bromochloroacetic-acid and Gingival-Overgrowth

The increasing frequency of using in the medical practice drugs that have the potential to induce gingival overgrowth (GO) and the existence of many unknown aspects in GO etiopathogenesis have prompted us to carry out this immunohistochemical experimental animal study. We conducted a cell proliferation study by Ki67 immunostaining and a cytokeratin (CK) study using anti-pan-CK AE1∕AE3 and anti-MNF116 antibodies, investigating the differences induced by different classes of drugs that are more frequently involved in the induction of GO. The results of our study indicate that CK AE1∕AE3 plays an important role not only in normal cellular proliferation, but also in hypertrophic tissues, and can be considered a marker of the proliferative process occurring in GO. Immunostaining for the anti-MNF116 antibody was weaker and inconsistent in intensity compared to anti-CK AE1∕AE3 antibody, its staining pattern appearing as diffuse or zonal.

Topics: Animals; Cell Proliferation; Female; Gingival Overgrowth; Humans; Immunohistochemistry; Keratins; Male; Rats

This investigation was undertaken to further study cyclosporin A (CsA)-induced gingival overgrowth. Thirty mg/kg/d of vehicle or CsA solutions were given orally to 6-wk-old male Sprague-Dawley rats. After 4, 9, 14 and 19 wk 2 control and 2 experimental rats were anaesthetized, tissues fixed by intracardiac perfusion of fixative solution and jaws processed for Epon inclusion. Histological and ultrastructural studies conducted in a gingival portion (free gingiva) revealed the presence of hyalinization areas and of multinucleated cells (MCs) containing collagen fibrils (connective tissue), of amorphous areas and disorders of keratinization (epithelia). Histomorphometric evaluation indicated that in the CsA rats the mean cross-sectional area of the free gingiva was 2.52-fold increased compared to the controls. The connective tissue comprised 41.43% of this area (instead of 31.49% in controls). Additional histomorphometric evaluation was performed in 3 groups of free gingival portions: control (C group), CsA-non-respondent (CsA-nR) and CsA-respondent (CsA-R). The cross-sectional gingival areas studied were slightly lower than the mean area of all the control sites previously defined (groups C and CsA-nR) or showed the higher degrees of enlargement (CsA-R). In the CsA-R group the mean cross-sectioned area of the vessel profiles was increased and the number of fibroblast profiles decreased. In the CsA-nR group the number of vessel profiles and that of MCs profiles were increased. In the epithelia of the CsA-R group were increased (a) keratinized epithelia: thickness; thickness of the inner and of the outer compartments; surface area of spinous cell profiles; (b) oral gingival epithelium: number of cell layers (inner compartment); (c) oral sulcular epithelium: surface area of granular cell profiles; (d) junctional epithelium: thickness; number of cell layers. These results indicate that (a) the CsA induced modifications are not limited to enlarged gingiva (b) the overgrowth of the GCT is the result of a vasodilatation and of an increase in the volume of the extracellular matrix and (c) the increase of the epithelial thickness is mainly the result of a cell hypertrophy in the keratinized epithelia and of a cell hyperplasia in the junctional epithelium.

Topics: Anatomy, Cross-Sectional; Animals; Cell Count; Collagen; Connective Tissue; Cyclosporine; Epithelial Attachment; Epithelium; Extracellular Matrix; Fibroblasts; Follow-Up Studies; Gingiva; Gingival Overgrowth; Hyalin; Hyperplasia; Immunosuppressive Agents; Keratins; Male; Microscopy, Electron; Pharmaceutical Vehicles; Rats; Rats, Sprague-Dawley; Vasodilation