Ameloblastoma is the most frequent odontogenic tumor and is considered benign, but locally invasive, neoplasm with variable clinico-pathological expression.1
Clinico radiographic types
Conventional, solid or multicystic.
Unicystic or intraosseous type
Peripheral or extraosseous type2
The local biologic behaviour of solid multicystic ameloblastoma is that of a low grade malignant tumour. Histologically, solid multicystic ameloblastoma (SMA) includes follicular, plexiform, acanthomatous, granular cell, and basal cell types.3 Unicystic ameloblastoma (UA), a variant of ameloblastoma is believed to be less aggressive.
Syndecan-1(SDC1), a transmembrane heparin sulphate proteoglycan, is also known as CD138, participates in odontogenesis and is known to regulate cytoskeletal organization, growth factor signaling, cell–cell adhesion, and extracellular matrix attachment.
Loss of expression of syndecan-1 is associated with tissue invasion, metastasis and poor prognosis.
Local invasiveness of some of the intraosseous ameloblastoma subtypes depending on its expression by epithelial cells and subsequent shifting to stromal and ECM.4
6.1 NEED FOR STUDY:
Amongst the ameloblastomas, there is now more detailed reference to the unicystic variety because both the surgical management and prognosis of these lesions are significantly different from that of other ameloblastomas.5
Measurement and assessment of tumour invasion may prove very valuable in predicting response to therapy and also assess post therapeutic response particularly in recurrent cases of Solid multicystic and unicystic ameloblastoma.3 6.2REVIEW OF LITERATURE:
In a similar study the pattern of syndecan-1 expression and proliferating activity of Ki67 was evaluated in a large series of solid/multicystic (SMA) and unicystic ameloblastomas (UA), possible correlation to their biological behavior showed the reduced expression of syndecan-1 for SMA. Results suggest that SA has a more aggressive biological behavior than the UA also lack of correlation between Ki67 and syndecan1 was reported.1
A different study to evaluate and compare the expression of CD105 (endoglin) in solid multicystic ameloblastoma (SMA) and unicystic ameloblastoma (UA) was done in which no significant difference found in mean vascular density mean vascular area and total vascular area, its measurement may be valuable in predicting response to antiangiogenic therapeutic strategies. Reports say that suggests that the angiogenesis has an important role in tumour progression and invasiveness of ameloblastoma.3
In another study involving the odontogenic lesions; ameloblastoma, keratocystic odontogenic tumor, and dentigerous cyst, immunohistochemical localization of syndecan-1 was found decreased in ameloblast like cells compared to stellate reticulum cells in ameloblastoma which also showed decreased expression than the other two odontogenic lesions. The present study reported SD-1immunoreactivity in the stromal cells of ameloblastoma, KCOT, and dentigerous cysts rather uniformly. This reported SD-1 expression by the tumor stroma is considered to be associated with poor prognosis of the lesions.6
In a study conducted using Aberrant Wingless type 1 glycoprotein (Wnt) pathway and syndecan- (SDC1) in ameloblastomas, SDC1 shifting from epithelium to stroma was reported in invasive non-odontogenic neoplasms which concluded the role of SDC1 in stromal cells and Extra Cellular Matrix can be carcinogenesis and local invasiveness of Ameloblastomas. A role of SDC1 in stromal cells and ECM can be hypothesized as a critical factor for carcinogenesis and local invasiveness.7
6.3OBJECTIVES OF THE STUDY:
1. To assess the distribution of the syndecan-1 in various cellular components of the solid multicystic and unicystic ameloblastomas.
2. To compare syndecan expression between solid and unicystic ameloblastomas and correlate with their differentiation and biological behaviour.
7. MATERIALS AND METHODS 7.1 Source of the data Cases of solid and unicystic ameloblastoma will be retrieved from the archives of the Department of oral maxillofacial pathology, V S Dental college and hospital, Bangalore and other dental colleges across Bangalore.
Samples in this study consist of 25 cases of solid multicystic ameloblastoma and 25 cases of unicystic ameloblastoma. 5 cases of normal mucosa will be taken as positive controls which will be run along with immunohistochemical panel slides.
7.2.2 Study materials:
Formalin fixed, paraffin-embedded tissue section are immunohistochemically analyzed for syndecan-1 markers.
7.2.3 Study method:
. The tissue sections will be immunohistochemically stained from the kit obtained from Dako Corporation (dilution 1:100). Sections were incubated with monoclonal antibodies against syndecan-1 (CD138) and the labeled polymer (Envision+ System/HRP, Dako Corporation).
The immunoreactivity of syndecan will be quantitatively scored using a 4-grade scoring: 0 (no staining); 1 (low), 1–10% positive cells; 2 (intermediate), 11–50% positive cells; 3 (high), >50% positive cells. The cases will be evaluated at two different levels: epithelial cells and the stromal cells.
Expression of syndecan will be measured under 400x in the solid ameloblastoma in epithelium where lesional cells are 4 types of cellular components; peripheral basal cells of tumour nests, central stellate reticulum like cells and foci of squamous and granular cells. Unicystic will be checked for its cystic lining. Stromal expression of syndecan1 also evaluated in fibroblast like or spindle cells. Sections of normal oral mucosa, will be stained in parallel as positive controls. Plasma cells serve as internal controls for the study. These readings will be statistically analysed.
7.2.4 Study design :Comparative study.
7.4 Statistical Analysis : Student t test and Chi Square test
7.5 Sample Design : Purposive sampling
7.6 Study place: V.S. Dental College and Hospital. Bangalore.
7.7 Study Duration: 11/2 years.
7.8 Inclusion criteria:
Histopathologically diagnosed benign cases of various types of primary and recurrent types of solid and unicystic ameloblastoma.
7.9 Exclusion criteria:
8.1 Does the study require any investigation or interventions to be conducted
Has ethical clearance been obtained from your institution in case of this study?
Yet to be obtained.
LIST OF REFERENCES:
1.Molina et al.Syndecan-1 (CD138) and Ki-67 expression in
different subtypes of ameloblastomas. J.oral oncology 2007; 10: 806-11.
2.Neville D, Allen B. Oral and maxillofacial pathology. 3rd Ed. W.B. Saunders: Philadelphia.
3. Hande et al. Comparative analysis of tumour angiogenesis in solid multicystic and Unicystic ameloblastoma by using CD 105 (endoglin). Archives of oral biology 2011;56:1635–40.
4. Yi Zhong et al. Molecular markers for tumor invasiveness in ameloblastoma: An update. Ann Maxillofac Surg 2011; 1: 145-9.
5. Latif et al. Clinicopathological and immunohistochemical study in odontogenic keratocysts and ameloblastoma (using laminin-1). American Journal Of Life Sciences 2013;1(3):130-35.
6. Ohoud Al-Otaibi1, Rita Khounganian1, Sukumaran Anil2, Ravindranath Rajendran. Syndecan-1 (CD 138) surface expression marks cell type and differentiation in ameloblastoma, keratocystic odontogenic tumor, and dentigerous cyst. J Oral Pathol Med 2013; 42:186–93.
7.P. Leocata et al. Syndecan-1 and Wingless-type protein-1 in human
Ameloblastomas. J Oral Pathol Med 2007; 36: 394–9.