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| Year : 2009 | Volume
: 20
| Issue : 1 | Page : 131-132 |
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| Odontogenic tumors |
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Shweta Nag, Shruti Nayak
Postgraduate Students, Meenakshi Ammal Dental College, Chennai, India
Click here for correspondence address and email
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How to cite this article:
Nag S, Nayak S. Odontogenic tumors. Indian J Dent Res 2009;20:131-2 |
Calretinin in odontogenic tumors
Alaeddini M, Etemad-Moghadam S, Baghaii F
Calretinin is a calcium-binding protein expressed primarily in certain subtypes of neurons in central and peripheral nervous systems and has been reported to be present in mesotheliomas and other tumours. Studies in rats have demonstrated expression of calretinin in neural elements of the tooth pulp, periodontal ligament and viscerosensory nerve fibres of oral and pharyngeal tissues, as well as in odontogenic epithelium during odontogenesis in molar tooth germs.
In this study, the investigators have assessed the expression of calretinin in selected odontogenic neoplasms (solid ameloblastomas, calcifying epithelial odontogenic tumours, adenomatoid odontogenic tumours, ameloblastic fibromas and odontogenic myxomas) using immunohistochemistry.
In all the immunopositive cases, strong reactivity was observed in both nucleus and cytoplasm. Ameloblastoma showed intense positivity of the ameloblastic epithelium with a diffuse distribution pattern. Immunoreactivity was restricted to the stellate reticulum-like epithelium. In contrast, none of the ameloblast-like peripheral cells were immunopositive for calretinin. Similarly, marked reactivity was observed in the cells that lined the macro- and microcysts. The intense positivity of the macrocysts occurred even when the epithelium lacked ameloblastic features. All other neoplasms were completely negative for calretinin.
In this study, the investigators due to paucity of cases did not study the pattern of calretinin expression. Evaluation of calretinin expression in these tumors and their comparison with ameloblastoma may provide additional information on the behaviour and tumorigenesis of odontogenic neoplasms. Considering that ameloblastomas were consistently reactive for calretinin, whereas the other studied tumours were invariably non-reactive, it has been hypothesized that calretinin plays a role in the aggressiveness of ameloblastoma compared to other odontogenic tumors.
Histopathology 2008;52:299-304
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Syndecan-1 and Wingless type protein-1 in ameloblastomas
Leocata P, Villari D, Fazzari C, Lentini M, Fortunato C, Nicotina PA
Syndecan-1 (SDC1), a transmembrane heparan sulphate proteoglycan, is also known as CD138 and participates in odontogenesis. SDC1 has been localized in different cell lines, including epithelial, endothelial and stromal tissues. In mature epithelia, SDC1 binds proteins of extracellular matrix (ECM), modulating epithelial-stromal interactions and cell proliferation. It is transiently expressed by mesenchymal cells and ameloblasts of tooth buds, as a developmentally regulated matrix receptor for growth factors and signalling transducers.
The Wingless type 1 glycoprotein (Wnt1), belonging to a large family of 19 secreted signalling transducers, besides promotes cell proliferation.Wnt1 assists embryogenesis and is normally involved in tooth development together with β-catenin and adenomatous polyposis coli (APC).
In this study, the investigators have assessed the immunohistochemical expression of SDC1 proteoglycan and Wnt1 protein in different subtypes of ameloblastomas and tooth buds. In ameloblastomas, SDC1 and Wnt1 were expressed in central ameloblast-like cells, central stellate reticulum-like cells, stromal cells and extracellular matrix. In tooth germs, SDC1 was expressed in stromal cells and extracellular matrix. Wnt1was expressed in the central ameloblast-like cells.
Most of the ameloblastoma subtypes expressed SDC1 in stromal cells and extracellular matrix and Wnt1 in tumour epithelial cells. Tis pattern of expression was more frequent in follicular and acanthomatous subtypes. Conversely, stromal SDC1 and epithelial Wnt1 reactions were infrequent in the plexiform and desmoplastic ameloblastomas.
It could be concluded from this study that SDC1 could be a critical factor for Wnt-induced carcinogenesis in the odontogenic epithelium and it might be involved in promoting local invasiveness of some ameloblastoma subtypes, depending on its expression by tumour epithelial cells and subsequent shifting to stromal cells and ECM.
J Oral Pathol Med 2007;36:394-9
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Wnt signalling in ameloblastomas with aberrant nuclear expression of β-Catenin
Tanahashi J, Daa T, Yada N, Kashima K, Kondoh Y, Yokoyama S
Wnt signaling molecules includes beta catenin, apc, axin1 and axin2, which are expressed during various stages of murine amelogenesis. Mutations in APC are associated with Gardner's syndrome which is often associated with dental abnormalities. Germline mutations in AXIN2 have been reported to be associated with tooth agenesis.
In this study, the expression of beta catenin and mutational status of genes involved in Wnt signaling pathway including CTNNB1, APC, AXIN1 and AXIN2 in ameloblastoma were analyzed using immunohistochemistry and polymerase chain reaction. Results showed a nuclear expression of beta catenin in solid/multicystic and unicystic variant. Cyclin D1 was expressed in the nucleus of tumor cells, while nuclear accumulation of beta catenin was absent. Expression of c-myc oncoprotein was not detected in any of the cases. Nuclear accumulation of beta catenin could be associated with tumorigenesis and cell proliferation of ameloblastoma.
J Oral Pathol Med. 2008 Oct; 37(9):565-70
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Notch signaling molecules in ameloblastomas
Kumamoto H, Ohki K
Notch was initially identified in Drosophila, where the first mutant allele gave rise to notches at the wing margin, and its complementary DNA was isolated and characterized to encode a transmembrane receptor. The first mammalian Notch homolog was found in chromosomal translocation in a subset of human T-cell leukemias. Notch receptors (Notch 1-4) are cleaved by proteinases in response to binding with cell surface-anchored Notch ligands (Delta1, Delta3, Delta4 and Jagged1, Jagged2) expressed by adjacent cells.
In this study the authors have investigated the expression of Notch signaling in ameloblastomas and tooth germs by Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Their results show that mRNA of Notch signaling molecules was expressed in all ameloblastomas and germ tissues. There was no distinct difference in the mRNA expression of Notch signaling molecules among the different types or variants of ameloblastomas.
In tooth germs, Notch1, Notch2, and Notch3 were expressed in many epithelial cells of stratum intermedium and fewer cells of stellate reticulum, outer enamel epithelium, and dental lamina. Expression of Notch receptors was not found in inner enamel epithelium. Expression of Delta1 and Jagged1 was detected in many epithelial cells of stratum intermedium and fewer cells of stellate reticulum, outer enamel epithelium, and dental lamina. Ameloblastomas also showed expression of Notch1, Notch2, and Notch3 in central polyhedral neoplastic cells.
It could be concluded from this study that Notch signaling might control cell differentiation and proliferation of normal and neoplastic odontogenic epithelium.
J Oral Pathol Med 2008;37:228-234.
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Platelet-derived growth factor-AA and platelet-derived growth factor-α receptor in ameloblastomas
Sulzbacher I, Wick N, Pichlhofer B, Mazal PR
Platelet-derived growth factors (PDGFs), especially PDGF-AA isoform and its tyrosine kinase receptor, PDGF-α receptor (PDGFRA) regulate the size and stage of tooth development via an autocrine mechanism during odontogenesis. In this study the immunohistochemical expression of PDGF-AA and PDGFRA in ameloblastomas has been analyzed.
In this study, PDGF-AA expression was granular and exclusively cytoplasmic and PDGFRA was cytoplasmic and membrane-bound staining pattern. All ameloblastomas showed variable staining levels with PDGF-AA antibody ranging from 0% to 78% positive cells. In unicystic ameloblastoma, the epithelial lining showed variable staining for both PDGF-AA and PDGFRA. In serial sections, they found coexpression of PDGF-AA and PDGFRA in the same tumor cells and some surrounding stroma cells.
Coexpression of PDGF-AA and PDGFRA in ameloblastomas, might stimulate tumor growth by receptor/ligan interaction via an autocrine/ paracrine loop.
J Oral Pathol Med 2008;37:235-240.
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Correspondence Address:
Shweta Nag
Postgraduate Students, Meenakshi Ammal Dental College, Chennai
India
 Source of Support: None, Conflict of Interest: None  | Check |
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