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Cartilage Intermediate Layer Protein Expression in Calcium Pyrophosphate Dihydrate Crystal Deposition Disease
KOJI YAMAKAWA, HIROSHI IWASAKI, IKUKO MASUDA, YUKO OHJIMI, ITSUO HONDA, KEN-ICHI IYAMA, EISUKE SHONO, MASATOSHI NAITO, and MASAHIRO KIKUCHI
ABSTRACT.
Methods. Histological sections and clinical data from 33 patients who fulfilled the criteria of Ryan and McCarty for CPPD were reviewed. Formalin fixed and paraffin embedded tissue sections of 33 patients with CPPDCD were stained with hematoxylin and eosin (H&E) and alizarin red S. Immunostaining was performed using affinity purified polyclonal antibody to synthetic peptide corresponding to the N-terminal sequence of the 61 kDa domain of porcine CILP. Results. The age of patients ranged from 49 to 89 years (median 73). The knee was the commonest site. Radiologically, almost all lesions exhibited fine, radiopaque, linear deposits in the meniscus, articular cartilage, and synovium or joint capsule. Histopathologically, all cases showed deposits of birefringent monoclinic or triclinic crystals, which were visualized by polarized light microscopy with a red analyzer filter. In alizarin red S staining, more numerous crystals were observed than in H&E staining. Crystal deposition was usually associated with adjacent variable amounts of hypertrophic and/or metaplastic chondrocytes in each type of tissue. Variable intensity of CILP immunostaining was found in deposits of each lesion. Hypertrophic/metaplastic chondrocytes in and around CPPD deposits were also positive for CILP. Small cartilaginous islands remote from the CPPD deposits exhibited a weak positivity for CILP. In addition, weakly positive chondrocytes were noted in a transitional zone between cartilaginous islands with and without the deposits. In addition to cytoplasmic immunoreactivity, immunostaining for CILP was observed in the pericellular fibrous matrix. Conclusion. Hypertrophic or metaplastic chondrocytes characteristic of CPPDCD may be directly involved in the formation of CPPD crystals. Our study suggests that increased CILP expression was closely associated with CPPDCD, and might play a role in promoting CPPD crystal formation. (J Rheumatol 2002;29:1746-53) Key Indexing Terms:
CALCIUM PYROPHOSPHATE DIHYDRATE CRYSTAL DEPOSITION DISEASE
From the First Departments of Pathology and Orthopedic Surgery, Fukuoka University School of Medicine, Fukuoka, Japan; the Department of Medicine, Division of Rheumatology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA; Department of Surgical Pathology, Kumamoto University School of Medicine, Kumamoto; and Department of Pathology, Kumamoto Orthopedic Hospital, Kumamoto, Japan. Dr. Masuda's work was supported by NIH grant AR44862. K. Yamakawa, MD, PhD; H. Iwasaki, MD, PhD, Professor, First Department of Pathology, Fukuoka University School of Medicine; I. Masuda, MD, PhD, Assistant Professor, Department of Medicine, Division of Rheumatology, Medical College of Wisconsin; Y. Ohjimi, MD, PhD, Instructor, First Department of Pathology, Fukuoka University School of Medicine; I. Honda, MD, PhD, Chief, Department of Pathology, Kumamoto Orthopedic Hospital; K. Iyama, MD, PhD, Associate Professor and Chief, Department of Surgical Pathology, Kumamoto University School of Medicine; E. Shono, MD, PhD, Instructor; M. Naito, MD, PhD, Chief Professor, Department of Orthopedic Surgery; M. Kikuchi, MD, PhD, Chief Professor, First Department of Pathology, Fukuoka University School of Medicine. Address reprint requests to Dr. K. Yamakawa, First Department of Pathology, Fukuoka University School of Medicine, Nanakuma 7-45-1, Jonan-ku, Fukuoka 814-0180, Japan. Submitted August 8, 2001; revision accepted February 14, 2002. |