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

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.

Agrandamiento gingival farmacoinducido: Serie de casos

“…El AG se manifiesta como consecuencia de una deficiente higiene oral en el paciente (4,8) , así como se pudo observar en los cuatro pacientes, quienes presentaron acúmulo de biopelícula que conlleva a una colonización de bacterias en los tejidos dentarios y gingivales desencadenando un proceso inflamatorio como mecanismo de defensa (1) . El tejido gingival ingresa en un ciclo de lesión y remodelación que induce la producción de distintos factores quimiotácticos que influirán en el control del proceso de reparación; se ha demostrado la participación de nifedipino, fenitoína y ciclosporina en la expresión de citoquinas a nivel gingival, sugiriendo un mecanismo de lesión específico en el tejido (18) .…”