## Pathophysiology of Osteoarthritis **Key Point:** Osteoarthritis is fundamentally a degenerative joint disease characterized by progressive cartilage loss, not inflammation-driven joint destruction. Understanding the structural and biochemical changes is essential for NEET PG. ### Correct Pathophysiological Features | Feature | Status in OA | Mechanism | |---------|-------------|----------| | Proteoglycan loss | Early & progressive | Enzymatic degradation by MMPs and ADAMTs | | Type II collagen fibrillation | Hallmark finding | Loss of tensile strength, surface fibrillation | | Inflammatory cytokines (IL-1, TNF-α) | Elevated | Drive chondrocyte apoptosis and MMP upregulation | | Synovial fluid viscosity | **Decreased** | Loss of hyaluronic acid; poor joint lubrication | | Subchondral bone changes | Progressive | Sclerosis, cyst formation, osteophyte formation | **High-Yield:** The decrease in synovial fluid viscosity in OA is a **direct consequence** of reduced hyaluronic acid synthesis by synovial cells. This impairs joint lubrication and accelerates cartilage wear — the opposite of what the distractor claims. ### Why Option 4 is Incorrect **Clinical Pearl:** In osteoarthritis, synovial fluid becomes less viscous and loses its protective lubricating properties. This is one reason why patients experience increased friction, pain, and accelerated cartilage damage with activity. The fluid may become more inflammatory (elevated IL-6, IL-8, prostaglandins) but less viscous. **Warning:** Do not confuse osteoarthritis with rheumatoid arthritis — RA has inflammatory exudative synovial fluid with high cell count; OA has non-inflammatory, low-viscosity fluid. ### Structural Changes in OA 1. **Cartilage:** Fibrillation → fissuring → full-thickness loss 2. **Bone:** Subchondral sclerosis, cyst formation, marginal osteophytes 3. **Synovium:** Mild chronic inflammation (not primary) 4. **Capsule & ligaments:** Fibrosis and laxity [cite:Robbins 10e Ch 26]
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