Cell proliferation, apoptosis and apoptosis‐related factors in odontogenic keratocysts and in dentigerous cysts

Kichi, Eisuke; Enokiya, Yasunobu; Muramatsu, Takashi; Hashimoto, Sadamitsu; Inoue, Takashi; Abiko, Yoshihiro; Shimono, Masaki

doi:10.1111/j.1600-0714.2005.00314.x

Cited by 87 publications

(105 citation statements)

References 42 publications

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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%

“…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%

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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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“…19,21 The released factors could contribute to the higher epithelial proliferative indexes observed in OKCs when compared to other odontogenic cysts. 1,3,11 Remodeling the epithelial basement membrane is a crucial step in many processes, from injury healing and keratinocyte migration 20 to tumor invasion and metastasis. 15 Many extracellular matrix substrates for matrilysins are epithelial and vascular basement membrane components, such as, laminin, fibronectin, and type IV collagen.…”

Section: Table II Immunoreactivity To Matrix Metalloproteinases In Omentioning

confidence: 99%

“…It is distinguished from other cystic lesions by its aggressive biological behavior and recurrence tendency. [1][2][3] Recent reports have shown that odontogenic keratocysts (OKCs) display high proliferative activity and protein expression associated with apoptosis inhibition, 1,3 as well as haploinsufficiency 4 and loss of heterozygosity of the tumoral suppressor gene PTCH. 1,5,6 These findings led the World Health Organization (WHO) to classify this cyst as a true neoplasm, giving rise to the term keratocystic odontogenic tumor.…”

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confidence: 99%

Immunohistochemical expression of MMPs 1, 7, and 26 in syndrome and nonsyndrome odontogenic keratocysts

Cavalcante

Pereira

Nonaka

et al. 2008

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, an

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Objective. The objective of this study was to analyze the expression of matrix metalloproteinases (MMPs) 1, 7, and 26 in odontogenic keratocysts (OKCs) associated with Gorlin syndrome (SOKCs) and nonsyndrome OKCs (NSOKCs). Study design. Twenty-one SOKCs and 20 NSOKCs were evaluated for epithelial expression of MMP-1, MMP-7, and MMP-26 and for mesenchymal expression of MMP-1 by immunohistochemistry. Results. Strong epithelial positivity to MMP-1 was observed in 76% of SOKCs and in 15% of NSOKCs (P Ͻ .05). Strong mesenchymal immunoreactivity to MMP-1 was observed in 38% of SOKCs and in 20% of NSOKCs (P Ͼ .05). Epithelial immunoreactivity to MMP-7 was strongly positive in 67% of SOKCs and in 40% of NSOKCs (P Ͼ .05). For MMP-26, strong positivity was found in 62% of SOKCs, in contrast to 35% of NSOKCs (P Ͼ .05). Conclusion. MMPs-1, Ϫ7 and Ϫ26 may play important roles in the biology of OKCs. Furthermore, the presence of these proteases at higher levels in SOKCs may help to explain increased OKC aggressiveness associated with nevoid basal cell carcinoma syndrome.

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“…Epithelial cells in KOTs seem to have a different proliferative potential from those of other odontogenic lesions [8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Odontogenic Epithelium: Immunolabeling of Ki-67, EGFR and Survivin in Pericoronal Follicles, Dentigerous Cysts and Keratocystic Odontogenic Tumors

Oliveira

Lauxen

Chaves

et al. 2010

Head and Neck Pathol

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Cell proliferation, apoptosis and apoptosis‐related factors in odontogenic keratocysts and in dentigerous cysts

Abstract: These results suggest that cellular proliferation and death is regulated in association with apoptosis-related proteins in the lining epithelia of OKCs, and subsequently those cysts are seen as cystic lesions but not as tumor masses.

Cited by 87 publications

References 42 publications

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

Immunohistochemical expression of MMPs 1, 7, and 26 in syndrome and nonsyndrome odontogenic keratocysts

Odontogenic Epithelium: Immunolabeling of Ki-67, EGFR and Survivin in Pericoronal Follicles, Dentigerous Cysts and Keratocystic Odontogenic Tumors

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