This is the authors' abstract. We don't add key points for this paper.
AIMS: To investigate the pathogenetic mechanisms of haemophilic arthropathy (HA) by comparing end-stage arthropathy with osteoarthritis (OA; a degenerative joint disorder) and rheumatoid arthritis (RA; an inflammation-mediated joint disease). METHODS AND RESULTS: Cartilage and synovium from patients with HA (n=10), RA (n=8), OA (n=14) and normal control subjects (n=6) were examined morphologically, biochemically and histochemically. Cartilage in HA exhibited characteristics of degenerative joint disease (OA), as evidenced by morphological, histochemical (Safranin-O fast green-iron haematoxylin, Mankin grade) and biochemical (proteoglycan synthesis, glycosaminoglycan content and DNA content) changes, whereas synovium in HA showed characteristics of inflammation-mediated joint disease (RA), as evidenced by histochemical (inflammation, haematoxylin and eosin (H&E) and iron deposition, Perls' blue) and biochemical changes (interleukin (IL)-1, IL-6, tumour necrosis factor (TNF)alpha and catabolic properties). CONCLUSION: Haemophilic arthropathy shows characteristics of both inflammatory and degenerative joint disease. On the basis of these results and published information, it appears that degenerative cartilage changes have a dominant role in HA and are augmented by relatively mild inflammation of the synovium.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Roosendaal et al. (1999) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: