Osteoarthritis

Osteoarthritis is the most common form of arthritis in the UK, affecting millions of people. It is no longer viewed simply as 'wear and tear' but as an active repair process of the joint that has become derailed. The core clinical features include joint pain (typically worse with activity), stiffness (lasting less than 30 minutes in the morning), and functional impairment. Risk factors include increasing age, female sex, obesity, previous joint injury, and repetitive occupational stress. In the hands, OA typically affects the distal interphalangeal (DIP) joints (Heberden's nodes) and proximal interphalangeal (PIP) joints (Bouchard's nodes), as well as the first carpometacarpal joint at the base of the thumb. Diagnosis can often be made clinically in patients over 45 with activity-related joint pain and no morning stiffness lasting longer than half an hour. Management follows a tiered approach based on NICE guidelines, prioritising weight loss and exercise. Pharmacological options are used for symptomatic relief, starting with topical NSAIDs (for knees/hands) or oral paracetamol, proceeding to oral NSAIDs (with PPI cover) if needed. Intra-articular corticosteroid injections may provide short-term relief. For patients whose quality of life is significantly impacted despite maximal conservative and medical therapy, surgical options like total hip or knee arthroplasty are considered.

The pathophysiology of OA involves a complex interplay of mechanical, inflammatory, and metabolic factors. Articular cartilage, composed of type II collagen and proteoglycans, loses its structural integrity due to an imbalance between degradative and synthetic activities of chondrocytes. Early OA is marked by increased water content and swelling of the cartilage, followed by fibrillation and erosion of the cartilaginous surface. As the protective cartilage layer thins, the underlying subchondral bone is exposed to increased mechanical stress, leading to subchondral sclerosis and the formation of subchondral cysts (as synovial fluid is forced through microfractures). Osteophytes (bone spurs) develop at the joint margins as a compensatory attempt to increase the surface area of the joint and redistribute the load. Low-grade inflammation within the synovium (synovitis) often accompanies the process, contributing to pain and joint effusion. Unlike rheumatoid arthritis, OA is not primarily an autoimmune systemic disease, though pro-inflammatory cytokines like IL-1 and TNF-alpha are involved locally within the joint microenvironment.

Patients typically present with chronic, insidious onset of joint pain that is exacerbated by movement and relieved by rest. Mechanical 'locking' or 'giving way' may occur. Physical examination may reveal joint line tenderness, bony enlargement, crepitus on movement, and restricted range of motion. Joint effusions are common but usually cool (non-inflammatory). In the hand, Heberden’s nodes (DIP) and Bouchard’s nodes (PIP) are classic; the thumb base (CMC joint) frequently shows 'squaring'. Functional impact is significant, particularly with hip and knee OA, leading to reduced mobility and loss of independence. Complications include secondary muscle atrophy due to disuse, chronic pain syndromes, and the risks associated with long-term NSAID use (GI bleeding, renal impairment). Red flags that should prompt investigation for alternatives include systemic symptoms (fever, weight loss), rapid progression, or nocturnal pain that prevents sleep.

- Bedside: Assessment of Body Mass Index (BMI), functional assessment (GALS screen).
- Bloods: Usually normal; ESR/CRP may be slightly raised but high levels suggest inflammatory arthritis. Rheumatoid factor and CCP are negative.
- Imaging: Plain X-ray of the affected joint is the gold standard. Look for 'LOSS': Loss of joint space, Osteophytes, Subchondral sclerosis, Subchondral cysts.
- Special Tests: Joint aspiration (arthrocentesis) ONLY if gout or septic arthritis is suspected; synovial fluid in OA is clear and non-inflammatory.

Management follows NICE (NG226) principles. Conservative: Patient education, therapeutic exercise (strengthening and aerobic), and weight loss if overweight. Footwear advice and local heat/cold packs. Medical: First-line involves topical NSAIDs (for knees/hands) or topical capsaicin. Oral paracetamol and oral NSAIDs (e.g., Ibuprofen 400mg TDS or Naproxen 500mg BD) can be used, but oral NSAIDs must be co-prescribed with a Proton Pump Inhibitor (PPI, e.g., Omeprazole 20mg). Weak opioids (Codeine) are for short-term use only. Intra-articular corticosteroid injections provide temporary relief. Surgical: Referral for joint replacement (Arthroplasty) if symptoms significantly impact quality of life and non-surgical management is exhausted.