Pathogenesis Of Hemophilic Arthropathy Research Articles

Blood-induced joint disease: the pathophysiology of hemophilic arthropathy.

Arthropathy is a frequent and serious complication of repeated joint bleeding in patients with hemophilia, resulting in pain, deformity, and disability. Although the pathogenesis of hemophilic arthropathy has not been fully elucidated, it appears to have similarities with the degenerative joint damage that occurs in osteoarthritis and the inflammatory processes associated with rheumatoid arthritis. This article reviews the potential actions of various blood constituents on joint components that culminate in the development of hemophilic arthropathy.

Pathogenesis of haemophilic arthropathy

The pathogenetic mechanism of haemophilic arthropathy is multifactorial and includes degenerative cartilage-mediated and inflammatory synovium-mediated components. Intra-articular blood first has a direct effect on cartilage, as a result of the iron-catalysed formation of destructive oxygen metabolites (resulting in chondrocyte apoptosis), and subsequently affects the synovium, in addition to haemosiderin-induced synovial triggering. Both processes occur in parallel, and while they influence each other they probably do not depend on each other. This concept resembles degenerative joint damage as found in osteoarthritis as well as inflammatory processes in rheumatoid arthritis. These processes finally result in a fibrotic and destroyed joint.

Pathogenesis of Hemophilic Arthropathy

Intra-articular bleeding is the most common clinical manifestation of hemophilia, and can adversely affect joints and lead to arthropathy. Affected joints are associated with changes to the synovium, bone, cartilage and blood vessels. Iron plays a critical role in the pathogenesis of this condition, and may exert its effects through a variety of different mechanisms. Hemophilic arthropathy shares some injury characteristics with rheumatoid arthritis, although the degree of analogy is a matter of some debate. The influences of the mechanisms underlying joint inflammation are better understood for rheumatoid arthritis than for hemophilia, and it is hoped that this knowledge can be used to provide a more comprehensive knowledge of the pathological process of hemophilic arthropathy. This, in turn, may enable novel targets for therapeutic intervention to be identified.