Osteoarthritis

Meet the patient

A 68-year-old retired farmer's wife arrives with right knee pain that has crept up over two years. It aches after a morning in the garden, settles by mid-afternoon, and never wakes her at night. Her right knee clicks loudly on stairs. Her fingers are knobbly at the tips — she cannot get her rings on.[1]

Two questions decide her next year, and they decide every OA consult: is this mechanical or inflammatory? (the pain pattern and the joint map answer it at the bedside) and what will actually change her trajectory? (core measures, not the next tablet). Hold those two and the page below slots into place.[1]

What OA is — and the three things it is not

It is a whole-organ failure of the synovial joint, not passive wear and tear. Articular cartilage thins and fibrillates while the bone beneath remodels — osteophytes at the margins, sclerosis and cysts underneath — and a low-grade synovitis smolders through it all. Once you call it "wear and tear" you stop treating it; call it an active, cell-mediated repair response that turns maladaptive under load, and the treatment logic (offload, strengthen, correct mechanics) writes itself.[1]

It is not inflammatory. Morning stiffness is measured in minutes, not hours; ESR and CRP are normal; there is no fatigue or fever. The contrast with rheumatoid arthritis is the central bedside decision in arthritis, and OA sits firmly on the mechanical side of it.[1]

It is not a blood test. There is no biomarker and no scan that makes the diagnosis. Investigations exist to exclude inflammatory, septic and metabolic mimics and to seek a secondary cause in atypical joints — they never confirm "osteoarthritis" on their own.[1]

It is not the X-ray. Radiographic severity correlates poorly with pain. Bone-on-bone change may sit under mild discomfort, and a near-normal film may belong to a patient who can barely walk. The film stages the joint; the patient dictates the treatment.[1]

The joint map — and the MCP that is always spared

The single highest-yield observation in OA is the distribution. Learn the map once and the diagnosis half-writes itself.[1]

• Knee — the medial tibiofemoral compartment fails first, so the leg drifts into varus (bow-leg) as disease advances. Patellofemoral OA hurts on stairs and rising from a chair.
• Hip — groin pain on weight-bearing and internal rotation that may refer to the knee through the obturator nerve. Internal rotation is lost first — test it early.
• Hand — Heberden nodes at the DIP, Bouchard nodes at the PIP, the first CMC squaring the base of the thumb. The MCP joints are characteristically spared.
• Spine — facet-joint OA causes mechanical back pain worse on extension and rotation, with referred buttock and thigh pain.
• First MTP — hallux rigidus, a stiff big toe with a dorsal osteophyte, distinct from hallux valgus.[1]

Etymology for viva gold: Heberden and Bouchard are eponyms, not mechanisms — William Heberden described the DIP nodes in 1802, Charles-Joseph Bouchard the PIP nodes a century later. The names survived because the bedside observation did.[1]

Mechanical versus inflammatory — the bedside fork

The pivotal decision at any arthritic joint is mechanical versus inflammatory, and a single question and a joint map settle it. OA pain is use-related with stiffness under 30 minutes and an asymmetric, patterned distribution. Rheumatoid arthritis is inflammatory with stiffness over an hour, symmetric small-joint swelling, raised ESR and CRP, and RF or anti-CCP positivity. Get this fork right and the entire downstream pathway diverges correctly.[1]

[1]

The discriminator line: the morning-stiffness clock and the MCP. Stiffness under 30 minutes with an asymmetric, MCP-sparing pattern is OA; stiffness over an hour with symmetric MCP and PIP swelling is rheumatoid arthritis. Everything else refines one of these two.[1]

Two mimics that bite. Avascular necrosis of the femoral head or knee produces sudden severe pain in a previously stable joint, often with night pain and a history of steroids, alcohol, sickle cell or trauma — the X-ray is normal early and MRI is diagnostic. Haemochromatosis must be considered whenever "OA" sits in the second and third MCP (a site primary OA spares): check iron studies and treat by venesection before cirrhosis, cardiomyopathy and diabetes arrive.[1]

How common, who, and why obesity burns the cartilage from inside

OA is the commonest form of arthritis and a leading cause of disability in older adults. Roughly 250 million people live with knee OA worldwide; radiographic knee OA is found in about 30 percent of those over 65, though only around half are symptomatic. The knee dominates; hand OA (especially nodal) is the commonest form in women beyond the menopause.[1]

[1]

The risk factors split cleanly. The non-modifiable set — age (the strongest; chondrocyte repair fades with time), female sex (women overtake men after the menopause, implicating oestrogen loss, especially in hand and knee OA), and genetics (heritability 40 to 65 percent for hand and knee OA) — set the substrate. The modifiable set is where treatment lives: obesity, prior joint injury (meniscectomy, ACL tear), repetitive occupational stress, and malalignment.[1]

The cultural geography the examiner likes. Farmers and those who squat or sit cross-legged — postures common across India and East Asia — concentrate contact stress on the posteromedial tibial plateau and the anterosuperior femoral head, accelerating cartilage failure in compartments already vulnerable to malalignment. It is one reason knee OA presents late and severe in those populations.[1]

Why the cartilage fails — the MMP and ADAMTS cascade

OA is not passive attrition; it is an active, cell-mediated destruction-and-repair process that turns maladaptive under load. A chondrocyte stressed by excessive or abnormal mechanical load — and already weakened by age, genes and metabolic stress — flips from a matrix-maintaining phenotype into a catabolic, pro-inflammatory one. It switches on matrix metalloproteinases (MMP-1, MMP-3, MMP-13) and the aggrecanases (ADAMTS-4, ADAMTS-5).[1]

The molecular hierarchy fixes the timeline. Type II collagen is the tensile scaffold — the steel reinforcement. Aggrecan is the water-binding proteoglycan that resists compression — the concrete. ADAMTS attacks aggrecan early (reversible water loss, swelling on MRI), while MMP-13 attacks type II collagen late (irreversible structural failure). This is why joint-space narrowing on X-ray is a late finding: by the time the gap visibly closes, much of the matrix is already gone.[1]

Once the collagen network disrupts, the cartilage loses its aggrecan-bound water, fibrillates, thins and ulcerates, progressing from superficial fraying to full-thickness erosions that expose subchondral bone. The bone does not sit idle: it remodels under the altered load, becoming denser and stiffer (subchondral sclerosis) and developing subchondral cysts (geodes) — fluid-filled cavities from synovial pressurisation of microfractures. At the margins, osteophytes form as a reparative response — and are the most specific radiographic feature of OA.[1]

Cartilage debris and calcium crystals released into the joint drive a low-grade synovitis, distinct from the high-grade pannus of rheumatoid arthritis; interleukin-1, TNF and interleukin-6 feed back to amplify catabolism. Periarticular quadriceps weakness and proprioceptive loss destabilise the joint further. Nerve ingrowth into subchondral bone and osteophytes, plus central sensitisation, explains the patient whose pain is severe out of all proportion to the film.[1]

What the X-ray does not tell you is who hurts. Severity on film and severity of pain correlate poorly — so never operate on a film, and never withhold core treatment because the film "looks mild". The patient is the scan.[1]

Primary or secondary — and when to hunt the driver

OA splits by cause into primary (idiopathic) and secondary forms, and the split matters because secondary OA demands a search for the underlying driver. Treat the cause and you may slow or localise the disease.[1]

Primary (idiopathic) OA has no identifiable precipitant and dominates in older adults. Its subtypes include generalised nodal OA (the classic Heberden phenotype — symmetric DIP, PIP and first CMC involvement in post-menopausal women, strongly familial) and erosive (inflammatory) OA, an aggressive hand subset marked by central erosions in the DIP and PIP (the "gull-wing" deformity) — distinguished from rheumatoid arthritis by DIP predominance, MCP and wrist sparing, and a self-limiting course.[1]

[1]

The rule of the atypical joint. When OA appears in a joint primary OA spares — the MCP, the wrist, the shoulder, the ankle — or in a young patient, hunt for a secondary cause: post-traumatic, developmental (DDH, FAI, SCFE, Perthes), metabolic (haemochromatosis, Wilson, acromegaly, hyperparathyroidism, ochronosis), neuropathic (Charcot), or crystal (CPPD). The young patient with hip OA mandates hip imaging — dysplasia is markedly more common in women and in breech presentations.[1]

The bedside round — bony, cool, and clicking

A focused joint examination confirms the mechanical, asymmetric, bony pattern and excludes inflammatory and septic mimics. Run it in this order.[1]

Inspect for bony swelling (Heberden at the DIP, Bouchard at the PIP), first CMC squaring, varus or valgus deformity at the knee, muscle wasting (quadriceps vastus medialis obliquus; interossei in hand OA), and gait (antalgic; Trendelenburg in hip OA). Palpate for bony enlargement — hard, cool and non-tender, in deliberate contrast to the soft, warm, boggy synovitis of rheumatoid arthritis — plus joint-line tenderness and a cool effusion (patellar tap or fluid thrill). A genuinely hot joint demands aspiration, not a diagnosis.[1]

Move the joint actively and passively. Crepitus — a palpable crunch on flexion-extension — is typical and mechanical. Restriction and functional limitation are graded. Named signs worth knowing: the squaring sign at the first CMC, varus thrust gait in medial-compartment knee OA, and a positive Faber (Patrick) test reproducing hip pain in hip OA.[1]

Functional impact is best quantified with a validated patient-reported tool — the WOMAC (24 items across pain, stiffness and function) or KOOS for the knee, and AUSCAN for the hand. In the elderly, add a gait and falls screen (get-up-and-go), because knee and hip OA are major contributors to falls.[1]

Investigations — a clinical diagnosis, confirmed by exclusion

OA is a clinical diagnosis. Investigations exist to exclude inflammatory and septic mimics and to seek secondary causes in atypical cases — never to make the diagnosis in isolation.[1]

Blood tests are used to rule out other arthritides. ESR and CRP are normal, the full blood count is normal (anaemia of chronic disease or leukocytosis argue against simple OA), RF and anti-CCP are negative, and urate may be normal or high but does not diagnose gout in a chronic joint. In atypical "OA" — young age, MCP, wrist or shoulder involvement, rapid onset, or a family history — add iron studies for haemochromatosis, calcium, phosphate, parathyroid hormone and vitamin D for hyperparathyroidism, and copper and caeruloplasmin for Wilson disease.[1]

X-ray is the imaging of choice and the four cardinal features live in the LOSS mnemonic: Loss of joint space, Osteophytes (the most specific sign), Subchondral sclerosis, and Subchondral cysts. Remember that X-ray severity correlates poorly with symptoms, so treatment follows the patient, not the film.[1]

MRI is reserved for red flags or diagnostic dilemmas — suspected avascular necrosis, stress fracture, early inflammatory arthritis with a normal X-ray, or a meniscal or root tear. Ultrasound guides intra-articular injections and detects effusion and synovitis. Synovial fluid analysis is mandatory in any acutely hot, swollen joint to exclude sepsis and crystals: OA fluid is clear, viscous (high hyaluronan), non-inflammatory with WBC under 2,000 cells per microlitre (predominantly mononuclear), whereas gout shows negatively birefringent needle crystals and sepsis shows WBC over 50,000 with a positive Gram stain.[1]

The ACR criteria — codifying the pattern examiners test

The ACR clinical classification criteria are designed for research and trial inclusion, but they codify the pattern an examiner rewards. For hand OA (Altman 1990): hand pain, aching or stiffness plus 3 of the following 4 — hard tissue enlargement of 2 or more of 10 selected joints (the second and third DIP, second and third PIP, and first CMC of both hands), fewer than 3 swollen MCP joints, hard tissue enlargement of 2 or more DIP joints, and deformity of at least 1 of the 10 selected joints — gives sensitivity 94 percent and specificity 87 percent.[3]

For knee OA (ACR 1986): knee pain plus at least 3 of 6 — age over 50, crepitus on active motion, morning stiffness 30 minutes or less, bony tenderness, bony enlargement, and no palpable warmth — captures the same mechanical signature at the bedside.[3]

Aspirate first — the acute hot joint is not a flare

Before attributing a worsening joint to an OA flare, exclude the dangerous mimics. Any sudden change in a chronic OA joint — new night pain, rest pain, severe acute pain, systemic features, a hot and tense effusion — mandates reassessment for fracture (insufficiency or stress), avascular necrosis, septic arthritis, or an acute crystal attack superimposed on chronic OA.[1]

The single safe rule, repeated: aspirate any acute hot joint before attributing it to an OA flare. Send synovial fluid for cell count, Gram stain, culture, and crystal microscopy. The missed septic joint is the catastrophic error in arthritis.[1]

Once sepsis and crystals are excluded, an OA flare is managed with rest, ice, simple analgesia, and a short course of oral NSAID (for example naproxen 500 mg twice daily for 7 to 14 days with a proton-pump inhibitor). For a clearly monoarticular flare, especially of the knee or hip, a single intra-articular corticosteroid injection (triamcinolone acetonide 40 mg for a large joint; methylprednisolone acetate 40 mg is an equivalent alternative), given with aseptic technique, peaks at 1 to 3 weeks and lasts 4 to 8 weeks. Limit injections to 3 to 4 per joint per year, and never inject a suspected septic or prosthetic joint.[1]

Core first — exercise and weight loss are disease-modifying

The most important sentence on this page: core non-pharmacological measures are first-line and disease-modifying, not adjuncts. Every patient, regardless of severity, begins here — and most stay here. The four core measures are education and self-management, aerobic and strengthening exercise (especially quadriceps strengthening for knee OA — strongly evidence-based), weight loss (target 5 kg, which cuts knee-OA symptom burden by roughly 50 percent), and biomechanical aids (appropriate footwear, lateral-wedge insoles for medial-compartment OA, bracing, walking aids). Physiotherapy delivers the structured exercise; occupational therapy the joint protection.[1]

[2]

Reframe it for the patient and adherence rises. Weight loss and exercise are not symptom relief — they slow progression of knee OA and outperform any single drug. That reframe is the difference between a patient who returns discouraged and one who walks daily.[1]

The pharmacological ladder — topical first, paracetamol last

The ladder is built on safety, and topical NSAIDs lead it. Each step is chosen by the balance of efficacy against gastrointestinal, renal and cardiovascular harm.[2]

Topical NSAIDs — diclofenac 1 percent gel (2 to 4 g applied four times daily) or ketoprofen 2.5 percent gel — are strongly recommended first-line for knee and hand OA because they match the symptomatic benefit of oral NSAIDs with a fraction of the systemic exposure and a far better safety profile.[2]

Oral NSAIDs are the next step, used at the lowest effective dose for the shortest time, always with a proton-pump inhibitor (for example omeprazole 20 mg once daily) for patients over 45 or with prior gastrointestinal history. The cardiovascular risk hierarchy is worth fixing: naproxen (lowest), then ibuprofen, then diclofenac and the COX-2 inhibitors (highest). Avoid oral NSAIDs in CKD with eGFR under 30, heart failure, active peptic ulcer, and bleeding diathesis.[2][4]

[2]

Capsaicin 0.025 to 0.075 percent cream applied four times daily is conditionally recommended by the ACR for hand and knee OA, useful when NSAIDs are contraindicated, though local burning limits adherence. Duloxetine 30 to 60 mg once daily (a serotonin–noradrenaline reuptake inhibitor) is conditionally recommended for chronic musculoskeletal pain of OA, particularly with central sensitisation, coexistent depression, or NSAID intolerance.[2]

[1] [2]

Paracetamol is no longer first-line

Paracetamol is the examinable reversal of the last decade. Once first-line everywhere, it is now no longer recommended as first-line by NICE (2022) and conditionally recommended against by the ACR 2019, because the Roberts 2016 systematic review showed minimal efficacy and a dose-dependent rise in mortality, gastrointestinal bleeding and cardiovascular events at chronic high doses (3 g per day or more). It retains only a limited short-term role as an add-on in patients who cannot take NSAIDs.[5][2]

Agents recommended against — do not prescribe

[2] [4] [5]

When to send for the surgeon

Surgery is reserved for end-stage OA with refractory pain and functional loss despite optimal conservative management. Total hip arthroplasty and total knee arthroplasty are among the most cost-effective interventions in medicine — over 90 percent of patients report substantial relief, and implant survival exceeds 90 percent at 10 to 15 years.[1]

High tibial osteotomy has a role in younger, active patients with isolated medial-compartment knee OA and varus malalignment, shifting the mechanical axis to delay arthroplasty. Unicompartmental knee replacement suits single-compartment disease. And — the recurring exam point — arthroscopic lavage and debridement have no role in uncomplicated OA: multiple sham-controlled trials ended the practice.[1]

How OA patients come to harm — the preventable list

OA does not shorten life, but it is a major cause of years lived with disability, and the preventable harms cluster around diagnostic error and drug toxicity.[1]

• The missed septic joint — attributing an acute hot swollen knee to "an OA flare" without aspirating is the catastrophic, avoidable error.[1]
• Missed avascular necrosis — sudden new hip or knee pain with a steroid or alcohol history; MRI is diagnostic when X-ray is normal.[1]
• Missed haemochromatosis — "OA" of the second and third MCP, unrecognised, while cirrhosis develops in the background.[1]
• Over-treating the film — operating on a bone-on-bone X-ray in a patient with mild symptoms, or withholding core treatment because the film "looks mild".[1]
• Long-term oral NSAIDs in the elderly without a PPI, renal monitoring, or review — gastrointestinal bleeding, acute kidney injury, and cardiovascular events accumulate silently.[2]
• Opioid escalation — dependence, falls, fracture and constipation in the elderly for marginal, non-durable benefit.[2]

Prognosis and disposition

OA is progressive but variable, and not life-threatening. Some patients run to bone-on-bone change over a few years; others stay stable for decades at the same radiographic grade. At the knee, obesity, malalignment, quadriceps weakness, bone-marrow lesions on MRI, and large effusions predict progression; pain, depression, comorbidity, and social isolation predict functional decline.[1]

Total hip and total knee arthroplasty transform outcomes in appropriately selected patients — over 90 percent report substantial relief, and implant survival exceeds 90 percent at 10 to 15 years. Revision rates rise with younger age, obesity, and high-impact activity. The disposition after a clinic visit is GP and physiotherapy-led conservative management for most, with rheumatology referral for diagnostic uncertainty or suspected inflammatory or secondary OA, and orthopaedic referral for end-stage refractory pain.[1]

The safety-net for every patient is the warning to return urgently with any sudden change — new night or rest pain, a hot swollen joint, systemic features — because none of these is explained by OA alone.[1]

Special populations

The elderly with comorbidity are the largest OA population. Prefer topical NSAIDs (knee and hand) over oral to avoid gastrointestinal, cardiovascular and renal harm; minimise polypharmacy; screen for falls and frailty; and treat depression and insomnia that amplify pain. Duloxetine helps when oral NSAIDs are contraindicated. Joint replacement is well tolerated even into the ninth decade in medically fit patients — age alone is never a contraindication.[2]

Obesity and knee OA — the single largest preventable driver. Weight loss of 5 kg cuts the knee-OA symptom burden by roughly half, and bariatric surgery in severe obesity produces sustained loss and substantial improvement. The message for the patient — that weight loss and exercise are disease-modifying — is what drives adherence.[1]

Younger patients with OA should prompt a search for a secondary cause: post-traumatic, developmental, metabolic, neuropathic, or crystal. In the young, prefer joint-preserving surgery (osteotomy, hip arthroscopy for FAI) to delay arthroplasty, because revision rates are higher in younger, high-demand patients.[1]

Pregnancy — OA is uncommon in women of reproductive age, but when symptomatic prefer topical NSAIDs (avoid oral NSAIDs in the third trimester — premature closure of the ductus arteriosus and oligohydramnios). A single intra-articular corticosteroid is acceptable for a disabling flare. Avoid duloxetine and opioids where possible.[2][5]

Anticoagulated patients — joint injection carries a small bleeding risk; do not stop warfarin if the INR is in range (under 3.0), and direct oral anticoagulants can be paused for one dose for high-risk injections. Aspiration of a hot joint in an anticoagulated patient should still be done — sepsis risk outweighs bleeding risk.[1]

Where the guidelines agree and disagree

Three contemporary guidelines dominate: NICE NG226 (2022), the ACR/Arthritis Foundation 2019 (Kolasinski), and the OARSI 2019 non-surgical guideline (Bannuru).[2][4]

[2] [4]

Where they agree: the four core non-pharmacological measures are first-line everywhere; topical NSAIDs are first-line pharmacological therapy for knee and hand OA; paracetamol is no longer first-line; hyaluronic acid, glucosamine, chondroitin, fish oil, strong opioids, stem cell and PRP are recommended against. The largest divergence is on hyaluronic acid (OARSI most permissive, ACR and NICE against).[2][4][5]

The trials that changed practice. Moseley 2002 (sham-controlled) ended routine arthroscopy for uncomplicated knee OA — no better than placebo. The Roberts 2016 systematic review moved paracetamol from first-line to conditionally against by showing dose-dependent mortality, gastrointestinal and cardiovascular harm. GAIT (Clegg 2006) showed glucosamine and chondroitin were no better than placebo for overall knee-OA pain.[2][4][5]

The mantra, and the mnemonic

[1]

The mantra: use-related pain, stiffness under thirty minutes, MCP spared — treat the patient, not the film.[1]

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic (answer)

The 68-year-old with right knee pain that aches after gardening, settles by afternoon, never wakes her at night, and clicks on stairs; knobbly fingertips. What is the diagnosis, and what is first-line treatment? Model: This is osteoarthritis — use-related pain, stiffness under 30 minutes, crepitus and bony swelling (Heberden nodes at the DIP), normal inflammatory markers expected, MCP spared. It is a clinical diagnosis; the X-ray (LOSS) supports but does not dictate. First-line is core non-pharmacological and disease-modifying: education, quadriceps strengthening exercise, weight loss toward 5 kg if obese, biomechanical aids, with topical diclofenac 1 percent gel four times daily as first-line pharmacological. No paracetamol first-line.[1][2]

Stem 2 — the hot knee that is not a flare (answer)

A known OA knee becomes acutely hot, swollen and exquisitely tender overnight, with a low-grade fever. The registrar calls it "an OA flare". What is the right first action? Model: Aspirate the joint before assuming anything. This could be septic arthritis (Staphylococcus aureus commonest; synovial WBC over 50,000, positive Gram stain and culture) or an acute gout or CPPD attack superimposed on chronic OA — and missing sepsis is the catastrophic, avoidable error. Send fluid for cell count, Gram stain, culture and crystal microscopy. Only when sepsis and crystals are excluded is an OA flare the working diagnosis (rest, short oral NSAID with a PPI, or a single intra-articular triamcinolone 40 mg injection).[1]

Stem 3 — the atypical hand (answer)

A 45-year-old man presents with "OA" of his second and third MCP joints, fatigue, and slightly bronze skin. The registrar plans topical NSAIDs and physiotherapy. What has been missed? Model: Primary OA does not affect the MCP. This distribution demands a search for a secondary cause — here, haemochromatosis is the classic fit (second and third MCP, fatigue, bronze skin). Check iron studies (transferrin saturation over 45 percent, raised ferritin) and treat by venesection to prevent progression to cirrhosis, cardiomyopathy and diabetes — even though the arthritis, once established, is largely irreversible. Topical NSAIDs alone would leave the underlying disease to cause silent end-organ damage.[1]

References

1. [1]Hunter DJ, Bierma-Zeinstra S. Osteoarthritis Lancet, 2019.PMID 31034380
2. [2]Kolasinski SL, Neogi T, Hochberg MC, et al. 2019 American College of Rheumatology/Arthritis Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee Arthritis Care Res (Hoboken), 2020.PMID 31908149
3. [3]Altman R, Alarcón G, Appelrouth D, et al. The American College of Rheumatology criteria for the classification and reporting of osteoarthritis of the hand Arthritis Rheum, 1990.PMID 2242058
4. [4]Bannuru RR, Osani MC, Vaysbrot EE, et al. OARSI guidelines for the non-surgical management of knee, hip, and polyarticular osteoarthritis Osteoarthritis Cartilage, 2019.PMID 31278997
5. [5]Roberts E, Delgado Nunes V, Buckner S, et al. Paracetamol: not as safe as we thought? A systematic literature review of observational studies Ann Rheum Dis, 2016.PMID 25732175