Primary Causes & Pathophysiology
Failure begins with cartilage (smooth lining) fibrillation and loss of proteoglycans (cushion molecules). Subchondral (beneath-cartilage) bone stiffens with sclerosis (thickening) and marrow lesions (bone stress areas). Osteophytes (bony spurs) form at margins by endochondral (cartilage-to-bone) remodelling. Synovitis (lining inflammation) is low-grade and contributes to pain and effusion (joint fluid). Cytokines (signalling proteins) with degradative enzymes (breakdown chemicals) sustain matrix (support-tissue) loss. Load overload with muscle weakness accelerates whole-joint failure.
Cumulative load with chondrocyte (cartilage-cell) ageing reduces matrix (support-tissue) repair leading to fibrillation (surface fraying) and thinning
Excess weight stresses cartilage (smooth lining) and subchondral (beneath-cartilage) bone driving sclerosis (thickening) and osteophyte (bony spur) formation
Altered congruence (fit) with instability (looseness) focuses load on small areas accelerating focal cartilage loss
Abnormal shape with varus (bow-leg) or valgus (knock-knee) alignment concentrates stress provoking bony remodelling
Crystals deposit in cartilage and synovium (joint lining) triggering flares (attacks) with chronic wear and chondrocalcinosis (cartilage calcification)
Persistent synovitis (lining inflammation) with erosions (breaks) damages cartilage and bone leaving secondary degenerative change
Abnormal deposits weaken cartilage and subchondral bone hastening joint failure
Loss of proprioception (position sense) permits repetitive microtrauma (small injury) without protective pain collapsing joint structure