Background <p>The aim of this study was to investigate the role of apoptosis in nifedipine-induced gingival overgrowth in a rat model using histologic, histomorphometric and immunohistochemical methods.</p> Methods <p>Thirty-two male Wistar rats were divided into the nifedipine (NIF) and control (C) groups. The NIF group received nifedipine for 30 days, after which the drug was discontinued, while the control group received no treatment. Gingival tissues from both groups were analyzed on days 30 and 70 using histomorphometry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling method for apoptotic cells.</p> Results <p>The NIF group showed significant increases in epithelial height, connective tissue height and width compared to the controls on both days 30 and 70 (<i>P</i> &lt; 0.05). Epithelial width increased only on day 30. Gingival overgrowth in the NIF group decreased significantly from day 30 to 70 (<i>P</i> &lt; 0.05); however, it remained elevated compared to the controls. No significant differences were found in the percentage of apoptotic cells within the groups over time or between groups at any time point (<i>P</i> &gt; 0.05).</p> Conclusions <p>Although nifedipine induced significant gingival overgrowth, apoptosis did not appear to play a major role in its progression or resolution. Further research is required to elucidate the precise molecular pathways involved.</p>

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Histomorphometric and immunohistochemical evaluation of apoptosis in nifedipine-induced gingival overgrowth

  • Cem Mangıroğlu,
  • İlhami Çelik,
  • Burcu Karaduman,
  • Mihtikar Gürsel

摘要

Background

The aim of this study was to investigate the role of apoptosis in nifedipine-induced gingival overgrowth in a rat model using histologic, histomorphometric and immunohistochemical methods.

Methods

Thirty-two male Wistar rats were divided into the nifedipine (NIF) and control (C) groups. The NIF group received nifedipine for 30 days, after which the drug was discontinued, while the control group received no treatment. Gingival tissues from both groups were analyzed on days 30 and 70 using histomorphometry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling method for apoptotic cells.

Results

The NIF group showed significant increases in epithelial height, connective tissue height and width compared to the controls on both days 30 and 70 (P < 0.05). Epithelial width increased only on day 30. Gingival overgrowth in the NIF group decreased significantly from day 30 to 70 (P < 0.05); however, it remained elevated compared to the controls. No significant differences were found in the percentage of apoptotic cells within the groups over time or between groups at any time point (P > 0.05).

Conclusions

Although nifedipine induced significant gingival overgrowth, apoptosis did not appear to play a major role in its progression or resolution. Further research is required to elucidate the precise molecular pathways involved.