Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Abstract

Braz Dent J 23(2) 2012Proliferation and apoptosis in odontogenic tumors 91 INTRODUCTIONAmeloblastoma (AM) is a locally invasive benign epithelial odontogenic tumor that may arise from rests of dental lamina, enamel organ rests, cell rests, the epithelial lining of an odontogenic cyst or from the basal cell layer of oral mucosa (1). Its occurrence varies from 10% to 45.2% of all odontogenic tumors and reaches approximately 1% of all oral cavity neoplasms (2). The usual clinical presentation includes a painless swelling with expansion of the jaws. It can be classified in 3 main groups: solid or multicystic ameloblastoma, unicystic and peripheral. Among these, the solid type is more common and histopathologically represented by follicular, plexiform, acanthomatous, desmoplastic, granular and basal cell patterns (3). A high proliferative activity of the odontogenic epithelium in ameloblastoma (AM) and keratocystic odontogenic tumor (KOT) has been demonstrated. However, no previous study has simultaneously evaluated cell proliferation and apoptotic indexes in AM and KOT, comparing both lesions. The aim of this study was to assess and compare cell proliferation and apoptotic rates between these two tumors. Specimens of 11 solid AM and 11 sporadic KOT were evaluated. The proliferation index (PI) was assessed by immunohistochemical detection of Ki-67 and the apoptotic index (AI) by methyl green-pyronine and in situ DNA nick end-labelling methods. KOT presented a higher PI than AM (p<0.05). No statistically significant difference was found in the AI between AM and KOT. PI and AI were higher in the peripheral cells of AM and respectively in the suprabasal and superficial layers of KOT. In conclusion, KOT showed a higher cell proliferation than AM and the AI was similar between these tumors. These findings reinforce the classification of KOT as an odontogenic tumor and should contribute to its aggressive clinical behavior. Cell Proliferation and Apoptosis in Ameloblastomas and Keratocystic Odontogenic Tumors

Immunohistochemical expression of Type IV Collagen and Autocrine Motility Factor Receptor in Odontogenic Tumours

“…Amorim RFB et al, [15] correlated the negative expression of type IV Collagen in basement membrane of Nevoid Basal Cell Carcinoma Syndrome (NBCCS) related KCOT with the aggressive biological behaviour of KCOT. Amaral FR et al, [16] studied the cell proliferative index and…”

Immunohistochemical expression of p63, epidermal growth factor receptor (EGFR) and notch-1 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors

“…Recent studies have focused on the etiopathogenesis of chronic periapical lesions, odontogenic cysts and tumors, using immunohistochemistry to investigate the role of cytokines, growth factors, cellular differentiation factors, tumor suppressor genes and oncogenes in the initiation, development, and progression of these lesions (4,6,(12)(13)(14)(15)(16)(17).…”

Targeting Ameloblatoma into Apoptosis

“…In accordance with the expressions of apoptotic ligand and receptor in central cells, expressions of p53 (8,15), phosphatase and tensin homolog (PTEN) (16), phosphorylated-PTEN (16), phosphorylated-Jun N-terminal kinase (JNK) (17), Bcl-2 associated X protein (Bax) (3,6), Bcl-2 homologous antagonist killer (Bak) (3,5,7), caspase 9 (18), apoptotic protease activating factor-1 (APAF-1) (18), caspase 3 (19), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) (14,20) were observed in central cells as well. Hence, some reports suggested that central cells have higher apoptotic activity than peripheral cells.…”

“…Hence, some reports suggested that central cells have higher apoptotic activity than peripheral cells. (3,6,14,20) Targeting ameloblastoma by inducing it into apoptosis could be a beneficial strategy, since many ameloblastoma cases were reported recurrent after surgical therapy. (1) Apoptosis-inducing Ligands TNF-α TNF-α is mainly produced by macrophages and monocytes.…”