Superficial fraying, splitting and fibrillation of articular cartilage as a consequence of ageing or mechanical injury is not always associated with joint pain. However, similar cartilage lesions accompanied by synovitis and engorgement of the subchondral vasculature generally is; the disorder being known as osteoarthritis (OA). In this hypothesis it is contended that the progression of early cartilage fibrillation to symptomatic OA arises as a consequence of the antigenic nature of cartilage components which when released into synovial fluid and the circulation can stimulate leukocytes (to a varying degree) to produce a number of factors some of which promote blood coagulation. While it is known that with ageing hyper-coagulation and plaque deposition is increased, the augmentation of this process by factors released by activated leukocytes is considered to exacerbate the problem. These haematological events may be particularly relevant in individuals whose leukocytes are hypersensitive to the cartilage-derived antigens, and whose fibrinolytic system is less capable of mobilizing the thrombi deposited in synovial tissues and the subchondral vascular tree.