Abstract
Objective: To compare the rate of cell proliferation and expression of antiapoptotic protein Bcl-2 between drug-induced gingival overgrowth (DIGO) and clinical healthy gingiva (CHG) and to establish associations with histopathological features. Material and Methods: Twenty specimens of DIGO and 20 CHG specimens were submitted to morphological and immunohistochemical analysis by light microscopy. Cell proliferation (Ki-67) and the expression of Bcl-2 were evaluated in epithelial cells and spindle-shaped mononuclear cells of the connective tissue by establishing the labeling index (LI). Results: In epithelial tissue, the mean LI for Ki-67 was 17.2% in DIGO and 21.71% in CHG ( p = 0.137). The mean LIs for Bcl-2 in epithelial tissue were 14.67% and 10.24% in DIGO and CHG, respectively ( p = 0.026). In connective tissue, DIGO and CHG specimens exhibited low LIs for Ki-67 and Bcl-2, with mean values of less than 0.5% in both groups. No significant differences in the LIs for Ki-67 or Bcl-2 in epithelial tissue were observed according to the degree of collagenization, degree of vascularization and intensity of inflammatory infiltration ( p > 0.05). No significant correlations were observed between the LIs for Ki-67 and Bcl-2 ( p > 0.05). Conclusion: The present results suggest that the pathogenesis of DIGO does not involve increased proliferation or decreased apoptosis of fibroblasts. On the other hand, the morphological pattern of elongated epithelial cristae observed in DIGO could mainly be due to the inhibition of keratinocyte apoptosis and not to increased proliferation of these cells.
Highlights
Drug-induced gingival overgrowth (DIGO) is an important side effect of the administration of certain drugs, anticonvulsants, immunosuppressants and calcium channel blockers (CCBs) [1]
The present results suggest that the pathogenesis of drug-induced gingival overgrowth (DIGO) does not involve increased proliferation or decreased apoptosis of fibroblasts
The morphological pattern of elongated epithelial cristae observed in DIGO could mainly be due to the inhibition of keratinocyte apoptosis and not to increased proliferation of these cells
Summary
Drug-induced gingival overgrowth (DIGO) is an important side effect of the administration of certain drugs, anticonvulsants, immunosuppressants and calcium channel blockers (CCBs) [1]. The etiopathogenesis of DIGO is not fully understood, studies suggest this disorder to be induced by the rupture of homeostasis between the synthesis and degradation of collagen and other extracellular matrix (ECM) components, as well as between cell proliferation and apoptosis involving the gingival epithelium and connective tissue [1,2,6,7,8,9,10]. The pathogenesis of DIGO has been suggested to be related to the presence of a genetically determined subpopulation of drug-sensitive fibroblasts, which may respond by increasing cell proliferation/survival or by altering the synthesis and remodeling of ECM [3,6,11,12,13].
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