Premium
Matrix metalloproteinase 7 and perlecan in oral epithelial dysplasia and carcinoma in situ : an aid for histopathologic recognition of their cell proliferation centers
Author(s) -
Tilakaratne W. M.,
Kobayashi T.,
IdaYonemochi H.,
Swelam W.,
Yamazaki M.,
Mikami T.,
Alvarado C. G.,
Shahidul A. Md.,
Maruyama S.,
Cheng J.,
Saku T.
Publication year - 2009
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.1600-0714.2009.00750.x
Subject(s) - epithelial dysplasia , pathology , immunohistochemistry , perlecan , dysplasia , stromal cell , biology , malignant transformation , epithelium , carcinoma in situ , carcinoma , matrix metalloproteinase , extracellular matrix , medicine , proteoglycan , microbiology and biotechnology , biochemistry
Background: As one of the valuable tools for differential diagnoses of oral epithelial dysplasia, carcinoma in situ (CIS) and squamous cell carcinoma (SCC), we have proposed the immunohistochemistry for perlecan, a heparan sulfate proteoglycan (HSPG). As HSPGs have been shown to be extracellular docking molecules for matrix metalloproteinase (MMP) 7, our aim was to determine the expression mode of MMP‐7 in these lesions for its possible diagnostic aid for oral borderline malignancies. Methods: Twenty cases each of moderate dysplasia, CIS, SCC, and normal/hyperplastic/mild dysplastic epithelia of the tongue and buccal mucosa were immunohistochemically examined for MMP‐1, ‐2 and ‐7 in reference to their perlecan immunolocalization. Results: The expression of all three MMPs in the normal mucosal epithelium was restricted mainly to the parabasal layers. The most striking finding was strong expression of MMP‐7 in epithelial dysplasia with a two‐phase appearance: a clear demarcation of MMP‐7‐immunopositive (+) lower dysplastic/basaloid cells from non‐positive upper keratinized cells. MMP‐7+ cells were spread over the whole epithelial layer of CIS. In SCC, MMP‐7 positivity was reduced from carcinoma cells but instead appeared in stromal cells. These expression profiles of MMP‐7 resembled those of perlecan. MMP‐1 and MMP‐2 exhibited a similar but much weaker staining than MMP‐7. Conclusion: These results suggest that the enhanced metabolism of perlecan associated with MMP‐7 plays an important role in the cell proliferation of oral epithelia in their malignant transformation process, and that MMP‐7 immunohistochemistry may be a valuable aid for identification of the cell proliferation center in oral CIS and dysplasia.