Joint damage due to (recurrent) joint
bleeding in
haemophilia causes major morbidity. Although the exact pathogenesis has not been fully elucidated, a central role for
iron is hypothesised. Likewise, in hereditary
haemochromatosis joint destruction is caused by
iron overload. A comparison between these types of
arthropathy could provide more insight in the influence of
iron in inducing joint damage. A literature review was performed to compare both disorders with respect to their clinical and histological characteristics, and preclinical studies on the influence of
iron on different joint components were reviewed. Similarities in the features of
arthropathy in
haemochromatosis and
haemophilia are cartilage degeneration, subchondral bone changes with
osteophyte and
cyst formation, and
osteoporosis. In both disorders synovial
inflammation and proliferation are seen, although this is much more explicit in
haemophilia. Other substantial differences are the age at onset, the occurrence of
chondrocalcinosis radiographically and
calcium pyrophosphate dihydrate deposition disease in
haemochromatosis, and a rapid progression with joint
deformity and neovascularisation in
haemophilia. Preclinical studies demonstrate detrimental effects of
iron to all components of the joint, resulting in synovial
inflammation and
hyperplasia, chondrocyte death, and impaired osteoblast function. These effects, particularly the synovial changes, are aggravated in the presence of a pro-inflammatory signal, which is prominent in haemophilic
arthropathy and minimal in
haemochromatosis. Additional research is needed to further specify the role of
iron as a specific target in treating these types of
arthropathy.