Osteoarthritis — Causes, Symptoms, Diagnosis & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Osteoarthritis (OA) is the most common joint disease, affecting approximately 500 million people worldwide and representing the leading cause of pain and physical disability in adults over 50 years. It is characterised by progressive degradation of articular cartilage, subchondral bone remodelling (osteophyte formation, sclerosis, cyst development), and synovial inflammation. OA most commonly affects the knee, hip, hand (distal and proximal interphalangeal joints, first carpometacarpal joint), and lumbar and cervical spine. The knee is the most commonly affected weight-bearing joint. OA is not merely 'wear and tear' but a metabolically active disease involving abnormal cartilage metabolism, low-grade synovial inflammation, and altered subchondral bone turnover. The socioeconomic burden is enormous: OA is the most common indication for total knee and hip replacement surgery globally, with over 1 million joint replacements performed annually in the USA alone.

OA results from an imbalance between cartilage synthesis and degradation, driven by mechanical, metabolic, and inflammatory factors. Primary (idiopathic) OA — most common, multifactorial, predominantly age-related. Secondary OA — results from identifiable causes: prior joint injury (ACL rupture, meniscal tear — increases OA risk 4-6 fold over 10-15 years), crystal deposition disease (gout, calcium pyrophosphate), congenital joint dysplasia, avascular necrosis, inflammatory arthritis, or infection. Key risk factors: age (cartilage repair capacity declines with age), female sex (higher risk after menopause), obesity (each 1-kg/m² increase in BMI raises knee OA risk by 15%), joint injury and repetitive occupational loading, quadriceps weakness, and genetic predisposition (heritability estimated at 40-70% for hand OA). Aberrant mechanical loading initiates chondrocyte apoptosis and disrupts the balance between MMP (matrix metalloproteinase) activity and TIMP (tissue inhibitor of metalloproteinase) activity, causing irreversible cartilage loss.

Joint pain is the cardinal symptom — typically activity-related (worse with use, better with rest), progressively worsening over years, with associated morning stiffness lasting less than 30 minutes (distinguishing OA from inflammatory arthritis, where stiffness lasts over 1 hour). Joint stiffness after periods of inactivity (gelling phenomenon). As OA advances: constant background pain including at rest and at night, reduced range of motion, crepitus (grating or clicking sensation with joint movement), bony enlargement (osteophytes — Heberden's nodes at DIP joints, Bouchard's nodes at PIP joints in hand OA), and joint deformity (varus knee deformity in medial compartment knee OA; valgus deformity in lateral compartment OA). Muscle wasting around the affected joint from disuse. Synovitis causes joint effusion (visible swelling) and warmth, particularly after activity. Severe OA causes significant restriction of daily activities — difficulty climbing stairs, rising from chairs, and walking distances.

OA is primarily a clinical diagnosis based on age, characteristic symptoms, and physical examination findings. X-ray (weight-bearing AP and lateral views) shows the 4 hallmarks: joint space narrowing (cartilage loss), subchondral sclerosis (increased bone density), osteophyte formation (bony outgrowths), and subchondral cysts. X-ray grading: Kellgren-Lawrence scale (0-4). MRI provides superior soft tissue detail — detects bone marrow lesions, meniscal tears, synovitis, and cartilage defects that precede radiographic changes; used before surgical planning. Ultrasound identifies synovitis and guides intra-articular injections. Blood tests (rheumatoid factor, anti-CCP, ESR, CRP, uric acid) are normal in OA but needed to exclude inflammatory arthritis, which may co-exist or mimic OA. Synovial fluid analysis (if effusion present) shows non-inflammatory fluid (WBC below 2000/mL) with no crystals in pure OA.

Conservative management is first-line and sufficient for most patients. Exercise: land-based exercise (strengthening, aerobic, balance) is the most evidence-based treatment, reducing pain by 40-50% — recommended by all guidelines regardless of severity. Aquatic exercise is beneficial for those with severe pain limiting land-based activity. Weight loss: each 1 kg weight loss reduces knee joint loading force by 4 kg — 10% body weight loss produces clinically significant pain reduction. Topical treatments: topical NSAIDs (diclofenac gel) preferred over oral for knee/hand OA, minimising systemic side effects. Oral NSAIDs (naproxen, ibuprofen, celecoxib): effective for moderate-to-severe OA; use lowest effective dose for shortest duration given GI, cardiovascular, and renal risks. Intra-articular corticosteroid injections: provide short-term pain relief (4-8 weeks) for acute OA flare, particularly with effusion. Intra-articular hyaluronic acid: modest benefit, particularly for knee OA in patients avoiding systemic medications. Surgery: total knee or hip arthroplasty (joint replacement) is highly effective for end-stage OA with severe pain and functional limitation inadequately controlled by conservative treatment — produces excellent pain relief and function improvement in 90% of patients with 15-20 year implant survival.

End-stage osteoarthritis causes complete loss of articular cartilage, bone-on-bone contact, severe chronic pain, and inability to walk or perform daily activities. Periarticular osteophyte formation causes joint deformity, locking, and recurrent effusions. OA is the most common indication for total knee replacement (over 900,000 procedures annually in the USA) and total hip replacement (450,000 annually). Severe OA-associated pain leads to disuse atrophy of periarticular muscles, increasing fall risk in elderly patients. Depression affects 25-35% of patients with severe OA. Prolonged NSAID use for pain relief increases risk of peptic ulcer disease, cardiovascular events, and acute kidney injury — particularly in older patients with comorbidities such as hypertension, heart failure, and chronic kidney disease.

Prevent joint injury: use appropriate protective equipment in sports; strengthen periarticular muscles (especially quadriceps for knee OA prevention and treatment). Maintain healthy weight throughout life — obesity is the single most modifiable risk factor for knee and hip OA. Regular aerobic and resistance exercise preserves joint health and reduces OA risk; inactivity is harmful. Avoid high-impact loading with inadequate conditioning. Treat sport and occupational injuries promptly to reduce post-traumatic OA risk. Fall prevention in elderly patients reduces joint injury. Screen for and treat conditions contributing to secondary OA: control gout effectively, manage haemochromatosis, treat dysplasia. There are currently no disease-modifying drugs for OA (DMOADs) approved for clinical use — multiple candidates (FGF-18/sprifermin, lorecivivint, anti-NGF antibodies) are in trials.

See a GP if joint pain persists for more than 6 weeks, causes functional limitation, or is associated with significant morning stiffness, constitutional symptoms, or rapidly progressive joint swelling — these features may suggest inflammatory arthritis requiring specialist evaluation. Urgent assessment is needed for sudden severe joint pain or swelling (possible joint infection/septic arthritis — a medical emergency), haemarthrosis following trauma, or features of locked or unstable joint. Refer to a rheumatologist if the diagnosis is uncertain, inflammatory arthritis is suspected, or to guide injection therapy. Orthopaedic referral is appropriate when conservative treatment has failed for at least 3-6 months and OA is severe enough to significantly impair daily living, sleep, and quality of life.