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Expression of fibronectin‐binding integrins in gingival epithelium in drug‐induced gingival overgrowth
Author(s) -
Walsh P.,
Häkkinen L.,
Pernu H.,
Knuuttila M.,
Larjava H.
Publication year - 2007
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2006.00927.x
Subject(s) - integrin , fibronectin , epithelium , fibrosis , connective tissue , immunohistochemistry , junctional epithelium , ctgf , chemistry , microbiology and biotechnology , medicine , pathology , biology , receptor , extracellular matrix , growth factor
Background and Objective: Gingival overgrowth is a side‐effect of nifedipine and cyclosporin medications. Integrins are transmembrane glycoproteins that mediate cell adhesion, regulate cell proliferation and participate in the regulation of tissue fibrosis. The aim of this study was to investigate whether expression of epithelial cell integrins is linked to the development of drug‐induced gingival overgrowth. Material and Methods: Human gingival biopsies of patients taking nifedipine, cyclosporin, or a combination of both medications, were used. Expression of the α5β1, αvβ1 and αvβ6 integrins, and of cellular extra domain A of fibronectin, was localized in frozen sections using immunohistochemistry. Results: The activated conformation of the β1, α5β1 and αvβ6 integrins were more frequently expressed in distinct locations in the oral epithelium in the combined drug group. Cellular extra domain A of fibronectin, a ligand for both α5β1 and αvβ6 integrins, was expressed within the connective tissue of all groups. It was also expressed around the basal keratinocytes of the control, nifedipine and cyclosporin‐induced gingival overgrowth groups, but not in the combined medication group. No relationship between the presence of inflammation and integrin expression was found. Conclusion: The results indicate that expression of certain integrins is up‐regulated in the epithelium of drug‐induced gingival overgrowth where they could participate in controlling the formation of elongated rete ridges and tissue fibrosis.