Osteoarthritis Overview and Knee Implications

Osteoarthritis (OA)

• OA is the most common form of arthritis and the most common musculoskeletal condition.
• Previously considered "wear and tear," OA is now recognised as a metabolically active disease affecting the entire joint (cartilage, bone, joint capsule, and muscle).
• OA is a disease of synovial joints, characterised by: -Progressive loss of articular cartilage. -Changes in subchondral bone, including hardening (sclerosis) and bone outgrowth (osteophytes). -Synovial inflammation (less severe than in rheumatoid arthritis). -Changes in periarticular muscle. -Pain and stiffness.

OA in the Knee

• OA is the most common type of non-inflammatory arthritis.
• Healthy knee vs Osteoarthritis knee
  • Healthy Knee: cartilage and bone are intact, joint capsule is intact, and meniscus is intact
  • OA Knee: cartilage is lost, bone is exposed, joint capsule is thickened, osteophytes, joint space narrowing, and degenerative changes in the meniscus.

OA Disease Progression

• Initial repair: chondrocytes proliferate and synthesise the extracellular matrix of bone (ECM).
• Early stage OA: ECM degradation exceeds chondrocyte activity, leading to net cartilage breakdown and increased subchondral bone remodelling.
• Intermediate stage OA: failure of ECM synthesis and increased breakdown of cartilage
• Late stage OA: extreme or complete loss of articular cartilage, joint space narrowing, bony outgrowth (osteophytes), and decreased bone remodelling and subchondral bone sclerosis.

OA Versus RA

• OA: Cartilage loss, often related to injury or overuse.
• RA: Overactive immune system, leading to chronic inflammation.

OA Risk Factors

• Increasing age (uncommon in <45 but common in >65, more prevalent in women).
• Gender (men <45, more prevalent in women 55-70).
• Ethnicity (less common in Asian, African-Caribbean and Chinese).
• Genetic predisposition (around 20%).
• Obesity.
• Physical stress and occupational factors.

OA Symptoms

• Joint pain and stiffness, weight-bearing joints (hip, knees, spine) and hands (base of thumb) commonly affected.
• Asymmetry of affected joints is common.
• Pain is worse with movement, no pain at rest.
• Morning stiffness lasting less than 30 minutes.
• Synovial thickening
• Deformity of joint.
• Bony swellings (heberden and bouchard's nodes).
• Joint effusion.
• Muscle weakness or wasting.
• Crepitus (joint clicking or crackling).
• Limited joint movement.

OA Diagnosis

• Clinical diagnosis (without investigations) is possible If person is 45+ years or older, with activity-related joint pain and minimal or no morning stiffness lasting <30 minutes

OA Management

• Core treatments: information, exercise, weight loss, and footwear advice.
• Activity and exercise: benefit of local muscle strengthening and general fitness.
• Weight loss intervention: lifestyle assessment and advice, dietary review, and exploration of physical activity levels.
• Non-pharmacological treatments (e.g. heat/cold therapy, TENS, aids and devices; for example, manual therapy, joint support, and walking aids; manipulation and stretching.
  • DO NOT OFFER nutraceuticals like glucosamine/chondroitin products
• Pharmacological treatments: Analgesics (e.g., topical NSAIDs, oral NSAIDs, COX-2 inhibitors, paracetamol, or opioids). NSAIDs may be insufficient for pain relief in some cases. Intra-articular corticosteroid injections; may be considered for moderate to severe pain
• Referral for consideration of joint surgery, surgical options.
• Follow-up and review.

OA Management: Core Treatments (cont.)

• Access to appropriate information (education)
• Discuss footwear.
• Activity and exercise benefits.
• Interventions to achieve weight loss (lifestyle, diet and physical activity levels).
• Environmental, social and family factors.

OA Management: Non-pharmacological Treatments

• Many patients report benefit from non-drug therapies as an adjunct to core treatment.
• Thermotherapy: use of local heat or cold.
• Electrotherapy: use of TENS (transcutaneous electrical nerve stimulation)
• Aids and Devices: Braces/supports/insoles, walking sticks, tap turners, and manual therapies (e.g. manipulation, stretching), particularly hip OA.

OA Management: Topical NSAIDs and Rubefacients

• Topical preparations of ibuprofen, ketoprofen, felbinac, and piroxicam.
• Systemic effects (hypersensitivity and asthma): discontinue if rash develops.
• Patient should avoid exposure to excessive sunlight.
• Rubefacients: relieve pain in joints, tendons, and/or muscles through mild counter-irritation
  • Rubefacients cause redness, dilate capillaries, increasing blood flow to area. e.g Capsaicin (0.025%)

Psoriatic Arthritis (PSA)

• Inflammatory arthritis, occurring in <15% of patients with psoriasis.
• Usually asymmetrical, affecting small joints (hands, feet) requiring X-ray or MRI confirmation.
• Pain, swelling, stiffness lasting >30 minutes.
• Dactylitis (sausage-shaped fingers/toes, 50%), enthesitis(inflammation where ligaments/tendons join bone).
• Less common types:
  • Rheumatoid-like symmetrical seronegative polyarthritis (RF-ve).
  • Arthritis mutilans (severe form).

PSA Treatment

• Non-progressive monoarthritis: local corticosteroid injections.
• Offer CDMARDs (combined disease-modifying antirheumatic drugs).
• If no relief after 3 months of max CDMARD, switch or combine to another standard CDMARD (consider oral NSAID as adjunct to cDMARD).
• Consider short-term oral steroid therapy. -NSAIDs use at lowest effective dose for the shortest possible time
  • Consider Gl protective treatment

Psoriatic Arthritis (PSA) Treatment (cont.)

• Use of biological therapies, or non-biological therapies; assess response to treatment after 12 weeks.
• If NSAIDs, colchicine or steroids are ineffective or unsuitable, consider Canakinumab (anti-IL-1) for frequent episodes of gout attacks.

Leflunomide

• Licensed for active psoriatic arthritis, specialist use only.
• Inhibitor of pyrimidine synthesis, affecting T cell proliferation, immunomodulatory.
• Active metabolite persists, washout procedure recommended if significant adverse effects.
• Side effects: Life-threatening hepatotoxicity, bone marrow toxicity, infection and malignancy.
• Pregnancy must be ruled out before treatment, effective contraception is required and should continue for at least two years after treatment in women and 3 months in men.
• Patients should be closely monitored.

Reactive Arthritis

• Inflammatory arthritis following infection (gastrointestinal or genitourinary).
• Believed that persistent bacterial antigens in inflamed synovium drive inflammation.
• Presents within 4 weeks post-infection and resembles psoriasis.
• Treatment: Antibiotics for infection, NSAIDs for pain relief.
• Condition often resolves in months, but recurrence possible.

Enteropathic Arthritis

• Arthritis linked to inflammatory bowel disease (IBD): ulcerative colitis or Crohn’s disease.
• Inflammatory arthritis, usually peripheral joints and spine.
• Arthritis activity mirrors bowel activity; better with improved bowel condition.
• Difficult to treat/manage (revisit drug treatment).
• NSAIDs for joint pain but might worsen bowel condition.

Crystal Deposition Diseases: Gout

• Most common inflammatory arthritis.
• Caused by monosodium urate crystal deposition (in joints and/or tissues in, fluid).
• Can present as acute inflammatory pain.
• Commonly affects the metatarsophalangeal joint of the great toe (75%).

Gout Risk Factors

• Uric acid metabolism/excretion abnormality (hyperuricaemia).
• Family history.
• Obesity.
• Excessive alcohol consumption.
• High purine diet.
• Diuretics.
• Acute infections, ketosis, and surgery.

Gout and Hyperuricaemia

• Single most important risk factor: sustained hyperuricaemia.
• Hyperuricaemia is caused by either overproduction of uric acid, or by impaired renal excretion (idiopathic, chronic renal disease, medications such as diuretics and low-dose aspirin, hypertension, increased lactic acid production, hyper/hypothyroidism).

Gout Diagnosis

• Physical examination: acute joint pain, redness, swelling, tophi.
• Serum uric acid levels: measurement 4–6 weeks after acute attack, often normal during acute attack. -Demonstration of monosodium urate crystals in synovial fluid by aspiration - rarely done in primary care.

Gout Management

• Acute gout attack:
  • NSAIDs (usually high dose, e g, naproxen or ibuprofen)
  • Colchicine.
  • Corticosteroids
• Prevention (long term):
  • Allopurinol, Febuxostat, and sulfinpyrazone

Gout: Colchicine

• Alkaloid extracted from autumn crocus.
• Mechanism: Prevents neutrophil/phagocyte migration into gouty joints by disrupting microtubules - reduced cell motility; prevents mediators release of inflammatory mediators by preventing/limiting the phagocytosis of urate crystals.
• Oral, well tolerated.

Gout Management: Uricosuric Agents

• Increase uric acid excretion by direct action on renal tubules.
• Second choice when gout cannot be controlled with allopurinol.
• Contraindicated in patients with renal stones, renal insufficiency.

Pseudogout

• Inflammatory arthritis, less common than gout, featuring attacks of pain and swelling in joints (typically larger ones; knee or wrist).
• Often presents in elderly, often familial and genetic.
• Acute attacks are less severe than gout; resembling OA sometimes.
• May be due to deposition of calcium pyrophosphate dihydrate (CPPD) crystal.
• May occur secondary to other conditions (e.g. OA, hyperparathyroidism, hypothyroidism, haemochromatosis).

Pseudogout Diagnosis

• Physical examination: joint pain and swelling.
• Diagnosis with detection of "brick-shaped crystals" in synovial fluid (aspiration), ultrasound, or X-ray (might find crystal and calcification of cartilage – chondrocalcinosis).
• Blood tests may show increased white blood cells, mineral imbalances.

Pseudogout Treatment

• Treatment: Rest, joint aspiration (to relieve pressure), NSAIDs, colchicine.
• Local corticosteroids sometimes useful, but not uric acid lowering meds like allopurinol.
• Severe or chronic cases may require specialist treatment (DMARDs).

This quiz covers the fundamentals of osteoarthritis (OA), the most common type of arthritis affecting synovial joints. It highlights the differences between healthy and OA-affected knees, including changes in cartilage, bone, and joint structure. Test your understanding of OA's effects and its classification as a metabolic disease.