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Rev Med Chir Soc Med Nat Iasi ; 112(4): 1026-33, 2008.
Article in Romanian | MEDLINE | ID: mdl-20209781

ABSTRACT

Human gingival overgrowth may occur as a side effect of chronic administration of some therapeutic agents. The mechanisms responsible for the gingival tissues lesions, fibrosis and inflamation, involve an impaired balance between the production and the degradation of type I collagen. It has been demonstrated that CCN2/CTGF, a connective tissue growth factor, is highly expressed in the gingival tissues and positively correlated with the degree of fibrosis in the drug-induced gingival overgrowth. The aim of this study was to identify the presence and localization of CCN2/CTGF and CCN1/Cyr61, members of the same molecular family, in gingival tissues of cyclosporin A- and nifedipine-treated rats, by immunohistochemistry. Staining was evaluated with light microscope and the results show cellular and extracellular CTGF in nifedipin gingival overgrowth tissues with intensity of labeling higher compared to the CsA gingival overgrowth tissues or the controls. The staining for Cyr61 shows its intracellular localization with no diference of labeling intensity between drug-induced gingival overgrowth and normal tissues. Also, we were interested in the gingival TGF-â expression in those animals. We didn't find any commercial anti-rat TGF antibody and our anti-human antibody shows no cross-reactivity with rat tissues. The data from our study sustain the involvement of CTGF and Cyr61 as growth factors in the gingival tissues and the CTGF association with drug-induced gingival overgrowth.


Subject(s)
Connective Tissue Growth Factor/metabolism , Cysteine-Rich Protein 61/metabolism , Gingival Hyperplasia/chemically induced , Gingival Hyperplasia/metabolism , Gingival Overgrowth/metabolism , Gingival Overgrowth/pathology , Animals , Cyclosporine/pharmacology , Disease Models, Animal , Fibromatosis, Gingival/metabolism , Fibromatosis, Gingival/pathology , Gingival Hyperplasia/pathology , Gingival Overgrowth/chemically induced , Immunohistochemistry , Immunosuppressive Agents/pharmacology , Male , Nifedipine/pharmacology , Rats , Rats, Wistar , Vasodilator Agents/pharmacology
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