Abstract for presentation at 13th International Congress on Oral Pathology and Medicine

The extracellular matrix proteins of odontogenic tumours

  • Sopee Poomsawat, Mahidol University, Thailand
  • Paisarn Vejchapipat, Chulalongkorn University, Thailand
  • Jirapa Punyasingh, Mahidol University, Thailand
  • Extracellular matrix (ECM) regulates cellular behaviours such as proliferation, migration and differentiation. Dynamic expression of ECM in the cells of tooth germ is observed. Dysregulation of these proteins may lead to an uncontrolled proliferation of the cells of tooth germ, resulting in odontogenic tumours.
    Purpose: To investigate the expression of ECM proteins including laminins 1 and 5, collagen type IV and fibronectin in 3 types of odontogenic tumours namely ameloblastoma (14 cases), calcifying odontogenic cyst (COC; 7 cases) and adenomatoid odontogenic tumour (AOT; 7 cases).
    Methods: Immunohistochemical study was performed. The primary antibodies against laminins 1 and 5, collagen type IV and fibronectin were used. Negative controls were omission of the relevant primary antibody.
    Results: Linear deposits of all proteins were found at the epithelial-mesenchymal junction in all tumours, but with different intensity. LM1 was expressed in the cytoplasm of tumour cells, regardless of cell types in ameloblastoma (14/14), COC (7/7) and AOT (6/7). In ameloblastoma, laminin 5 (14/14) and fibronectin (13/14) was seen in the cytoplasm of central cells, but only laminin 5 was occasionally present in the ameloblast-like cells (9/14). In COC, weak cytoplasmic expression of fibronectin was seen in basal (6/7), suprabasal (7/7) and ghost cells (7/7). Laminin 5 was found as weak intensity in the stellate and squamous cells (5/7) and very strong intensity in ghost cells (7/7). In AOT, strong expression of laminin 5 (6/7) and weak expression of fibronectin (6/7) was noted focally in a group of stellate cells.
    Conclusions: The expression of ECM proteins in ameloblastoma, COC and AOT were characterized. The profiles of these proteins among these tumours were different, suggesting that the origin of these 3 tumours derives from either different cell sources or similar cell types but different stages of tooth development.

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