Quantitative and qualitative analysis of argyrophilic nuclear organizer regions in follicular cyst, keratocystic odontogenic tumor and ameloblastoma

Seifi, Safoura; Shafigh, E; Allaie, Ayoub

doi:10.4103/0973-1482.87017

Cited by 9 publications

(5 citation statements)

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“…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%

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Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

et al. 2012

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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

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

et al. 2012

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“…While the proliferation index and expression of apoptosis‐related proteins in OCLs seems to be quite significant for their clinical behavior (Seifi et al , 2011; Soluk Tekkeşın et al , 2012), interestingly, it has been proposed that immune reactions can to contribute with the proliferation and differentiation of the cystic epithelium (Yanagisawa, 1980; Gao et al , 1988; Piattelli et al , 2002). Accordingly, several researches have been developed focusing the study of different cells of the immune system, as well as cellular receptors and inflammatory cytokines, in an attempt to elucidate the mechanisms involved in the pathogenesis of OCLs (Matthews and Browne, 1987; Gao et al , 1988; Murase et al , 1990; Akhlaghi and Dourov, 1995; Suzuki et al , 2001; Piattelli et al , 2002; de Noronha Santos Netto et al , 2012).…”

Section: Introductionmentioning

confidence: 99%

Immunophenotypic characterization and distribution of dendritic cells in odontogenic cystic lesions

et al. 2012

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Oral Diseases (2012) 19, 85–91 Objective: To analyze the expression and distribution patterns of mature dendritic cells (mDCs) and immature DCs (imDCs) in radicular cysts (RCs), dentigerous cysts (DtCs), and keratocystic odontogenic tumors (KCOTs). Materials and methods: Forty‐nine odontogenic cystic lesions (OCLs) (RCs, n = 20; DtCs, n = 15; KCOTs, n = 14) were assessed using the following markers: S100, CD1a and CD207 for imDCs; and CD83 for mDCs. Results: Almost all cases were S100, CD1a, and CD207 positive, whereas 63% were CD83 positive. RCs presented greater number of immunostained cells, followed by DtCs, and KCOTs. The number of S100+ cells was greater than both CD1a+ and CD207+ cells (P < 0.001), which showed approximately similar amounts, followed by lower number of CD83+ cells (P < 0.001) in each OCL type. Different from S100+ cells, both CD1a+ and CD207+ cells on the epithelium (P < 0.05) and CD83+ cells on the capsule (P < 0.05) were preferentially observed. In RCs, significant correlation was found between the thickness epithelium with S100+ and CD1a+ cells, and between the degree of inflammation with CD83+ cells. Conclusions: Dendritic cell populations in OCLs can be phenotypically heterogeneous, and it could represent distinct lineages and/or functional stages. It is suggested that besides DC‐mediated immune cell interactions, DC‐mediated tissue differentiation and maintenance in OCLs should also be considered.

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“…23 However, the finding of similar mAgNORs in SA and UA is in contrast to previous reports of a statistically higher mAgNOR in SA. [24][25][26] A closer comparison of studies revealed differences in AgNOR quantification criteria, as well in sample size (see Supplemental Table I). One important factor that can explain the different results with regard to cells counted, is that both basal and parabasal cells were considered in our study, whereas Colemann et al 24 quantified only basal cells, Ananthaneni et al 26 did not specify which cells were counted (basal or parabasal), and Seifi et al 25 used different criteria for quantification, considering also AgNORs outside the nucleus, which may explain why they observed much higher values than the other studies.…”

Section: Discussionmentioning

confidence: 99%

Ameloblastic neoplasia spectrum: a cross-sectional study of MMPS expression and proliferative activity

Silva

Nóbrega

Saudades

et al. 2016

Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology

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Quantitative and qualitative analysis of argyrophilic nuclear organizer regions in follicular cyst, keratocystic odontogenic tumor and ameloblastoma

Cited by 9 publications

References 0 publications

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Immunophenotypic characterization and distribution of dendritic cells in odontogenic cystic lesions

Ameloblastic neoplasia spectrum: a cross-sectional study of MMPS expression and proliferative activity

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