OA General Principles

General MSK Principles

Overview

Osteoarthritis (OA) is the most common joint disease worldwide and the leading cause of musculoskeletal disability, affecting approximately 8.75 million people in the UK and driving the majority of joint replacement surgery. OA is not simply 'wear and tear' - it is an active, dynamic whole-joint process involving cartilage, subchondral bone, synovium, ligaments, capsule, and periarticular muscles. Characteristic features are cartilage degradation, subchondral bone remodelling, osteophyte formation, low-grade synovitis, and progressive loss of joint function. OA most commonly affects the knees, hips, hands (DIP joints with Heberden's nodes, PIP joints with Bouchard's nodes, and 1st CMC joint), spine, and 1st MTP joint. UK practice is anchored by NICE NG226 (Osteoarthritis in over 16s, 2022) which permits a clinical diagnosis without imaging when the typical presentation criteria are met. Management centres on three core treatments - therapeutic exercise, weight management, and information/support - with pharmacological, injection, and surgical options as adjuncts. OA is NOT an inevitable consequence of ageing: modifiable risk factors (obesity, physical inactivity, joint injury, occupational loading) offer real opportunities for prevention.

Anatomy & Pathophysiology

OA is a whole-joint disease - not just cartilage loss.

  • Articular cartilage: progressive loss of hyaline cartilage is the hallmark. Normal cartilage is maintained by chondrocytes and composed of type II collagen, proteoglycans (aggrecan), and water. In OA, degradation driven by matrix metalloproteinases and aggrecanases outpaces repair; chondrocyte apoptosis accelerates the imbalance. The cartilage surface becomes fibrillated, fissured, and eventually eroded. Loss is typically focal and asymmetric.
  • Subchondral bone: sclerosis (thickening) and subchondral cyst formation; bone marrow lesions on MRI correlate with pain and progression.
  • Osteophytes: new bone at joint margins - the most characteristic radiographic feature; an attempt to increase surface area and redistribute load.
  • Synovium: low-grade synovitis is present in many OA joints (not exclusive to inflammatory arthritis). Inflammatory mediators (IL-1, TNF-alpha, IL-6) contribute to cartilage degradation, pain, and effusion.
  • Joint capsule and ligaments: capsular thickening, contracture, and ligamentous laxity.
  • Periarticular muscles: weakness and wasting are both a consequence and a contributor - weak muscles reduce joint protection, increase abnormal loading, and accelerate degeneration. This is why therapeutic exercise (including strengthening) is a core treatment.

Pathogenesis - the vicious cycle: joint injury or abnormal loading triggers cartilage damage, inflammatory mediator release, subchondral remodelling, osteophyte formation, synovitis, and muscle weakness, which produces further abnormal loading and progressive degeneration. Breaking this cycle through exercise, weight management, and biomechanical optimisation is the basis of conservative management.

Risk factors:

  • Non-modifiable: age (the strongest risk factor), female sex (especially post-menopause), genetic predisposition (particularly hand and generalised OA), previous joint injury (post-traumatic OA), and joint malalignment (varus/valgus).
  • Modifiable: overweight and obesity (the major modifiable risk, especially for knee OA), physical inactivity, occupational loading (repetitive kneeling, squatting, heavy lifting), and muscle weakness (particularly quadriceps for knee OA).

Patterns: primary (idiopathic) is most common; secondary OA has an identifiable cause - post-traumatic (the dominant cause at the ankle), inflammatory arthritis (RA, gout, CPPD), metabolic disease (haemochromatosis, Wilson''s, ochronosis), developmental abnormalities (hip dysplasia, Perthes, SUFE), AVN, or Charcot joint. Generalised (nodal) OA is polyarticular (DIP, PIP, 1st CMC, knees, hips) with strong genetic component, more common in post-menopausal women. OA at the ankle, wrist, or elbow is atypical for primary OA and should prompt search for a secondary cause.

Clinical Pearl
  • OA is a WHOLE-JOINT disease - not just cartilage loss; cartilage, subchondral bone (sclerosis, cysts), osteophytes, synovium, capsule, ligaments, and periarticular muscles are all involved.
  • Overweight and obesity are major MODIFIABLE risk factors, especially for knee OA - every 1 kg of body weight is about 3-6 kg of force across the knee in walking.
  • OA in atypical joints (ankle, wrist, elbow) should prompt a search for a secondary cause: post-traumatic, inflammatory, haemochromatosis ('iron fist' 2nd/3rd MCP OA), Wilson's, ochronosis.
  • Heberden's nodes = DIP; Bouchard's nodes = PIP; squaring of the thumb base = 1st CMC OA.
  • Muscle weakness is both a consequence AND a contributor - quadriceps strengthening is core management for knee OA.

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