Research Article: Differences in E-Cadherin and Syndecan-1 Expression in Different Types of Ameloblastomas

Date Published: April 23, 2018

Publisher: Hindawi

Author(s): Ramón G. Carreón-Burciaga, Rogelio González-González, Nelly Molina-Frechero, Sandra López-Verdín, Vanesa Pereira-Prado, Ronell Bologna-Molina.


Ameloblastomas are a group of benign, locally aggressive, recurrent tumors characterized by their slow and infiltrative growth. E-Cadherin and syndecan-1 are cell adhesion molecules related to the behavior of various tumors, including ameloblastomas. Ninety-nine ameloblastoma samples were studied; the expression of E-cadherin and syndecan-1 were evaluated by immunohistochemistry. E-Cadherin and epithelial syndecan-1 were more highly expressed in intraluminal/luminal unicystic ameloblastoma than in mural unicystic ameloblastoma and solid/multicystic ameloblastoma, whereas the stromal expression of syndecan-1 was higher in mural unicystic ameloblastoma and solid/multicystic ameloblastoma. Synchronicity was observed between E-cadherin and epithelial syndecan-1; the expression was correlated with intensity in all cases. There was a strong association between expression and tumor size and recurrence. The evaluation of the expression of E-cadherin and syndecan-1 are important for determining the potential aggressiveness of ameloblastoma variants. Future studies are required to understand how the expression of these markers is related to tumor aggressiveness.

Partial Text

The ameloblastoma is an epithelial neoplasia originating in the enamel and has been described as a tumor that is usually unicentric, intermittent in growth, and persistent [1]. According to the recent classification by the World Health Organization (WHO) [2], ameloblastoma is defined as a benign epithelial odontogenic neoplasia, characterized by tumor expansion, progressive growth, and a tendency for recurrence if not completely removed. Ameloblastomas are classified as follows according to their clinical and histopathological features: solid multicystic (SMA), unicystic (UAM), extraosseous/peripheral, and metastasizing ameloblastoma; the two most common types are SMA and UAM [2]. SMA is an aggressive tumor with high recurrence rates if not treated promptly; the early manifestation of this tumor is characterized by slow growth and painless expansion, which later exhibits accelerated growth with several complications that can be fatal if its growth is not controlled. SMA has two common types of histopathological growth patterns that are not related to prognosis [2]. UAM is characterized by slow growth that occurs as a single cystic cavity, in which different types of epithelial extension can occur, namely, luminal, intraluminal (UAM-L/I), and mural (UAM-M). The mural component displays aggressive behavior, like that observed in SMA [2].

Ameloblastomas are locally aggressive, recurrent, benign tumors with the potential for malignant transformation into ameloblastic carcinomas [18]. UAM and SMA are most often located in the ascending limb of the mandible, followed by the body and the mandibular symphysis. Radiographically, they present as well-defined unilocular neoplasms and, in most cases, are associated with impacted dental organs, sometimes showing root resorption and cortical perforation [2]. Recent WHO guidelines [2] indicate that invasion of the cystic wall (mural invasion) by ameloblastic tumor cells in UAM is an important histopathological factor, as this mimics a behavior similar to that found in SMA [2].

In this study, we evaluated clinical, radiographic, and histopathological findings from ninety-nine cases of ameloblastoma and related these data to the expression of Ecad, Syn1E, and Syn1S. Importantly, we found that the expression of these proteins had an association with radiographic patterns and tumor size as important risk factors for recurrence. We established a possible relationship between Ecad and Syn1E expression in ameloblastomas; a synchronous reduction in Ecad and Syn1E expression was found to be associated with a high expression of Syn1S. This is a potential factor contributing to the aggressive behavior of these tumors. Additional studies with more ameloblastoma cases are required and should include clinical follow-up and coexpression studies in which Ecad and Syn1 are evaluated with proteins involved in cell proliferation, apoptosis, and growth factor proteins, as well as proteins involved in bone remodeling and ECM interactions. This can help to determine whether Syn1S expression and the simultaneous decreases in Ecad and Syn1E expression are also associated with mechanisms of bone remodeling, tumor invasion, and cellular immortality.




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