Osteoarthritis — Symptoms, Causes & Treatment | MyMedicPlus

Osteoarthritis (OA) is the most prevalent joint disease worldwide, affecting over 500 million people — approximately 7% of the global population and the leading cause of disability in older adults. It is a whole-joint disease characterised by progressive loss of articular hyaline cartilage, subchondral bone remodelling and sclerosis, formation of marginal osteophytes (bony outgrowths), synovial inflammation and thickening, and periarticular soft tissue changes — collectively causing pain, stiffness, and functional limitation. OA is not simply 'wear and tear' but an active pathological process involving chondrocyte dysfunction, metalloproteinase-mediated cartilage matrix degradation, inflammatory cytokines (IL-1β, TNF-α), and subchondral bone micro-fractures. The knee is the most commonly affected joint (affecting 250 million people globally), followed by the hip, hand joints (distal interphalangeal and proximal interphalangeal joints — causing Heberden's and Bouchard's nodes), the first carpometacarpal joint (base of thumb), and the facet joints of the lumbar and cervical spine. OA prevalence rises steeply with age, affecting over 50% of adults over 65 years; it is significantly more common in women than men, particularly after the menopause. The global burden of OA is increasing rapidly due to population ageing and the obesity pandemic. Total knee and hip replacement surgery — performed over 1 million times annually in the USA alone — represents the definitive treatment for end-stage OA.

OA aetiology is classified as primary (idiopathic) or secondary to an identifiable joint disorder. Primary OA risk factors: older age (radiographic OA is nearly universal above 65 years, though symptoms vary widely); female sex (twice the prevalence of hip and knee OA in post-menopausal women compared to age-matched men — oestrogen may be chondroprotective, and loss at menopause accelerates cartilage degradation); obesity (the most important modifiable risk factor for knee OA — each 5 BMI unit increase raises knee OA risk by 35%, both through increased mechanical loading and through pro-inflammatory adipokines secreted by visceral adipose tissue — leptin, adiponectin, IL-6); genetic susceptibility (heritability of 60% for hip and hand OA; polygenic risk including GDF5 and ALDH1A2 variants); and occupation (repetitive kneeling, squatting, and heavy lifting — construction workers, farmers, athletes in high-impact sports). Secondary OA follows prior joint pathology: anterior cruciate ligament (ACL) tears and meniscal injuries increase knee OA risk 3-5 times; congenital hip dysplasia predisposes to early hip OA; post-traumatic OA after joint fractures; previous inflammatory arthritis (rheumatoid arthritis causing secondary degenerative changes after joint inflammation); avascular necrosis of the femoral head (from steroid use, alcohol, sickle cell disease); and metabolic disorders depositing calcium pyrophosphate crystals in cartilage (pseudogout, haemochromatosis, hyperparathyroidism, Wilson's disease — always consider secondary metabolic OA in atypical distribution).

The hallmark symptom of OA is use-related (mechanical) joint pain — pain that is worse with weight-bearing activity (walking, standing, climbing stairs) and relieved by rest, in contrast to inflammatory arthritis where pain is worst with prolonged rest and improves with movement. OA pain is typically: dull or aching in character, located within the joint or over periarticular structures, and may radiate distally (hip OA may refer pain to the anterior thigh, medial knee, or groin); it worsens progressively over years and may progress to rest and nocturnal pain in end-stage disease. Brief morning stiffness (lasting less than 30 minutes — often under 15 minutes) on waking or after inactivity — the 'gelling phenomenon' — distinguishes OA from inflammatory arthritis where morning stiffness exceeds 45-60 minutes. Crepitus — the palpable or audible grinding or creaking sensation during joint movement — results from roughened cartilage surfaces and is a characteristic finding on examination. Reduced range of motion from cartilage loss, osteophyte impingement, and contracture of the joint capsule causes progressive functional limitation — difficulty squatting, kneeling, and climbing stairs in knee OA; reduced hip abduction and internal rotation in hip OA. Bony deformity develops in advanced OA: varus (bow-legged) or valgus (knock-kneed) malalignment in knee OA; Heberden's nodes (bony swelling at the DIP joints) and Bouchard's nodes (at PIP joints) in hand OA. Synovial inflammation with joint effusion (palpable in the knee — ballottement of the patella) occurs during OA flares. Muscle wasting from disuse — particularly the quadriceps in knee OA — further destabilises the joint.

OA is primarily a clinical diagnosis — NICE guidelines recommend diagnosing OA clinically without routine investigation in patients over 45 with typical activity-related joint pain and either no morning joint-related stiffness or morning stiffness lasting no more than 30 minutes. Plain X-rays are the standard initial imaging: the four radiographic hallmarks of OA are joint space narrowing (from cartilage loss), subchondral sclerosis (increased density of bone immediately below the joint surface), osteophytes (bony outgrowths at the joint margins visible as spurs), and subchondral cysts (lucent areas in the subchondral bone from synovial fluid forced into the bone under increased pressure). Kellgren-Lawrence grading (0-4) classifies OA severity radiologically; however, radiographic severity correlates poorly with symptom severity — severe X-ray changes may be asymptomatic, and significant pain can occur with minimal radiographic change. MRI is not routinely indicated for OA but provides superior assessment of cartilage thickness, bone marrow oedema (BML — correlates with pain and progression), meniscal degeneration, synovitis, and subchondral bone changes — useful when diagnosis is uncertain or surgery is planned. Blood tests: FBC, ESR, CRP, rheumatoid factor, anti-CCP antibodies, uric acid, and ANA are used to exclude inflammatory arthritis (rheumatoid arthritis, psoriatic arthritis, gout) and should be performed if atypical features are present. Joint aspiration of an effusion: crystal examination (calcium pyrophosphate, uric acid) differentiates inflammatory from non-inflammatory synovitis; synovial fluid WBC below 2,000/mm³ is characteristic of OA.

OA management follows a stepped, multimodal approach combining non-pharmacological, pharmacological, and surgical interventions. Core treatments (OARSI and NICE endorsed for all OA patients): land-based therapeutic exercise — aerobic (swimming, cycling, walking) and strengthening exercises, particularly quadriceps strengthening for knee OA (reduces pain by 30-40% and improves function — NICE recommends offering exercise regardless of age, radiographic severity, or pain level); weight loss — every 1% weight loss reduces knee pain by 0.5%; a 5-10% body weight reduction significantly reduces OA pain, functional limitation, and progression; self-management education and patient activation. Pharmacological management: topical NSAIDs (diclofenac 1% gel or diclofenac 2.32% 1% w/w gel — Voltarol) are first-line for knee and hand OA, providing equivalent analgesia to oral NSAIDs with minimal systemic exposure and side effects; paracetamol (no longer recommended as routine first-line by NICE NG226 2022 due to limited efficacy evidence); oral NSAIDs (naproxen 500mg twice daily, ibuprofen 400-600mg three times daily, celecoxib 100-200mg twice daily) — effective for moderate-severe OA pain; use with a proton pump inhibitor (omeprazole) in patients over 45 and assess cardiovascular/renal risk; duloxetine 30-60mg daily for central pain sensitisation and those with anxiety/depression comorbidity. Intra-articular (joint) injections: corticosteroid injections (triamcinolone, methylprednisolone) provide short-term relief for 4-12 weeks during flares — effective for synovitis but repeated use may accelerate cartilage loss; hyaluronic acid injections have modest evidence and are not recommended by NICE. Surgical options: total knee arthroplasty (TKA) and total hip arthroplasty (THA) — the most effective interventions for end-stage OA, achieving 80-90% patient satisfaction; osteotomy (realignment for unicompartmental knee OA in younger active patients); unicompartmental knee arthroplasty (UKA) for isolated medial compartment disease.

Progressive OA leads to significant functional impairment: reduced walking distance, inability to climb stairs or rise from a chair, and ultimately loss of independent ambulation — causing dependency, nursing home placement, and social isolation. Falls risk is substantially increased in OA patients from joint instability, muscle weakness (quadriceps atrophy in knee OA), and fear of movement — hip fracture from falls is a major cause of morbidity and mortality. Severe, uncontrolled chronic OA pain causes sleep disruption (present in 60-70% of patients with severe OA), depression and anxiety (comorbid in 40-50% of OA patients), and significant reduction in quality-of-life. Long-term NSAID use — often necessary for adequate OA pain control — carries important risks: peptic ulcer disease and gastrointestinal haemorrhage (mitigated by co-prescription of a PPI — omeprazole, lansoprazole); increased cardiovascular events (myocardial infarction, stroke — particularly with diclofenac and COX-2 inhibitors); and renal impairment (renal prostaglandins are required for normal haemodynamics — NSAIDs reduce eGFR, particularly in the elderly, hypertensive, or diabetic). Post-surgical joint replacement complications: deep vein thrombosis and pulmonary embolism (requiring thromboprophylaxis — LMWH or rivaroxaban for 28-35 days post-surgery); peri-prosthetic joint infection (1-2% risk — the most serious complication, may require prosthesis removal and 2-stage revision); implant loosening and wear requiring revision surgery (10-15% need revision within 15-20 years); and intra-operative fracture or nerve injury.

The most impactful preventive strategies for OA address the major modifiable risk factors. Maintaining a healthy BMI (18.5-25) throughout adult life is the most important individual preventive measure for knee OA — weight loss of 5-10% body weight in overweight individuals significantly reduces OA risk and symptom progression; each BMI unit reduction is associated with proportional risk reduction. Regular physical activity (150 minutes weekly of moderate aerobic exercise and twice-weekly resistance training) strengthens the periarticular muscles, particularly the quadriceps for knee OA, which absorb joint loading forces and protect cartilage from excessive stress — contrary to popular belief, moderate exercise is not detrimental to OA-affected joints. Occupational injury prevention: ergonomic interventions to reduce repetitive kneeling, squatting, and heavy lifting; use of knee pads and mechanised lifting equipment for high-risk occupations. Sport injury prevention: structured anterior cruciate ligament (ACL) injury prevention programmes (warm-up and neuromuscular training — FIFA 11+ for football players) substantially reduce ACL tears; prompt surgical reconstruction and rigorous rehabilitation after ACL or meniscal injury reduces long-term OA risk. Early OA management: initiating exercise therapy at the first diagnosis of OA (even early radiographic change) reduces symptom progression and delays need for surgery. Weight loss and exercise delivered together in a structured programme (NICE-endorsed structured weight management plus physiotherapy) provide additive benefit. Patients who undergo joint replacement should be aware that activity modification and weight management post-operatively prolongs the life of the prosthesis.

See your GP for: joint pain lasting more than 6 weeks, significant joint stiffness in the morning (lasting less than 30 minutes — longer morning stiffness suggests inflammatory arthritis), swelling of knee or hip joints, worsening difficulty with everyday activities (walking, stairs, dressing), or a sudden significant increase in joint pain or swelling in established OA. Seek urgent assessment for: a single hot, acutely swollen joint with fever — this may indicate septic arthritis (not OA) requiring emergency joint aspiration and treatment. See an orthopaedic surgeon for assessment of joint replacement (total hip or total knee arthroplasty) when pain is inadequately controlled with maximal conservative and medical management, quality of life is significantly impaired, and conservative measures have failed over 6-12 months.