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  • Title: Immunohistochemical analysis of hip arthritis in ankylosing spondylitis: evaluation of the bone-cartilage interface and subchondral bone marrow.
    Author: Appel H, Kuhne M, Spiekermann S, Köhler D, Zacher J, Stein H, Sieper J, Loddenkemper C.
    Journal: Arthritis Rheum; 2006 Jun; 54(6):1805-13. PubMed ID: 16736521.
    Abstract:
    OBJECTIVE: Previous histopathologic and magnetic resonance imaging studies suggest that the subchondral bone marrow might be the primary site of inflammation in patients with ankylosing spondylitis (AS) and that this might be reflected by inflammation found in hip joints. The aim of this study was to conduct an immunohistologic assessment of the bone-cartilage interface and subchondral bone marrow in AS patients with hip arthritis. METHODS: We collected femoral heads from patients with AS, osteoarthritis (OA), and rheumatoid arthritis (RA) who were undergoing hip replacement. The subchondral bone marrow and bone-cartilage interface were assessed immunohistochemically by evaluating infiltrating T cells, microvessel density, and osteoclasts. Areas of the femoral head surface with and without cartilage were assessed separately. RESULTS: At sites with surface cartilage, we found subchondral infiltration of CD3+ T cell aggregates at significantly higher numbers in AS patients as compared with OA patients, but not RA patients. At sites of complete cartilage destruction, the frequency of CD3+ T cell aggregates was significantly reduced as compared with sites with cartilage on the surface in AS patients, but not in RA patients. Similar differences were found for CD4+ and CD8+ T cells. Only at sites with surface cartilage, but not those without, angiogenesis and osteoclastic foci in the subchondral bone marrow in AS patients were significantly increased as compared with RA patients and with OA patients. CONCLUSION: These findings suggest that the subchondral bone marrow and bone-cartilage interface are primary sites of inflammation in AS and that cartilage might be necessary for the induction of inflammation.
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