MRI and Histological Characterization of Bone Marrow Oedema In Chronic Topahceous Gout

S. Bugatti1, F. Paparo2, G. Garlaschi2, L. Molfetta3, R. Andracco4, C. Montecucco1, M.A. Cimmino4 1Cattedra ed Unità Operativa di Reumatologia, Università di Pavia, Fondazione IRCCS Policlinico San Matteo, Pavia; 2Sezione di diagnostica per immagini, DI.M.I., Università di Genova; 3Clinica Ortopedica, Università di Genova; 4Clinica Reumatologica, DI.M.I., Università di Genova, Genova, Italy

Background: Bone marrow oedema (BME) on magnetic resonance imaging (MRI) is common in both degenerative and inflammatory arthropathies, where it is thought to represent a considerable pain trigger and a significant prognostic factor. Though the appearance of BME on MRI is fairly consistent across different pathologies, its histopathologic correlates may considerably vary, with possible pathophysiological implications. No data on BME are available in chronic gout, a condition significantly associated with changes in articular and periarticular structures.

Objectives: To investigate the frequency of BME in chronic tophaceous gout and to evaluate its immunohistologic features.

Methods: Nine consecutive patients with chronic tophaceous gout (8M/1F; mean age 71.3±11.5 years, mean disease duration 98.1±44.9 months, mean serum uric acid concentration 9.2±2.8 mg/L) were studied. MRI was performed with a 0.2 T extremity-dedicated system (ESAOTE, Genova, Italy). To image BME a short tau inversion recovery sequence (TR/TE 1500/24, TI 85, FOV 200x180) was used. Synovium and subchondral bone samples were obtained from 1 patient undergoing tophus removal from the 2nd metacarpophalangeal joint scanned by MRI the day before surgery. In this patient, MRI documented synovitis, synovial tophi, bone erosions and BME. Tissue sections were analyzed histologically and after specific immunostainings.

Results: Ten tophi of 9 patients were studied (3 MCP joints, 2 DIP joints, 1 wrist, 1 elbow, 1 knee, 2 MTP joint). BME was found in association with bone erosions in 7/9 joints, whilst 2 joints did not show signs of neither bone erosions nor BME. The immunohistochemical analysis of the synovium revealed numerous multinucleated cells expressing the osteoclast markers TRAP and cathepsin K surrounding synovial tophi. The inflammatory infiltrate was composed of CD68+ macrophages, whereas CD3+ T and CD20+ B lymphocytes were lacking. Areas of bone erosions were characterized by penetration of osteoclast-enriched synovial tissue into broken cortical bone barrier. MRI signal alterations indicative of BME corresponded to discrete marrow fibrosis, increased number of blood vessels and mild infiltration of CD68+ mononuclear cells. No marrow lymphocytes were found. BME areas adjacent to the erosion front were also characterized by few scattered TRAP+ cathepsin+ multinucleated cells adherent to the subchondral trabecular bone.

Conclusion: This study represents the first imaging and histological description of BME in gout. Though BME is a frequent finding in the bone adjacent to tophi, it can only be observed in association with bone erosions. The subchondral marrow inflammatory lesions corresponding to MRI BME are milder in gout compared to rheumatoid arthritis and mainly consist of fibrosis and minimal infiltration of monocytes/macrophages. Although osteoclast-like cells can be found within the subchondral bone compartment in areas of BME, the largely predominate in the synovium. We propose that bone marrow involvement in gout is a secondary phenomenon which follows the intra-marrow invasion of the synovial membrane through bone erosions.

Disclosure of Interest: None declared

Citation: Ann Rheum Dis 2010;69(Suppl3):304

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