Objective: This study used Ki-67 to evaluate the proliferative activity of ameloblastoma in an attempt to provide a scientific basis for any differences in the biologic behaviour that exists between the different type...Objective: This study used Ki-67 to evaluate the proliferative activity of ameloblastoma in an attempt to provide a scientific basis for any differences in the biologic behaviour that exists between the different types of ameloblastoma and correlate the results with the recurrence rate. Study design: We assessed Ki-67 expression by immunohistochemistry in 32 cases of mandibular ameloblastoma. Formalin-fixed, paraffinembedded blocks were sectioned and used for Haematoxylin & Eosin (H&E) staining. H&E slides were used to re-evaluate the histological types of the ameloblastoma. Immunohistochemical analysis for Ki-67 with a labelled streptavidin-biotin-peroxidase complex technique was performed on tumour sections using Monoclonal Mouse Anti-Human Ki-67 Antigen (clones MIB1, code M7240, Dako Corporation). Lymph nodes (lymphoma) were used as positive control for Ki-67. Results: The specimens comprised 18 cases of Follicular ameloblastoma, 7 cases of Cystic ameloblastoma, 4 cases of plexiform ameloblastoma, and 3 cases of Acanthotic ameloblastoma. The results showed that cellular proliferative activity varied within the ameloblastoma types. There was no statistically significant difference in the Ki-67 Acanthotic, cystic and follicular types of ameloblastoma, while plexiform type showed statistically significantly higher levels than the other 3 types. The mean Ki-67 labelling index of plexiform ameloblastoma ranged from 13 to 30 with a mean of 19.75. The mean values of Ki-67 were statistically significantly higher in recurrent than?non-recurrent cases. Conclusion: The significant expression of Ki-67 could provide useful prognostic markers for proliferative activity and good prognostic indicators for recurrence rate of mandibular ameloblastoma.展开更多
文摘Objective: This study used Ki-67 to evaluate the proliferative activity of ameloblastoma in an attempt to provide a scientific basis for any differences in the biologic behaviour that exists between the different types of ameloblastoma and correlate the results with the recurrence rate. Study design: We assessed Ki-67 expression by immunohistochemistry in 32 cases of mandibular ameloblastoma. Formalin-fixed, paraffinembedded blocks were sectioned and used for Haematoxylin & Eosin (H&E) staining. H&E slides were used to re-evaluate the histological types of the ameloblastoma. Immunohistochemical analysis for Ki-67 with a labelled streptavidin-biotin-peroxidase complex technique was performed on tumour sections using Monoclonal Mouse Anti-Human Ki-67 Antigen (clones MIB1, code M7240, Dako Corporation). Lymph nodes (lymphoma) were used as positive control for Ki-67. Results: The specimens comprised 18 cases of Follicular ameloblastoma, 7 cases of Cystic ameloblastoma, 4 cases of plexiform ameloblastoma, and 3 cases of Acanthotic ameloblastoma. The results showed that cellular proliferative activity varied within the ameloblastoma types. There was no statistically significant difference in the Ki-67 Acanthotic, cystic and follicular types of ameloblastoma, while plexiform type showed statistically significantly higher levels than the other 3 types. The mean Ki-67 labelling index of plexiform ameloblastoma ranged from 13 to 30 with a mean of 19.75. The mean values of Ki-67 were statistically significantly higher in recurrent than?non-recurrent cases. Conclusion: The significant expression of Ki-67 could provide useful prognostic markers for proliferative activity and good prognostic indicators for recurrence rate of mandibular ameloblastoma.
