Benign odontogenic tumors comprise a complex group of lesions described in the 2005 WHO classification based on the presence of odontogenic epithelium, odontogenic ectomesenchyme, or both. Ameloblastic fibroma (AF) is defined in WHO classification as “neoplasm composed of proliferating odontogenic epithelium embedded in a cellular ectomesenchymal tissue that resembles dental papilla, and with varying degrees of inductive change and dental hard tissue formation. Both the epithelial and the connective tissue components of AF are neoplastic.[1] The neoplastic nature of AF is supported by reports of recurrence after surgery and by cases of malignant transformation from a pre‑existing AF.[2,3] AF is a rather uncommon tumor, accounting for only 2.5% of all odontogenic tumors. AF raises at any age, ranging from 6 months to 42 years (mean 3.6-15.5 years); it does not show sex predilection. The lesion occurs in nearly 50‑80% of cases in posterior areas of the mandible, molar, or premolar locations as well. About 25% of AF are associated with permanent tooth eruption disturbances and impacted tooth, affecting several teeth too.[4] The rare extraosseous and soft tissue localization of the lesion is defined “peripheral AF”. The initial and small lesions are asymptomatic, whereas large and advanced ones lead to swelling and jawbone deformities.[2,5] The dimension and growth of the lesion are not related with patient’s complain, and the neoformation is frequently discovered accidentally during a simple dental radiological examination.[4] AF may appear radiographically as a well‑defined uni or multilocular radiolucent lesion, giving rise to expansion of the cortex, associated or not with the crown of an unerupted tooth.[2,3,5] Differential diagnosis may involve dentigerous cyst and ameloblastoma on a radiological point of view.[4,6] Tumor size varies from 1 to 8.5 cm.[3,5] Amina et al. described an exceptionally large AF localized in the upper jaw, unlike the most common site in the posterior mandible.[7] AF exhibits a slower clinical growth than, for example, an unicystic ameloblastoma, and it does not demonstrate an infiltrative pattern among trabeculae of the surrounding bone. It produces a enlargement of jawbone through a gradual expansion of cortex so that bony surface appears intraoperatively smooth.[4,5] Conservative or extensive (radical) approaches over AF treatment are advocated by different authors. In consideration of the innocuous behavior of the lesion, several authors proposed a meticulous enucleation or curettage as the initial treatment, keeping a block resection for recurrence.[5] Recurrence rate after surgery is a controversial issue, and it is estimated between 18.3 and 43.5%.[2,3] Residual tumor left at the time of curettage or enucleation gives rise to recurrence, and this induce some authors to advocate a more extensive surgery as first removal of the lesion. Zallen and coworkers recommends, in detail, a wide excision of the tumor unless a significant cosmetic deformity is produced.[3] Detection of residual tumor and early recurrence is possible through a long‑term postoperative control. The follow‑up management does not have a well‑defined protocol. Pereira plans to see the patient twice a year and to obtain TC/OPT on yearly basis for 2 years; any suspicion of recurrence needs earlier clinical and radiological control.[8] Long‑term follow‑up carried out by different authors report no recurrence after conservative procedure (enucleations and curettage).[2,3,5] Recurrence of AF may potentially occur as the malignant histological counterpart, i.e., as an ameloblastic fibrosarcoma. Ameloblastic fibrosarcoma develops de novo or in recurrent fibro‑odontoma or AF. The malignant transformation in an ameloblastic fibrosarcoma is rare, even though 30‑45% of ameloblastitc has developed in pre‑existing or recurrent AF or in ameloblastic fibro‑odotomas.[9] Ameloblastic fibrosarcoma does not give rise to metastasis and is associated with a high recurrence rate (35%) and 20% of patients have died because of disease within 3 months to 19 years. Most of these patients had undergone a curettage or an enucleation at the same site 1‑10 years before the malignant transformation.[9] In ameloblastic fibrosarcoma transformation the mesenchymal component becomes malignant, while the epithelial component does not show signs of malignant transformation.[5] The mesenchymal part may show a step‑wise progression to malignancy, making difficult to differentiate ameloblastic fibrosarcoma from AF. Immunoistochemical studies (Ki‑65, p53, PCNA) are useful for identifying the malignancy.[9]

Commentary to: An aggressive ameloblastic fibroma in a 9‑year‑old child treated with buccal fat graft / Anesi, Alexandre. - In: JOURNAL OF CRANIO-MAXILLARY DISEASES. - ISSN 2278-9588. - STAMPA. - 2:(2013), pp. 85-86.

Commentary to: An aggressive ameloblastic fibroma in a 9‑year‑old child treated with buccal fat graft

ANESI, Alexandre
2013

Abstract

Benign odontogenic tumors comprise a complex group of lesions described in the 2005 WHO classification based on the presence of odontogenic epithelium, odontogenic ectomesenchyme, or both. Ameloblastic fibroma (AF) is defined in WHO classification as “neoplasm composed of proliferating odontogenic epithelium embedded in a cellular ectomesenchymal tissue that resembles dental papilla, and with varying degrees of inductive change and dental hard tissue formation. Both the epithelial and the connective tissue components of AF are neoplastic.[1] The neoplastic nature of AF is supported by reports of recurrence after surgery and by cases of malignant transformation from a pre‑existing AF.[2,3] AF is a rather uncommon tumor, accounting for only 2.5% of all odontogenic tumors. AF raises at any age, ranging from 6 months to 42 years (mean 3.6-15.5 years); it does not show sex predilection. The lesion occurs in nearly 50‑80% of cases in posterior areas of the mandible, molar, or premolar locations as well. About 25% of AF are associated with permanent tooth eruption disturbances and impacted tooth, affecting several teeth too.[4] The rare extraosseous and soft tissue localization of the lesion is defined “peripheral AF”. The initial and small lesions are asymptomatic, whereas large and advanced ones lead to swelling and jawbone deformities.[2,5] The dimension and growth of the lesion are not related with patient’s complain, and the neoformation is frequently discovered accidentally during a simple dental radiological examination.[4] AF may appear radiographically as a well‑defined uni or multilocular radiolucent lesion, giving rise to expansion of the cortex, associated or not with the crown of an unerupted tooth.[2,3,5] Differential diagnosis may involve dentigerous cyst and ameloblastoma on a radiological point of view.[4,6] Tumor size varies from 1 to 8.5 cm.[3,5] Amina et al. described an exceptionally large AF localized in the upper jaw, unlike the most common site in the posterior mandible.[7] AF exhibits a slower clinical growth than, for example, an unicystic ameloblastoma, and it does not demonstrate an infiltrative pattern among trabeculae of the surrounding bone. It produces a enlargement of jawbone through a gradual expansion of cortex so that bony surface appears intraoperatively smooth.[4,5] Conservative or extensive (radical) approaches over AF treatment are advocated by different authors. In consideration of the innocuous behavior of the lesion, several authors proposed a meticulous enucleation or curettage as the initial treatment, keeping a block resection for recurrence.[5] Recurrence rate after surgery is a controversial issue, and it is estimated between 18.3 and 43.5%.[2,3] Residual tumor left at the time of curettage or enucleation gives rise to recurrence, and this induce some authors to advocate a more extensive surgery as first removal of the lesion. Zallen and coworkers recommends, in detail, a wide excision of the tumor unless a significant cosmetic deformity is produced.[3] Detection of residual tumor and early recurrence is possible through a long‑term postoperative control. The follow‑up management does not have a well‑defined protocol. Pereira plans to see the patient twice a year and to obtain TC/OPT on yearly basis for 2 years; any suspicion of recurrence needs earlier clinical and radiological control.[8] Long‑term follow‑up carried out by different authors report no recurrence after conservative procedure (enucleations and curettage).[2,3,5] Recurrence of AF may potentially occur as the malignant histological counterpart, i.e., as an ameloblastic fibrosarcoma. Ameloblastic fibrosarcoma develops de novo or in recurrent fibro‑odontoma or AF. The malignant transformation in an ameloblastic fibrosarcoma is rare, even though 30‑45% of ameloblastitc has developed in pre‑existing or recurrent AF or in ameloblastic fibro‑odotomas.[9] Ameloblastic fibrosarcoma does not give rise to metastasis and is associated with a high recurrence rate (35%) and 20% of patients have died because of disease within 3 months to 19 years. Most of these patients had undergone a curettage or an enucleation at the same site 1‑10 years before the malignant transformation.[9] In ameloblastic fibrosarcoma transformation the mesenchymal component becomes malignant, while the epithelial component does not show signs of malignant transformation.[5] The mesenchymal part may show a step‑wise progression to malignancy, making difficult to differentiate ameloblastic fibrosarcoma from AF. Immunoistochemical studies (Ki‑65, p53, PCNA) are useful for identifying the malignancy.[9]
2013
85
86
Anesi, Alexandre
Commentary to: An aggressive ameloblastic fibroma in a 9‑year‑old child treated with buccal fat graft / Anesi, Alexandre. - In: JOURNAL OF CRANIO-MAXILLARY DISEASES. - ISSN 2278-9588. - STAMPA. - 2:(2013), pp. 85-86.
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