Ameloblastoma

Ameloblastoma is a benign albeit locally aggressive odontogenic tumor originating from remnants of the dental lamina, primarily affecting the mandible, and potentially mutilating if is left untreated. Ameloblastomas are classified as ameloblastoma (conventional), unicystic ameloblastoma, and peripheral ameloblastoma. Annual incidence is estimated to be 0.5/1 million population. In the Helsinki University Hospital (HUS) district, approximately five ameloblastoma patients are treated each year. Etiology has yet to be elucidated, although new genetic findings have emerged relating to the mitogen-activated protein kinase (MAPK) pathway. We surveyed the Q-pati system to identify all ameloblastoma patients (n = 64) treated at the Head and Neck Surgery Unit of HUS. A total of 30 to 36 patient records and the formalin-fixed paraffin-embedded tumor tissue samples were suitable for use from the Department of Pathology at HUS (HUSLAB) from 1985 through 2016. All patient reports were studied, and the parameters were collected using clinical data, Q-pati records, and imaging reports. A total of 26 ameloblastoma patients’ radiological findings were re-evaluated and studied. All tissue samples were revised microscopically, and representative paraffin blocks were chosen for immunohistochemistry with tested dilutions and protocol methods including positive and negative controls. BRAF, MMP-7, MMP-8, MMP-9, E-cadherin, and beta-catenin were of interest. For statistics, we used R studio, seeking correlations between parameters using the Fisher’s exact test, z-test, t-test, χ², and logistic regression to determine statistical significance. We considered p < 0.05 significant. Our results mostly coincide with previous knowledge with minor deviations and some notable differences to consider in future studies. Specifically, maxillary tumors occurred mostly in older, male patients. BRAF-positive tumors seemed to recur more often than BRAF-negative tumors in the mandible area. In addition, all maxillary tumors were BRAF-negative. Maxillary tumors are likely to recur easily, presumably along complex anatomical structures. Unlike previous studies, ameloblastoma cells did not express MMP-7, MMP-8, or MMP-9. MMP-9 positivity, however, was observed in inflammatory cells, macrophages, and osteoclasts. Beta-catenin expression appeared on the cell membranes. E-cadherin expression varied, although maxillary tumors presented with a weak E-cadherin expression. Radiologic re-evaluation revealed that ameloblastomas eradicate cortical bone already during the early stages of tumor growth. Ultimately, we found that CT and MRI imaging remain essential in differential diagnostics, serving to protect the patient from radical surgery. In conclusion, maxillary tumors might be reasonable to study separately from mandibular tumors because of their different protein properties. Our investigations among this Finnish ameloblastoma patient cohort have expanded our knowledge of a rare odontogenic tumor and further substantiated previous findings.