scholarly journals CD1a-positive Langerhans cells and their relationship with E-cadherin in ameloblastomas and keratocystic odontogenic tumors

2012 ◽  
Vol 42 (6) ◽  
pp. 454-461 ◽  
Author(s):  
Leonardo Araújo Mello ◽  
Andréia Leal Figueiredo ◽  
Eduardo Antônio Gonçalves Ramos ◽  
Clarissa Araújo Silva Gurgel ◽  
Manoela Domingues Martins ◽  
...  
Keyword(s):  
Langerhans Cells ◽  
Odontogenic Tumors ◽  
Keratocystic Odontogenic Tumors ◽  
E Cadherin

scholarly journals E-cadherin regulators are differentially expressed in the epithelium and stroma of keratocystic odontogenic tumors

2015 ◽  
Vol 45 (4) ◽  
pp. 302-311 ◽  
Author(s):  
Lia Pontes Arruda Porto ◽  
Jean Nunes dos Santos ◽  
Luciana Maria Pedreira Ramalho ◽  
Andreia Leal Figueiredo ◽  
Bráulio Carneiro Júnior ◽  
...  
Keyword(s):  
Differentially Expressed ◽  
Odontogenic Tumors ◽  
Keratocystic Odontogenic Tumors ◽  
E Cadherin

scholarly journals Disruption of Smad4 in Odontoblasts Causes Multiple Keratocystic Odontogenic Tumors and Tooth Malformation in Mice

2009 ◽  
Vol 29 (21) ◽  
pp. 5941-5951 ◽  
Author(s):  
Yuanrong Gao ◽  
Guan Yang ◽  
Tujun Weng ◽  
Juan Du ◽  
Xuejiu Wang ◽  
...  
Keyword(s):  
Transforming Growth Factor Beta ◽  
Hedgehog Signaling ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Bmp Signaling ◽  
Odontogenic Tumors ◽  
High Recurrence Rate ◽  
Signal Molecules ◽  
Cystic Tumors ◽  
Keratocystic Odontogenic Tumors

ABSTRACT Keratocystic odontogenic tumors (KCOTs) are cystic epithelial neoplasias with a high recurrence rate. However, the molecular mechanisms underlying the initiation and progression of KCOTs are still largely unknown. Here, we show that specific ablation of Smad4 in odontoblasts unexpectedly resulted in spontaneous KCOTs in mice. The mutant mice exhibited malformed teeth characterized by fractured incisors and truncated molar roots. These abnormalities were mainly caused by disrupted odontoblast differentiation that led to irregular dentin formation. The cystic tumors arising from the reactivation of epithelial rests of Malassez (ERM), in which Smad4 remained intact, proliferated and formed stratified and differentiated squamous epithelia that exhibited a dramatic upregulation of Hedgehog signaling. Odontoblasts, which are responsive to transforming growth factor beta (TGF-β)/bone morphogenetic protein (BMP) signals, may produce signal molecules to inhibit the activation of ERM. Indeed, we observed a downregulation of BMP signals from Smad4 mutant odontoblasts to the adjacent Hertwig's epithelial root sheath (HERS). Intriguingly, KCOTs frequently emerged from Smad4-deficient ERM in keratinocyte-specific Smad4 knockout mice, suggesting a novel mechanism in which reciprocal TGF-β/BMP signaling between odontoblasts and HERS was required for tooth root development and suppression of KCOT formation. These findings provide insight into the genetic basis underlying KCOTs and have important implications for new directions in KCOT treatment.

Poster 25: Bacterial Identification in Odontogenic Cysts and Keratocystic Odontogenic Tumors

2012 ◽  
Vol 70 (9) ◽  
pp. e55-e56
Author(s):  
P. Boffano ◽  
C. Gallesio ◽  
J. Roana ◽  
D. Scalas ◽  
S. Berrone ◽  
...  
Keyword(s):  
Odontogenic Tumors ◽  
Odontogenic Cysts ◽  
Bacterial Identification ◽  
Keratocystic Odontogenic Tumors
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