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Syndecan‐1 (CD 138) surface expression marks cell type and differentiation in ameloblastoma, keratocystic odontogenic tumor, and dentigerous cyst
Author(s) -
AlOtaibi Ohoud,
Khounganian Rita,
Anil Sukumaran,
Rajendran Ravindranath
Publication year - 2013
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.1600-0714.2012.01195.x
Subject(s) - dentigerous cyst , ameloblastoma , keratocystic odontogenic tumor , pathology , odontogenic tumor , stromal cell , biology , keratocyst , immunohistochemistry , odontogenic cyst , lesion , cyst , medicine , anatomy , odontogenic , maxilla
J Oral Pathol Med (2013) 42 : 186–193 Background: The altered expression of syndecan‐1 (SD‐1), a transmembrane heparan sulfate proteoglycan, in ameloblastomas and cysts of odontogenic origin suggests that this molecule could have prognostic value in assessing the clinical outcome of those lesions. The purpose of this study was to analyze SD‐1 expression profile immunohistochemically in archival, paraffin‐embedded tissue sections of ameloblastomas and in common odontogenic cysts arising from the same locale. Methods: SD‐1 expression was investigated in 32 ameloblastomas, 26 keratocystic odontogenic tumors (KCOT), and 21 dentigerous cysts from the archives of the histopathology laboratory which were routinely processed. The cases were reviewed and assessed according to the established criteria. Sections were immunostained with monoclonal antibody against SD‐1 (CD138). Sections of normal oral mucosa, site matched, were stained in parallel as positive controls. The plasma cells in sections served as internal positive controls. Results: SD‐1 expression was observed in the epithelial and stromal elements of the sections, and the expression was significantly associated with the lesion’s extension and involvement of adjacent structures ( P = 0.025). Stellate‐reticulum cells showed higher expression than the ameloblasts, which was at a significant level ( P < 0.0001). Highly significant difference was reported among the three groups of lesion for the epithelial staining ( P < 0.0001). The mean rank scores (Kruskal–Wallis test) of ameloblastomas were significantly lower than those of KCOT and dentigerous cysts. Non‐significant comparison was made between KCOT and dentigerous cyst groups. Conclusions: The present study revealed SD‐1 immunoreactivity in the stromal cells of ameloblastoma, KCOT, and dentigerous cysts rather uniformly. This reported SD‐1 expression by the tumor stroma is considered to be associated with poor prognosis of the lesions.