Re: Controversies in Odontogenic Tumours Review

Re: Controversies in Odontogenic Tumours Review


Subject and more

  • LCC Subject Category: Biochemistry, Biomedicine, Medicine
  • Publisher's keywords: Controversies, Odontogenic Tumours
  • Language of fulltext: english
  • Full-text formats available: PDF


    Divya Gopinath, Rohit K. Menon



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We read with great interest the recent review article by Siwach et al. published in the August 2017 issue of SQUMJ.1 We congratulate the authors on their elaborative narrative review of the controversies regarding various tumours of odontogenic origin. We would like to further contribute by adding an interesting odontogenic tumour to the debate—adenoid ameloblastomas with dentinoid. First reported by Slabbert et al., this tumour shows histopathological features of both an ameloblastoma and an adenomatoid odontogenic tumour (AOT), along with hard tissue formation (i.e. dentin or dentinoid-like material).2 While ameloblastic elements such as epithelial whorls, duct-like structures and occasional signs of induction cover a major portion of the tumour, AOT-like areas are also visually evident, indicating a composite odontogenic tumour.2 Initially known as dentinoameloblastomas, the suggestion that these tumours were the result of the hybridisation of an ameloblastoma and AOT with fbrous separation resulted in signifcant controversy, as numerous cases revealed duct-like structures with bordering cells displaying subnuclear vacuoles.2,3 Subsequently, Loyola et al. described a similar neoplasm with the potential for recurrence and suggested the term ‘adenoid ameloblastoma with dentinoid’ for such lesions.3 To date, adenoid ameloblastomas have not yet been included by the World Health Organization (WHO) in the histological classifcation of odontogenic tumours.4 Te exclusion of this entity is interesting as other tumours with comparatively fewer documented cases, such as sclerosing odontogenic carcinomas, have nevertheless been incorporated in the latest WHO classifcation of odontogenic tumours.4 While the nature of the hard tissue in these tumours is unknown, ectomesenchymal cells showing odontoblastic differentiation can be completely absent.5 According to Sonone et al., the formation of dysplastic dentin in these tumours may be the result of a metaplastic process rather than the currently accepted theory of epithelial-ectomesenchymal interaction.5 Tis new hypothesis is further supported by the expression of certain genes by ameloblastic epithelial cells usually present in ectomesenchymal cells, thereby resulting in the conversion and co-expression of a mesenchymal phenotype.6 Further studies with more detailed molecular profling are needed to determine whether the hard tissue in adenoid ameloblastoma is the result of a metaplastic process or a true inductive phenomenon. Te co-occurrence of multiple phenotypes of ameloblastoma within the same lesion is not uncommon.4 In general, the diverse histological hybridisation of subtypes of solid and multicystic ameloblastoma does not impact the clinical behaviour of the lesion. However, substantial evidence indicates that adenoid ameloblastomas are locally aggressive.3 Adenoid ameloblastomas can present with hypercellularity and atypia, thus posing a challenge in distinguishing these lesions from ameloblastic carcinomas. Nevertheless, features of loss of ameloblastic differentiation, basilar hyperplasia, necrosis and vascular/perineural invasion can assist in differentiating a true ameloblastic carcinoma from an adenoid ameloblastoma.

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