Expressions of bax, bcl-2 and ki-67 in odontogenic keratocysts (keratocystic odontogenic tumor) in comparison with ameloblastomas and radicular cysts

Tekkeşın, Merva Soluk; Mutlu, Serdar; Olgaç, Vakur

doi:10.5146/tjpath.2012.01097

Cited by 36 publications

(45 citation statements)

References 19 publications

(16 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is in accordance with previous reports (10,11). In contrast, studies have also demonstrated a higher cell proliferation in AM in relation to KOT (7)(8).…”

Section: Discussionsupporting

confidence: 46%

“…Since KOT had been classified as an odontogenic cyst, several authors have compared cell proliferation between KOT and odontogenic cysts (8,12,13). Although several authors have assessed cell proliferation and apoptosis in the odontogenic epithelium in AM and in the epithelial lining in KOT (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22), few studies have compared cell proliferation between these tumors (7,8,11) and no previous study has simultaneously evaluated cell proliferation and apoptotic indexes in AM and KOT, comparing both lesions. Therefore, this is the first study assessing comparatively cell proliferation and apoptosis indexes in AM and KOT, although tissue cell population is controlled by a balance among these processes.…”

Section: Discussionmentioning

confidence: 99%

“…A higher proliferation activity in AM epithelium in relation to KOT epithelial lining has been demonstrated (7)(8)(9), even though opposite results have also been reported (10,11). Several studies have evaluated apoptosis and related apoptotic factors in the odontogenic epithelium of AM and epithelial lining of KOT (10)(11)(12)(13)(14)(15)(16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

“…Several studies have evaluated apoptosis and related apoptotic factors in the odontogenic epithelium of AM and epithelial lining of KOT (10)(11)(12)(13)(14)(15)(16)(17)(18)(19). Nevertheless, despite the fact that the cell population is controlled by the balance between cell proliferation and apoptosis, no study has evaluated simultaneously apoptotic and proliferation indexes in AMs and KOTs.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

et al. 2012

View full text Add to dashboard Cite

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

show abstract

“…This is in accordance with previous reports (10,11). In contrast, studies have also demonstrated a higher cell proliferation in AM in relation to KOT (7)(8).…”

Section: Discussionsupporting

confidence: 46%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Ki-67 can be difficult to detect using IHC, especially in decalcified tissue samples where IHC staining can become unstable. It is overexpressed in both SMAs and UAs compared to both normal tooth germs and other odontogenic lesions, with the exception of the KCOT which consistently has a higher PI compared to the ameloblastoma [32,[36][37][38]. Certainly our results did not indicate a significant difference between SMA (4.9 %) and UA tumors (4.3 %), although the ameloblastic carcinoma showed a noticeably higher PI of 11.4 %.…”

Section: Proliferation Index (Pi)contrasting

confidence: 36%

Immunohistochemistry of Five Molecular Markers for Typing and Management of Ameloblastomas: A Retrospective Analysis of 40 Cases

Singh

Chandu

Clement

et al. 2016

J. Maxillofac. Oral Surg.

View full text Add to dashboard Cite

Purpose The aims of this study are to elucidate if molecular markers can be used to differentiate between the two main types of ameloblastoma (unicystic and solid/multicystic), and to determine whether a biologically 'less-aggressive' subtype exists. Methods A retrospective analysis of 33 solid/multicystic ameloblastomas and six unicystic ameloblastomas was completed using immunohistochemistry for five molecular markers: P16, P53, MMP-9, Survivin, and Ki-67. Tumors were graded as either negative or positive (mild, moderate, strong), and the results were related to both ameloblastoma subtypes and outcomes following treatment.Results Unicystic ameloblastomas were more likely to test strongly positive for P53 than solid/multicystic ameloblastomas (p \ 0.05), whereas the latter were more likely to be negative for Survivin (p \ 0.05). Solid/multicystic and Type 3 unicystic ameloblastomas that were positive for P16, but also negative for MMP-9 and Survivin, were less likely to recur than all other tumors (p \ 0.05). The proliferation index of an ameloblastic carcinoma (11 %) was shown to be higher than benign ameloblastomas (4.5 %).Conclusions Immunohistochemistry can be valuable in lesions where histological sub-typing of an ameloblastoma is unclear. A biologically 'less-aggressive' subtype may exist, and hence further research into this area is required.

show abstract

Clinicopathological and cell proliferation evaluation of ameloblastomas and keratocystic odontogenic tumors: a 10 year retrospective study

Silva

Serpa

Santana

et al. 2016

Eur Arch Otorhinolaryngol

View full text Add to dashboard Cite

Odontogenic tumors (OTs) are important lesions of the gnathic bones due to their clinicopathological heterogeneity and variable biological behavior; therefore, epidemiological studies are needed to outline the incidence and behavior of these tumors. To evaluate the incidence and epidemiological profile of ameloblastoma (AMB) and keratocystic odontogenic tumor (KCOT) from an oral pathology service, and correlate morphological findings of these tumors with the immunoexpression of a cellular proliferation marker (Ki-67), a retrospective study (2002-2012) was conducted to characterize demographic, clinical, radiological, and morphological data of AMBs and KCOTs. Then, a representative sample composed of 49 cases of each tumor was selected to perform immunohistochemical (IHC) analysis of Ki-67 through the streptavidin biotin peroxidase technique. For statistical analysis, we used Fisher's exact test (p < 0.05). A total of 279 OTs were found in the service, in which 91 (32.6%) were AMB and 98 (35 %) were KCOT. Most cases occurred in white women, and the average age of patients with AMB and KCOT was 32 and 33 years, respectively. The maxilla-mandible ratio was 1:6 and 1:3.6 for AMB and KCOT, respectively. Regarding IHC analysis, AMB and KCOT had similar levels of cellular proliferation. However, KCOTs with intense inflammation showed higher Ki-67 expression (p < 0.001). Recurrent cases had similar Ki-67 immunoexpression. The demographic profile of the studied tumors corroborates with data reported in the literature, and the levels of cellular proliferation were similar in both tumors, although the inflammation seems to induce a differential proliferative behavior in KCOT.

show abstract

Expressions of bax, bcl-2 and ki-67 in odontogenic keratocysts (keratocystic odontogenic tumor) in comparison with ameloblastomas and radicular cysts

Cited by 36 publications

References 19 publications

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Immunohistochemistry of Five Molecular Markers for Typing and Management of Ameloblastomas: A Retrospective Analysis of 40 Cases

Clinicopathological and cell proliferation evaluation of ameloblastomas and keratocystic odontogenic tumors: a 10 year retrospective study

Contact Info

Product

Resources

About