopic lavage or debridement should not be offered.
• Prevention centres on healthy weight, activity, strengthening, injury prevention and early core treatment.

Musculoskeletal and skin topics such as rheumatoid arthritis, gout, calcium pyrophosphate deposition disease, Paget disease of bone, slipped capital femoral epiphysis, developmental dysplasia of the hip, knee injuries and ligament tears, and obesity and bariatric surgery provide useful adjacent context for osteoarthritis. Some of these topics may be marked as coming soon until published.