الفهرس 
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Abstract
Odontogenic tumours are a group of heterogenous lesions that ranges from hamartomatous benign or malignant neoplasms with variable aggressiveness.
Odontogenic tumours are lesions derived from the epithelial and/or ectomesenchymel remnants of the tooth-forming apparatus.
The odontogenic developmental cysts frequently affect the gaws even though they are believed to arise from odontogenic epithelium, they have different clinical behavior ranging from benign behaviors such as dentigerous cyst to aggressive behavior such as odontogenic keratocyst.
The keratocystic odontogenic tumour, was previously known as odontogenic keratocyst, and was reclassified as keratocystic odontogenic tumour (KCOT) under the 2005 WHO histologic classification of odontogenic tumours to emphasize its neoplastic character.
The controversies over the nature of KCOT are in fact a reflection of our limited knowledge of molecular basis of this fascinating entity.
Ameloblastoma is the most frequently encountered tumor arising from odontogenic epithelium. It is characterized by a benign but locally invasive behavior, with a high risk of recurrence.
The aim of the present study is to evaluate the odontogenic tumours (KCOT and ameloblastoma) with dentigerous cyst on basis of their clinical presentation and to investigate the expression of P63 protein.
The material of this study consisted 20 archival cases of odontogenic tumours (10 KCOT and 10 ameloblastoma) and 5 cases of the dentigerous cysts.
Specimens were routinely processed and sections of 4 microns were obtained for histological evaluation using hematoxylin and eosin staining.
Serial paraffin sections were immunohistochemically stained by monoclonal antibody P63 protein – Clone 4A4 using a labeled streptavidin biotin complex method (LSABI).
The results of this work revealed that out of 5 examined cases of dentigerous cyst, 3 (60%) cases showed weak reactivity to P63 in the thin epithelial lining, the other 2 (40%) revealed moderate reaction, the first case showed epithelium rests in the fibrous capsule and the second case showed hyperplastic epithelial lining.
(70%) of KCOT cases revealed moderat immunoreactions to P63 mainly in the basal and suprabasal cell layer, while (30%) showed moderate immunoreactions to P63 in all the layers of the corrugated parakeratinized odontogenic epithelium.
All the ameloblastoma cases were immunopositive to P63 with different intensities. The conventional ameloblastoma (60%) as well as desmoplastic ameloblastoma (10%) revealed strong immunopositivity to P63 protein. While, unicystic ameloblastoma cases (30%) showed moderate positivity to P63.
Immunohistological sections were examined by the image analyzer computer system using the software Leica Qwin 500. The device includes a light microscope cabled to a microcomputer that performs high speed digital image processing.
The immunoreactivity for P63 was measured in the form of: area percent and optical density.
In this study it was concluded that detection of in ameloblastomas was found to be higher than cystic odontogenic lesions. The P63 protein could be an effective tool in recognizing cystic dontogenic lesions with more aggressive behavior