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Expression of extracellular matrix proteins in adenomatoid odontogenic tumor
Author(s) -
Modolo Filipe,
Biz Michelle Tillmann,
Martins Marília Trierveiller,
Machado de Sousa Suzana Orsini,
De Araújo Ney Soares
Publication year - 2010
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.1600-0714.2009.00846.x
Subject(s) - osteonectin , osteopontin , extracellular matrix , decorin , biglycan , pathology , tenascin , immunohistochemistry , chemistry , fibronectin , adenomatoid odontogenic tumor , calcification , proteoglycan , microbiology and biotechnology , biology , osteocalcin , medicine , anatomy , immunology , biochemistry , ameloblastoma , maxilla , alkaline phosphatase , enzyme
J Oral Pathol Med (2010) 39 : 230–235 Altered expression of extracellular matrix (ECM) components has been reported in several pathologies; however, few ECM proteins have been evaluated in adenomatoid odontogenic tumor (AOT). The aim of this study was to analyze the expression and distribution of the ECM proteoglycans: biglycan and decorin; and glycoproteins: osteonectin, osteopontin, bone sialoprotein and osteocalcin in the AOT. Three‐micrometer sections from paraffin‐embedded specimens were evaluated employing a streptavidin–biotin immunohistochemical method with the antibodies against the proteins previously cited. Only the osteonectin was expressed in the epithelial cells. The eosinophilic amorphous material and the connective tissue showed expression of all components studied. The calcification foci expressed only osteopontin. In conclusion, the low expression of the components studied in neoplastic epithelial cells suggests that the epithelial cells act probably as stimulators of the expression by the stroma, which in turn can act as agonist or antagonist of the tumor growth. These results suggest that the components studied probably have a key role in the biological behavior of the AOT.