Immunohistochemical Analysis of Cell Proliferation and Bcl-2 Expression in Drug-Induced Gingival Overgrowth

Ana Luzia Araújo Batista, Angélica Kercya Pereira de Mendonça, Roseana de Almeida Freitas, Pollianna Muniz Alves, Gustavo Pina Godoy, Cassiano Francisco Weege Nonaka, Ruthineia Diógenes Alves Uchôa Lins

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.

Keywords


Gingival Overgrowth; Ki-67 Antigen; Genes, bcl-2; Immunohistochemistry

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References


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DOI: http://dx.doi.org/10.4034/PBOCI.2017.171.08

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