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Immunohistochemical detection of MT1‐MMP, RECK, and EMMPRIN in ameloblastic tumors
Author(s) -
Kumamoto H.,
Ooya K.
Publication year - 2006
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2006.00432.x
Subject(s) - immunohistochemistry , ameloblastoma , matrix metalloproteinase , extracellular matrix , basement membrane , pathology , odontogenic tumor , mesenchymal stem cell , medicine , biology , odontogenic , molar , dentistry , microbiology and biotechnology
Background: To evaluate the roles of matrix‐degrading proteinase regulators in progression of odontogenic tumors, expression of membrane‐bound matrix metalloproteinase (MMP) MT1‐MMP, MMP inhibitor RECK and MMP inducer EMMPRIN was analyzed in ameloblastic tumors as well as in tooth germs. Methods: Tissue specimens of 11 tooth germs, 40 ameloblastomas, and five malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against MT1‐MMP, RECK, and EMMPRIN. Results: Immunohistochemical reactivity for MT1‐MMP, RECK and EMMPRIN was detected predominantly in odontogenic epithelial cells near the basement membrane in tooth germs and benign and malignant ameloblastic tumors. The level of immunoreactivity for MT1‐MMP was slightly higher in benign and malignant ameloblastic tumors than in tooth germs. RECK expression was lower in ameloblastomas than in tooth germs. Follicular ameloblastomas showed significantly lower expression of RECK than plexiform ameloblastomas, and immunoreactivity for RECK in acanthomatous ameloblastomas was slightly lower than that in other cellular variants. Conclusion: Expression of MT1‐MMP, RECK and EMMPRIN in tooth germs and ameloblastic tumors suggests that these normal and neoplastic epithelial components control MMP‐dependent extracellular matrix (ECM) degradation during tooth development and tumor progression via epithelial‐mesenchymal interactions.