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Hemosiderin / iron / arthritis
Hemosiderin / iron / arthritis -- Posted by doe on 04-17-04 14:21
This shows cleary hemosiderin deposits / iron deposits IN .. arthritis ..
induced either by trauma / injury or simple bleeding into the joints ..
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Hemosiderin was found in the synovial membrane
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Haemophilia. 2004 May;10(3):280-7. Related Articles, Links
Experimental haemophilic synovitis: rationale and development of a murine model
of human factor VIII deficiency.
Valentino LA, Hakobyan N, Kazarian T, Jabbar KJ, Jabbar AA.
Departments of Pediatrics and Immunology/Microbiology, Rush Children's Hospital
and Rush University, Chicago, IL, USA.
Summary. Haemophilia is a genetic disease as a result of the deficiency of
blood coagulation factor VIII or IX. Bleeding is common, especially into joints
where an inflammatory, proliferative synovitis develops resulting in a
debilitating arthritis, haemophilic arthropathy. The pathogenesis of
blood-induced haemophilic synovitis (HS) is poorly understood. The gross,
microscopic and ultrastructural changes that occur in the synovial membrane
following human and experimental hemarthrosis have been described. Repeated
episodes of bleeding induce synoviocyte hypertrophy and hyperplasia, an intense
neovascular response and inflammation of the synovial membrane. The
component(s) in blood that initiates these changes is(are) not known, although
iron is often proposed as one possibility. Here, we describe a novel murine
model of human haemophilia A, which facilitates the examination of large number
of animals and tissue specimens. The effects of hemarthrosis on the physical,
gross and microscopic changes evoked following joint bleeding are described.
Controlled, blunt trauma to the knee joint consistently resulted in joint
swelling because of a combination of bleeding and inflammation. Hemosiderin was
found in the synovial membrane. Similar to hemarthrosis in human haemophilia,
joint bleeding resulted in acute morbidity evidenced by inactivity, weight loss
and immobility. With time the animals recovered. The model of experimental
murine HS described here has utility in the study of the pathogenesis of HS.
This is the first of a series of articles, which will discuss the
pathophysiology and characterize the model, with comparison of his model to
others which have been published previously. It should provide a useful model
to test potential therapeutic interventions.
PMID: 15086328 [PubMed - in process]
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