Adenoid Ameloblastoma with Dentinoid

Abstract

Ameloblastoma and adenomatoid odontogenic tumors are the most common odontogenic neoplasms. However, hybrid variant of the two lesions, Adenoid Ameloblastoma with dentinoid is extremely rare. The lesion comprises of characteristic histopathological features of Ameloblastoma and Adenomatoid odontogenic tumor and also shares certain clinical characteristics with either of the entities. Adenoid Ameloblastoma with dentinoid may be considered at the more aggressive end of spectrum of benign odontogenic neoplasms. Owing to the frequent tendency of lesion to be underdiagnosed, careful histopathological screening of submitted biopsies is warranted. With the increase in number of reported cases in the recent years, it is likely to be included as a separate entity in the upcoming WHO classification. The present systematic review aims at collectively presenting the demographic, clinical, radiographic and histopathological features, treatment performed along with its outcome for all the cases of Adenoid Ameloblastoma with dentinoid reported in scientific literature till date.
 Keywords: Hybrid Odontogenic Tumor; Adenomatoid Odontogenic Tumor; Adenoameloblastoma; dentinoameloblastoma; Immunohistochemistry

Adenoid Ameloblastoma Shares Clinicopathologic, Immunohistochemical, and Molecular Features With Dentinogenic Ghost Cell Tumor

“…All cytokeratins markers were detected, but CK8/18 was not statistically significant in differentiating AA from DGCT and CK8/18 was slightly higher in DGCT compared with AA. Nuclear β-catenin were identified in all AA and DGCT cases analyzed, and Ki-67 index ranging from 2% to 13% was detected in both types of tumors, consistent with previous reports 5,19 . Regarding the distinction between AA and AM, dentinoid is typically absent in AM, although the occasional presence of ghost cells in AM, indicating some overlap between them.…”

“…The mandible was the most frequently affected site (69%) in AA whereas the DGCT were mainly located in the maxilla (64%). The cumulative probabilities of recurrence were not statistically significant ( P =0.4940) between AA and DGCT, either in curettage groups ( P =0.2810) or osteotomy groups ( P =0.7679), which were inconsistent with previous reports 4,5,19 . Regarding the comparison between AA and AM, AA presents with demographic similarities to conventional AM, but exhibited distinct histopathologic differences and a higher rate of multiple recurrences, indicating its biological aggressiveness 20 …”

“…The cumulative probabilities of recurrence were not statistically significant (P = 0.4940) between AA and DGCT, either in curettage groups (P = 0.2810) or osteotomy groups (P = 0.7679), which were inconsistent with previous reports. 4,5,19 Regarding the comparison between AA and AM, AA presents with demographic similarities to conventional AM, but exhibited distinct histopathologic differences and a higher rate of multiple recurrences, indicating its biological aggressiveness. 20 Upon microscopic examination, AA is defined as a distinct entity characterized by epithelium resembling conventional AM, duct-like or cribriform architecture, and cellular condensations called morules or whorls.…”

“…Nuclear β-catenin were identified in all AA and DGCT cases analyzed, and Ki-67 index ranging from 2% to 13% was detected in both types of tumors, consistent with previous reports. 5,19 Regarding the distinction between AA and AM, dentinoid is typically absent in AM, although the occasional presence of ghost cells in AM, indicating some overlap between them. However, based on the observed genetic mutations and nuclear β-catenin reactivity of AA, it is not exactly what one would expect if this were a variant of AM.…”

Histopathological Insight of a Case of Adenoid Ameloblastoma: A Rare Odontogenic Tumor

“…Now, it has been universally accepted and adopted by the 5 th edition of the WHO classification for odontogenic tumors [ 1 ]. The word “ameloblastoma” from adenoid ameloblastoma is justified histopathologically by the presence of ameloblast-like cells showing intense, focal expression of calretinin, a specific marker for neoplastic ameloblastic epithelium [ 10 ]. However, these ameloblast-like cells fail to express BRAF p.V600E, the most common activating mutation seen in mandibular ameloblastoma [ 11 , 12 ].…”