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(American Journal of Pathology. 2001;158:1465-1472.)
© 2001 American Society for Investigative Pathology

Regular Articles

Cartilage-Specific Matrix Protein Chondromodulin-I Is Associated with Chondroid Formation in Salivary Pleomorphic Adenomas

Immunohistochemical Analysis

Kimihide Kusafuka^*, Yuji Hiraki, Chisa Shukunami, Akira Yamaguchi, Teruo Kayano^§ and Tamiko Takemura^*

From the Department of Pathology,^*
Japanese Red Cross Medical Center, Tokyo; the Department of Molecular Interaction and Tissue Engineering,
Institute for Frontier Medical Sciences, Kyoto University, Kyoto; the Department of Oral Pathology,
School of Dentistry, Nagasaki University, Nagasaki; and the Section of Forensic Dentistry,^§
Division of Public Health, Department of International Health Development, Graduate School, Tokyo Medical and Dental University, Tokyo, Japan

Chondromodulin-I (ChM-I) is a novel cartilage-specific matrix protein. In the growth plates of the long bones, ChM-I was shown to be expressed in mature to upper hypertrophic chondrocytes, and to be deposited in the cartilage matrix. As ChM-I strongly inhibits angiogenesis, cartilage is avascular. Also, ChM-I has bifunctional activity against chondrocyte proliferation. On the other hand, pleomorphic adenomas of the salivary glands frequently have chondroid elements. To elucidate the relationship between chondroid formation and hypovascularity in salivary pleomorphic adenomas, we immunohistochemically examined the expression and localization of ChM-I in 35 cases of this tumor. ChM-I was immunolocalized to the lacunae in the chondroid elements of pleomorphic adenomas (100%). Type II collagen and aggrecan were immunolocalized throughout the matrix around lacuna cells of the chondroid element (100%, 91.7%), and ChM-I was infrequently immunolocalized to the spindle-shaped myoepithelial cells in the myxoid element (37.5%). Fibroblast growth factor-2 was strongly immunolocalized to the lacuna cells in the chondroid element (100%), among the neoplastic myoepithelial cells in the myxoid elements (96.9%), and on the basement membranes around the solid nests of neoplastic myoepithelial cells (71.4%). Although CD34 is a marker of endothelial cells, CD34 was expressed in the endothelial cells in only a few areas around the epithelial elements and in the fibrous element of pleomorphic adenomas. No signals for CD34 were observed in chondroid elements in pleomorphic adenomas (P < 0.001), but a few signals were seen in the myxoid elements (P < 0.05). These findings suggested that lacuna cells and neoplastic myoepithelial cells expressed ChM-I, and that this molecule may play an important role in hypovascularity and chondroid differentiation in pleomorphic adenoma. In conclusion, pleomorphic adenoma expressed ChM-I, which is involved in hypovascularity and chondroid formation in this type of tumor.