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. 2007 Sep;86(9):888-92.
doi: 10.1177/154405910708600916.

Apoptosis in gingival overgrowth tissues

A Kantarci  1 , P Augustin, E Firatli, M C Sheff, H Hasturk, D T Graves, P C Trackman
Affiliations

Apoptosis in gingival overgrowth tissues

A Kantarci et al. J Dent Res. 2007 Sep.

Abstract

Variations in the balance between cell proliferation and apoptosis could contribute to the etiology of gingival overgrowth. The aim of this study was to test the hypothesis that, in fibrotic gingival lesions, fibroblast proliferation is stimulated and apoptosis is decreased. Apoptotic index, caspase 3 expression, the proliferative index, FOXO1 expression, and histological inflammation were measured in situ. Analysis of data showed that apoptosis decreased in all forms of gingival overgrowth examined (p < 0.05), and inflammation caused a small but significant increase compared with non-inflamed tissues (p < 0.05). The greatest decrease of apoptosis occurred in the most fibrotic tissues. Cell proliferation was elevated in all forms of gingival overgrowth tested, independent of inflammation (p < 0.05). To identify potential mechanisms of transcriptional regulation of apoptosis, we assessed FOXO1 and caspase 3 expression levels and found them to correlate well with diminished apoptosis. Analysis of data suggests that increased fibroblast proliferation and a simultaneous decrease in apoptosis contribute to gingival overgrowth.

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Figures

Figure 1
Figure 1
Apoptotic index (% TUNEL-positive fibroblasts) (A) and proliferative index (% PCNA-positive fibroblasts) (B) in gingival overgrowth and control tissue samples. Data are expressed as means ± SD. In (A), the numbers of independent samples (n) per group are: no overgrowth control, 6; phenytoin overgrowth, 8; cyclosporin A overgrowth, 7; nifedipine overgrowth, 7; and gingival fibromatosis, 12. *p < 0.05 compared with control, cyclosporin A, and nifedipine; **p < 0.05 compared with control; #p < 0.05 compared with non-inflamed. In (B), (n) per group is: control, 6; phenytoin, 6; cyclosporin A, 6; nifedipine, 6; gingival and fibromatosis, 12. *p < 0.05 compared with control.
Figure 2
Figure 2
Caspase 3 expression in gingival tissues. Quantitative histomorphometric analyses of caspase 3 immunostaining in all forms of gingival overgrowth in inflamed and non-inflamed tissue areas (0.09 mm2). (n) per group is: control, 6; phenytoin, 8; cyclosporin A, 7; nifedipine, 7; and gingival fibromatosis, 12. *p < 0.05 compared with control and cyclosporin A; **p < 0.05 compared with control.
Figure 3
Figure 3
FOXO1 expression in gingival overgrowth and no overgrowth control tissues. (A) Representative sections for the immunohistochemical staining of FOXO1 expression in phenytoin and control tissues. Black arrows designate fibroblasts stained positive for FOXO1. Each bar represents 200 μm at a magnification of 200×. (B) Histomorphometric and quantitative analyses of FOXO1 immunostaining in all forms of gingival overgrowth in inflamed and non-inflamed tissue areas (0.09 mm2). (n) for control, 6; for phenytoin, 6; for cyclosporin A, 6; for nifedipine, 6; and for gingival fibromatosis, 8. *p < 0.05 compared with control; #p < 0.05 compared with non-inflamed.
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References

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