OBJECTIVE: The aim of this study was to determine the demographic and clinical profile of the adenomatoid odontogenic tumors in a Sri Lankan population.
METHODS: Data gathered from the cases received for a period of 38 years from the Department of Oral Pathology, Faculty of Dental Sciences, University of Peradeniya. Request forms, biopsy reports and electronic data base of the department were used to obtain relevant information. Demographic data including age, gender and location of the tumor were included in the analysis.
RESULTS: Out of 116 cases of adenomatoid odontogenic tumor, the mean age was 21.02 ± 11.24. It occurs more fre quently in the second decade of life, more prevalent in females, most often associated with the maxilla, predominantly affecting anterior jaw bones and presenting mostly in the right side of the jaw bone. The results from the present study showed the statistically significant relationship with site of occurrence (maxilla/mandible) and age (p 0.05).
CONCLUSIONS: Adenomatoid odontogenic tumor occurs more frequently in the second decade of life with a significant female predominance and the commonest site is anterior maxilla. This study revealed few differences on demographic and clinical presentations of adenomatoid odontogenic tumor from some regions of the world.
MATERIALS AND RESULTS: Thirty-five paraffin-embedded ameloblastoma cases, ameloblastoma-derived cell lines (AM-1), and primary cultures of ameloblastoma stromal fibroblasts (ASF) were used. Immunohistochemistry, MTT assay, Western blotting, and RT-PCR were performed on these samples. Parenchyma-stromal CCN2 overexpression correlated significantly with fibrous-type stroma, but not with myxoid-type stroma, suggesting a role of CCN2 in fibrosis (P < 0.05). Recombinant CCN2 induction of enhanced ASF proliferation in AM-1 medium supports this view. Conversely, BMP4 and TGF-β were expressed in myxoid-type fibroblasts, but little expression was found in parenchyma. RANKL-positive and CD68-positive stromal cell populations were significantly greater in myxoid-type tumor areas than in fibrous-type tumor areas, while a higher Ki-67 labeling index was recorded in ameloblastoma with fibrous-type stroma. These data suggest that stromal properties influence bone resorption-related activities and growth rates, respectively.
CONCLUSIONS: These results suggest that the effects of secreted growth factors are governed by ameloblastoma parenchyma-stromal interactions. CCN2 promotes fibrogenesis independent of TGF-β signaling. Absence of CCN2 expression is associated with a phenotypic switch to a myxoid-type microenvironment that is conducive for TGF-β/BMP4 signaling to promote osteoclastogenesis.
MATERIALS AND METHOD: Eighty-seven paraffin-embedded ameloblastoma cases (20 unicystic, 47 solid/multicystic, 3 desmoplastic and 17 recurrent) were subjected to immunohistochemistry for expression of cortactin, N-WASP, WIP, Src kinase and F-actin, and findings correlated with clinicopathological parameters.
RESULTS: Invadopodia proteins (except Src kinase) and F-actin were widely detected in ameloblastoma (cortactin: n = 73/87, 83.9%; N-WASP: n = 59/87; 67.8%; WIP: n = 77/87; 88.5%; and F-actin: n = 87/87, 100%). Protein localization was mainly cytoplasmic and/or membranous, and occasionally nuclear for F-actin. Cortactin, which functions as an actin-scaffolding protein, demonstrated significantly higher expression levels within ameloblastoma tumoral epithelium than in stroma (P < 0.05). N-WASP, which coordinates actin polymerization and invadopodia-mediated extracellular matrix degradation, was overexpressed in the solid/multicystic subtype (P < 0.05). WIP, an upstream regulator of N-WASP, and F-actin were significantly upregulated along the tumour invasive front compared to tumour centres (P < 0.05). Except for males with cortactin overexpression, other clinical parameters (age, ethnicity and anatomical site) showed no significant correlations.
CONCLUSIONS: Present results suggest that local invasiveness of ameloblastoma is dependent upon the migratory potential of its tumour cells as defined by their distribution of cortactin, N-WASP and WIP in correlation with F-actin cytoskeletal dynamics.
METHODS: This is a retrospective non-randomized study of outcomes and tumor recurrence of all patients diagnosed with mandibular ameloblastoma from August 1997 until August 2017 (20 years) requiring free fibula osteocutaneous flap reconstruction at a single institution. The patients were identified through an electronic operative database; subsequently, their medical records and photo documentation were retrieved.
RESULTS: Twenty-seven patients were included in this study. Eighteen patients were male, while nine were female. The majority of the patients (48.1%) were in their third decade of life when they were diagnosed with ameloblastoma. All of them underwent radical resection of the tumor with a surgical margin of 2 cm (hemimandibulectomy in cases with a large tumor) and immediate mandibular reconstruction with a free fibula osteocutaneous flap. Two patients required revision of a vascular anastomosis due to venous thrombosis postoperatively, while one patient developed a flap recipient site infection. The flap success rate was 100%. There was no tumor recurrence during a mean follow-up period of 5.6 years.
CONCLUSIONS: Mandibular ameloblastoma should be treated with segmental mandibulectomy (with a surgical margin of 2 cm) to reduce the risk of recurrence. Subsequent mandibular and adjacent soft tissue defects should be reconstructed immediately with a free fibula osteocutaneous flap.