Clinical meaning
Osteoarthritis (OA) is the most common joint disease, resulting from progressive loss of articular cartilage with secondary bony changes. Mechanical stress and inflammatory mediators (IL-1, TNF-alpha, MMPs) cause chondrocyte apoptosis and extracellular matrix degradation. Subchondral bone sclerosis, osteophyte formation, and synovial inflammation follow. OA characteristically affects weight-bearing joints (knees, hips) and DIP/PIP joints (Heberden and Bouchard nodes). Gout is a crystal arthropathy caused by monosodium urate (MSU) crystal deposition in joints when serum uric acid exceeds the saturation threshold (> 408 mcmol/L). MSU crystals activate the NLRP3 inflammasome in macrophages, triggering IL-1-beta release and intense neutrophilic inflammation. The first MTP joint (podagra) is the most common site. Pseudogout (calcium pyrophosphate deposition disease, CPPD) presents similarly but with calcium pyrophosphate crystals, typically affecting knees and wrists.
Diagnosis & workup
Diagnostics & workup: - OA: clinical diagnosis (no labs needed); XR: joint space narrowing, osteophytes, subchondral sclerosis, cysts - Gout: serum uric acid (may be normal during acute attack), joint aspiration showing negatively birefringent needle-shaped MSU crystals - CPPD: joint aspiration showing weakly positively birefringent rhomboid crystals; XR: chondrocalcinosis - Inflammatory markers (ESR, CRP) elevated in gout/CPPD, normal in OA - Renal function (eGFR) before starting urate-lowering therapy - Dual-energy CT for tophaceous gout if aspiration not feasible