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Amelogenin positive cells scattered in the interstitial component of odontogenic fibromas
  1. Y Kabasawa1,
  2. K Nagumo2,
  3. Y Takeda3,
  4. N Kawashima4,
  5. N Okada2,
  6. K Omura1,
  7. A Yamaguchi5,
  8. K Katsube5
  1. 1
    Oral and Maxillofacial Surgery, Graduate School of Tokyo Medical and Dental University, Tokyo, Japan
  2. 2
    Oral Diagnostic Pathology, Graduate School of Tokyo Medical and Dental University, Tokyo, Japan
  3. 3
    Pulp Biology and Endodontics, Graduate School of Tokyo Medical and Dental University, Tokyo, Japan
  4. 4
    Oral Pathology, Iwate Medical University School of Dentistry, Iwate, Japan
  5. 5
    Oral Pathology, Graduate School of Tokyo Medical and Dental University, Tokyo, Japan
  1. Dr K Katsube, Oral Pathology, Graduate School of Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549, Japan; katsube.mpa{at}tmd.ac.jp

Abstract

Background: Odontogenic tumours are often biphasic, consisting of epithelial and interstitial components, with an origin that is not well understood. Odontogenic fibromas are rich in mesenchymal component, but also have many epithelial nests.

Aims: To investigate the origin of this tumour by immunohistochemistry.

Methods: The expression of several odontogenic and epithelial markers, including amelogenin, was investigated by immunofluorescent studies.

Results: Immunohistochemical analysis showed that epithelial nests exhibited E-cadherin expression, but not amelogenin. Amelogenin positive cells were scattered in the fibrous tissue, which did not exhibit epithelial marker expression except for epithelial membrane antigen. In one case that had received a test biopsy before whole resection of tumour, amelogenin positive cells were distributed in the regenerating mucosal epithelium or subepithelial tissue.

Conclusions: Results indicate that amelogenin positive cells of odontogenic fibromas have an epithelial origin and may have the potential for epithelial mesenchymal transition, which has not to date been investigated in benign tumours.

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Footnotes

  • Competing interests: None.

  • Funding: This work was supported by Grant-in-Aid for Scientific Research from the Japan Society for the Promotion of Science to YK, AY and KK (19791493, 19209059 and 15390552).

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