Syndecan-1 (CD138) and Ki-67 expression in odontogenic cystic lesions

Nadalin, Michele Regina; Fregnani, Eduardo Rodrigues; Silva-Sousa, Yara Teresinha Corrêa; Perez, Danyel Elias da Cruz

doi:10.1590/s0103-64402011000300008

Cited by 29 publications

(30 citation statements)

References 20 publications

(36 reference statements)

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“…In our series, all ameloblastomas were unicystic. In the study of Nadalin et al (29), CD138 expression was detected in all epithelial layers of KCOTs, RCs and DCs. Our results were similar to the findings of previous studies, but we also observed CD138 expression in the stromal cells.…”

Section: Some Authors Suggested That Loss Of E-cadherin Expression Inmentioning

confidence: 87%

“…Although there are several studies related to role of these proteins in odontogenic lesions in English literature (8,9,18,24,(27)(28)(29), no comparative and comprehensive study, in which the expression of these proteins or adhesion molecules in odontogenic cystic lesions have been evaluated, to our knowledge. Therefore, we aim to evaluate the immunohistochemical expressions of CD138 (syndecan-1), CD38, E-cadherin and survivin in these cystic odontogenic lesions and investigate the potential implications of their expressions among these lesions.…”

Section: Introductionmentioning

confidence: 99%

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Immunohistochemical characteristics of cystic odontogenic lesions: a comparative study

Özcan

Yavan²,

Günhan³

2015

TJPATH

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Objective: Cystic ameloblastoma, keratocystic odontogenic tumor, dentigerous cyst, and radicular cyst are the most commonly encountered cystic odontogenic lesions. The aim of this study was to investigate the expressions of survivin, E-cadherin, CD138, and CD38 in these lesions and their potential diagnostic usage. Material and Method:A total of 20 cases, consisting 5 radicular cysts, 5 dentigerous cysts, 5 keratocystic odontogenic tumors and 5 cystic ameloblastomas were included in our series. For all cases, sections from the selected blocks were stained against the antibodies for survivin, E-cadherin, CD138, and CD38 on an automated device.Results: All cystic ameloblastomas and keratocystic odontogenic tumors showed diffuse and strong nuclear survivin expression. No specific survivin immunoreactivity was observed in the dentigerous and radicular cysts. E-cadherin expression was stronger in all dentigerous cysts and radicular cysts when compared to others. CD138 expression in stromal cells was prominent in cystic ameloblastomas, but gradually decreased in the other three lesions. All cases were negative for CD38. Conclusion:In the present study, loss of E-cadherin expression in epithelial cells, strong CD138 expression in stromal cells and strong nuclear survivin expression both in epithelial and stromal cells in cystic ameloblastomas and keratocystic odontogenic tumors were the most remarkable findings. These findings are also reinforced by the studies suggesting their role in the aggressiveness and pathogenesis of these tumors. Key Words: Odontogenic tumors, Odontogenic cysts, Immunohistochemistry ÖzAmaç: Kistik ameloblastoma, keratokistik odontojenik tümör, dentijeröz kist ve radiküler kist en sık karşılaşılan kistik odontojenik lezyonlardır. Çalışmada bu lezyonlarda survivin, E-cadherin, CD138 ve CD38 ekspresyonları ve bunların potansiyel tanısal kullanımları araştırılmıştır. Gereç ve Yöntem:Çalışma serimiz 5 kistik ameloblastoma, 5 keratokistik odontojenik tümör, 5 dentijeröz kist ve 5 radiküler kist olmak üzere toplam 20 olgudan oluşmaktadır. Bütün olgulara ait seçilmiş bloklardan sağlanan kesitler otomatize bir cihazda survivin, E-cadherin, CD138, and CD38 antikorları ile boyandı. Bulgular:Kistik ameloblastoma ve keratokistik odontojenik tümörlerin hepsi yaygın ve kuvvetli nükleer survivin ekspresyonu gösterdi. Dentijeröz ve radiküler kistlerde spesifik survivin ekspresyonu gözlenmedi. E-cadherin ekspresyonu diğer lezyonlarla karşılaştırıldığında, dentijeröz ve radiküler kistlerde daha belirgindi. CD138 ekspresyonu kistik ameloblastomalarda stromal hücrelerde daha belirgindi, ancak diğer lezyonlarda giderek azalan oranlardaydı. CD38 olguların hepsinde negatifdi.Sonuç: Çalışmada, keratokistik odontojenik tümörlerde ve kistik ameloblastomada epitelyal hücrelerde E-cadherin kaybı, stromal hücrelerde kuvvetli CD138 ekspresyonu ve hem epitelyal hem de stromal hücrelerde kuvvetli nükleer survivin ekspresyonu en karakteristik bulgulardır. Bu bulguların bu tür lezyonların patogenezini ve agresif davranış...

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Section: Some Authors Suggested That Loss Of E-cadherin Expression Inmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Immunohistochemical characteristics of cystic odontogenic lesions: a comparative study

Özcan

Yavan²,

Günhan³

2015

TJPATH

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“…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).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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The aim of this study was to assess the immunohistochemical expression of p63 protein, epidermal growth factor receptor (EGFR) and Notch-1 in the epithelial lining of radicular cysts (RC), dentigerous cysts (DC) and keratocystic odontogenic tumors (KOT). For this study, 35 RC, 22 DC and 17 KOT were used. The clinical and epidemiological data were collected from the patient charts filed in the Oral Pathology Laboratory, University of Ribeirão Preto, Brazil. Immunohistochemical reactions against the p63, EGFR and Notch-1 were performed in 3-µm-thick histological sections. The slides were evaluated according to the following criteria: negative: <5% of positive cells, low expression: 5-50% of positive cells, and high expression: >50% of positive cells. Moreover, the intensity of EGFR and Notch-1 expressions was also evaluated. Fisher's exact test and Spearman's correlation coefficients were used for statistical analysis, considering a significance level of 5%. Almost all cases demonstrated p63, EGFR and Notch-1 expressions. The p63 expression was significantly higher in KOT (p<0.001). Positive correlation between these immunomarkers was observed. These findings suggest the participation of p63, EGFR and Notch-1 in the development, maintenance and integrity of cystic odontogenic epithelial lining, favoring lesion persistence. The high expression of p63 in KOT suggests that it may be related to their more aggressive biological behavior and marked tendency to recurrence.

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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%

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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Syndecan-1 (CD138) and Ki-67 expression in odontogenic cystic lesions

Cited by 29 publications

References 20 publications

Immunohistochemical characteristics of cystic odontogenic lesions: a comparative study

Immunohistochemical characteristics of cystic odontogenic lesions: a comparative study

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

Cell proliferation and apoptosis in ameloblastomas and keratocystic odontogenic tumors

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