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The Journal of Nuclear Medicine Vol. 39 No. 9 1638-1645
© 1998 by Society of Nuclear Medicine
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Rat Antigen-Induced Arthritis: Cartilage Alterations Assesed with Iodine-123-Antileukoproteinase

Raimund W. Kinne, Philipp Meyer, Winfried Gründer, Eberhard Buchner, Ernesta Palombo-Kinne, Regina Heinzel-Wieland, Wolfgang Becker, Friedrich Wolf, Joachim R. Kalden and Harald Burkhardt

Institute of Clinical Immunology and Transfusion Medicine and Institute of Biophysics, University of Leipzig, Leipzig, Germany
Fachbereich Chemische Technologie, Fachhochschule Darmstadt, Darmstadt, Germany
Department of Nuclear Medicine and Institute of Clinical Immunology and Rheumatology, Department of Internal Medicine III, University of Erlangen-Nuremberg, Nuremberg, Germany

Correspondence: For correspondence or reprints contact Raimund W. Kinne, MD, Experimental Rheumatology Unit, Bachstr. 18, D-07740 Jena, Germany.

ABSTRACT

Imaging of cartilage alterations was attempted in joints of rats with chronic antigen-induced arthritis (AIA)using the cationic 123-labeled seine proteinase inhibitor antileukoproteinase (123I-ALP; pl > 10), which selectively accumulates in normal cartilage, presumably through interaction with negatively charged proteoglycans. Methodes:Iodine-123-ALP or 123I-myoglobin, a control protein of comparable size but with different isoelectric point (pl= 7.3) was injected intravenously into normal or AIA rats. Joint accumulation was followed by scintigraphy for 14 hr. Tissue radioactivity was assessed by well-counter measurements after dissection. The content of charged molecules in articular cartilage was determined by toluidine blue staining; the degree of joint destruction was assessed in parallel by x-ray, ex vivo MRI and histopathology. Results: In intact articular cartilage, ALP accumulated to a significantly higher degree than myoglobin. This preferential accumulation was lost in rats with chronic AIA. The target-to-background ratio for 123I-ALP negatively correlated with the loss of toluidine blue staining in cartilage, which documents depletion of charged matrix molecules (r = -0.92,p < 0.01 at 4 hr; r = -0.97,p < 0.01 at 13 hr). ALP scintigraphy was sensitive in detecting cartilage alterations, even though the degree of joint destruction and inflammatory infiltration was mild, as demonstrated by x-ray, MRI and histopathology. Conclusion: In rat AIA, loss of ALP accumulation appears to document proteoglycan depletion in mildly altered arthritic cartilage. ALP scintigraphy may represent a functional assay for early, premorphological cartilage alterations in human arthritis as well.

Key Words: scintigraphy • x-ray • MRI • iodine-123 • antileukoproteinase







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