A physiological approach to the pathogenesis of rheumatoid and other high-protein arthropathies.

In many types of arthropathy the synovial fluid (SF) oxygen tension and glucose levels often are low and associated with lactic acidosis which, unless joints are insensitive to the lack of fuel and oxygen, must contribute to joint damage. To such hypoxic-ischaemic changes can contribute quite a number of rheological and other mechanisms and synovial necroses, but also tamponade due to increased SF hydrostatic pressure caused by colloid osmotic forces (pi) in SF with a high protein concentration. pi in SF can be increased by numerous mechanisms, many of which are active in patients with rheumatoid and other arthropathies. The present compilation shows that the above in a dynamic fashion can be covered by equations elaborated by physiologists.