SECONDARY OA: Appears at any age in apreviously damaged or congenitally abnormaljoint . OA is a “wear and tear” phenomenon.Indeed the vertebrae , hips and knees are mostaffected . OA can be superimposed uponRHEUMATOID ARTHRITIS.
Two main theories:1)BIOMECHANICAL THEORY2)BIOCHEMICAL THEORY
This maintains the wear and tear leads to deranged function,focal death, and reactive proliferation of chondrocytes. Collagen breakdown , fissuring and flaking and osteophyte formation occurs.
maintains that aging leads to lessenedmatrix maintenance and excess oflytic enzymes , which in turns lead tosynovitis . Synovitis further results ina release of inflammatory mediatorsand cytokines(especially IL-1) ,degradative enzymes and freeradicals and eventually chondrocytedeath.
Primary abnormality is thinning and fragmentation of the articular cartilage. Loss of articular cartilage leads to exposure of subchondral bone , which appears as shiny foci on the articular surface( enburnation ). New bone formation , usually in the form of nodules (spurs). Formation of osteocartilagenous loose bodies (“joint mice”). Inflammation is absent.
CLINICAL FEATURES:Although OA may be asymptomatic,most patients experience morning stiffness in affected joints . There is usually no local heat or tenderness , but affected joints often show restricted range of motion , small efusions and crepitus. A slowly progressive disease characterized by joint disability.It is associated with ALKAPTONUREA and FOOTBALL PLAYERS.