T Rosenstein1, M A Pogrel, R A Smith, J A Regezi. 1. Department of Oral and Maxillofacial Surgery, University of California, San Francisco, San Francisco, CA 94143-0440, USA.
Abstract
PURPOSE: This article presents a series of cystic ameloblastomas in which an unexpected capacity for bony destruction and recurrence was shown. Proliferation rates were evaluated to see if there is a correlation to the biologic behavior of these lesions. MATERIALS AND METHODS: Clinical and histologic material on 21 consecutive cystic ameloblastomas was retrieved and reviewed. Immunohistochemical analysis of proliferation-associated Ki-67 protein was carried out to determine mitotic indices for 10 cystic ameloblastomas, and these were compared to 10 solid ameloblastomas and 10. dentigerous cysts. RESULTS: Lesions from 10 males and 11 females (age range, 12 to 72 years; mean age, 35 years) were included. All lesions were in the mandible; 18 in posterior sites. Lesion size ranged from 2 to 8 cm in greatest dimension. Cortical perforation was evident in 7 lesions, and multilocularity (more often in older patients) was evident in 6 lesions. Recurrences were seen in 9 cases (43%), and the time between initial treatment and recurrence was as long as 10 years. The characteristic histopathologic feature was a thin, stratified squamous cystic lining with spongiosis and basal palisades. Ten cases also showed mural invasion, and 4 had plexiform luminal proliferation. The proliferation rate of the cystic ameloblastomas (represented as a percentage of cells in cell cycle) was 4.3%, compared with solid tumors at 2.8% and dentigerous cysts at 6.6%. CONCLUSIONS: Cystic ameloblastomas occur within a wide age range, but at slightly lower mean age than solid lesions. There is a very strong predilection for the mandible, and there appears to be no gender difference. Lesions frequently become large, destructive, and/or multilocular. There is a significant recurrence potential, and extended follow-up is advisable. The deceptively innocent histology of cystic ameloblastomas belies the biologic potential of these lesions. The mechanism(s) by which cystic ameloblastomas gain their destructive behavior seems less likely associated with acceleration of the cell cycle than with other factors. Simple enucleation or curettage of these lesions may be inappropriate treatment. Copyright 2001 American Association of Oral and Maxillofacial Surgeons
PURPOSE: This article presents a series of cystic ameloblastomas in which an unexpected capacity for bony destruction and recurrence was shown. Proliferation rates were evaluated to see if there is a correlation to the biologic behavior of these lesions. MATERIALS AND METHODS: Clinical and histologic material on 21 consecutive cystic ameloblastomas was retrieved and reviewed. Immunohistochemical analysis of proliferation-associated Ki-67 protein was carried out to determine mitotic indices for 10 cystic ameloblastomas, and these were compared to 10 solid ameloblastomas and 10. dentigerous cysts. RESULTS: Lesions from 10 males and 11 females (age range, 12 to 72 years; mean age, 35 years) were included. All lesions were in the mandible; 18 in posterior sites. Lesion size ranged from 2 to 8 cm in greatest dimension. Cortical perforation was evident in 7 lesions, and multilocularity (more often in older patients) was evident in 6 lesions. Recurrences were seen in 9 cases (43%), and the time between initial treatment and recurrence was as long as 10 years. The characteristic histopathologic feature was a thin, stratified squamous cystic lining with spongiosis and basal palisades. Ten cases also showed mural invasion, and 4 had plexiform luminal proliferation. The proliferation rate of the cystic ameloblastomas (represented as a percentage of cells in cell cycle) was 4.3%, compared with solid tumors at 2.8% and dentigerous cysts at 6.6%. CONCLUSIONS:Cystic ameloblastomas occur within a wide age range, but at slightly lower mean age than solid lesions. There is a very strong predilection for the mandible, and there appears to be no gender difference. Lesions frequently become large, destructive, and/or multilocular. There is a significant recurrence potential, and extended follow-up is advisable. The deceptively innocent histology of cystic ameloblastomas belies the biologic potential of these lesions. The mechanism(s) by which cystic ameloblastomas gain their destructive behavior seems less likely associated with acceleration of the cell cycle than with other factors. Simple enucleation or curettage of these lesions may be inappropriate treatment. Copyright 2001 American Association of Oral and Maxillofacial Surgeons
Authors: Andrew C McClary; Robert B West; Ashley C McClary; Jonathan R Pollack; Nancy J Fischbein; Christopher F Holsinger; John Sunwoo; A Dimitrios Colevas; Davud Sirjani Journal: Eur Arch Otorhinolaryngol Date: 2015-04-30 Impact factor: 2.503