This shows cleary hemosiderin deposits / iron deposits IN ..
arthritis .. induced either by trauma / injury or simple
bleeding into the joints ..
<<snip>> Hemosiderin was found in the synovial
membrane <<snip>>
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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