Immunohistochemical Evaluation of Ki-67 Expression and Apoptosis in Cyclosporin A-Induced Gingival Overgrowth

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Abstract

Background:

This study was planned to evaluate cell division rate and apoptosis by immunohistochemical and in situ hybridization techniques in cyclosporin A (CsA)-induced gingival overgrowth tissue samples to determine whether these processes played a role in the pathogenesis of this condition.

Methods:

Fourteen CsA-induced overgrowth tissues from renal transplant recipients, 10 control tissues from patients with plaque-induced gingivitis, and 14 control tissues from systemically and periodontally healthy subjects were evaluated. In patient groups, clinical periodontal recordings and tissue sampling were performed before initiation of any periodontal intervention. Numbers of Ki-67-positive cells/field and apoptotic cells/field in formalin-fixed/paraffin-embedded tissue sections were determined. Data were evaluated by oneway analysis of variance, post hoc Sidak test with modified Bonferroni correction, and Pearson correlation analysis. Three phenytoin- and five nifedipine-induced overgrowth tissues were also processed in the same way, and findings in these tissue specimens were evaluated as case series.

Results:

The number of keratinocytes was significantly greater in the CsA-induced gingival overgrowth group than in the healthy control group (P <0.05). Cells labeled by in situ end labeling, namely the apoptotic cells, were significantly fewer in the CsA group than in the gingivitis and healthy control groups (P <0.01). Overall, statistically significant positive correlations were found between the numbers of Ki-67-positive cells and probing depth and hyperplastic, bleeding, and plaque indices (P <0.01). Phenytoin and nifedipine samples exhibited obviously higher expression of Ki-67-positive cells than the CsA, gingivitis, and healthy control groups.

Conclusion:

Our findings suggest that decreased apoptosis may have a more prominent role than increased cell division in the pathogenesis of CsA-induced gingival overgrowth. J Periodontol 2007;78:282-289.

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