Apoptosis in gingival overgrowth tissues.
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.
Kantarci
A
A
Department of Periodontology and Oral Biology, Boston University, Goldman School of Dental Medicine, Boston, MA 02118, USA.
Augustin
P
P
Firatli
E
E
Sheff
M C
MC
Hasturk
H
H
Graves
D T
DT
Trackman
P C
PC
D000927:Anticonvulsants / Q000009:adverse effects; D017209:Apoptosis / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000009:adverse effects; D016022:Case-Control Studies; D053148:Caspase 3 / Q000096:biosynthesis; D049109:Cell Proliferation; D016572:Cyclosporine / Q000009:adverse effects; D005347:Fibroblasts / Q000473:pathology; D005351:Fibromatosis, Gingival / Q000473:pathology; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D019214:Gingival Overgrowth / Q000139:chemically induced / Q000473:pathology*; D005891:Gingivitis / Q000473:pathology; D006801:Humans; D007166:Immunosuppressive Agents / Q000009:adverse effects; D020287:In Situ Nick-End Labeling; D009543:Nifedipine / Q000009:adverse effects; D010672:Phenytoin / Q000009:adverse effects; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis
D000927:Anticonvulsants; D002121:Calcium Channel Blockers; C085126:FOXO1 protein, human; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors; D007166:Immunosuppressive Agents; D018809:Proliferating Cell Nuclear Antigen; D010672:Phenytoin; D016572:Cyclosporine; D053148:Caspase 3; D009543:Nifedipine