Ahlqvist J. (Department of Pathology, Aurora Hospital, Helsingfors, Finland.) Can increased generalized vascular leakage in ambulant individuals induce joint effusions, synovitis, hypoxia and destruction? Scand J Rheumatol, Suppl 52: 86-92, 1984.Fundamental points of a hypothesis on the pathogenesis of non-specific synovitides can be summarized as follows: ))Many mechanisms can make blood vessels leaky to fluid and protein. In people in whom some of these mechanisms work, fluid tends to accumulate in and around joints because mechanical stress enhances fluid influx into these structures from which the removal of protein by lymphatics is poor. When joints are used, the pressure in the effusion increases, especially if the surrounding tissue is scarry, disturbing circulation, and swollen tissues containing extra protein tend to become inflamed, and later to die if they do not get enough oxygen from the blood.)) The (combination of) leakage-inducing mechanisms to which patients are hyperresponsive need not be the same in two patients fulfilling the criteria of, e.g., rheumatoid arthritis. It is suggested that the significance of combinations of such ())contributing))) mechanisms should be uprated to give ))multifactorial)) a wider meaning.Discrepancies between existing theories on the pathogenesis of rheumatoid and other nonspecific synovitides, and clinical, laboratory and morphological findings (1, 3) induced me to search for explanations that do not disagree with such findings. The present hypothesis has been dealt with at length elsewhere (3, 4).