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Objectives Ameloblastoma is a benign, locally aggressive odontogenic tumor with high recurrence rates. Matrix metalloproteinases (MMPs) mediate extracellular integrity in normal and pathological conditions, and exert multiple functions coordinating inflammation and tumor progression. E‐cadherin and beta‐catenin are adherence junction molecules in cell‐to‐cell connections. We investigated the involvement of MMP‐7, ‐8, ‐9, E‐cadherin, and beta‐catenin in ameloblastoma and the surrounding extracellular matrix. Material and methods Our material consisted of 30–34 tissue samples from ameloblastoma patients of Helsinki University Hospital. We used immunohistochemistry to detect the expression of the biomarkers. Two oral pathologists independently scored the immunoexpression intensities and statistical calculations were made based on the results. Results E‐cadherin expression was weaker in the maxillary than in mandibular ameloblastomas. Beta‐catenin was expressed in the ameloblastoma cell membranes. We detected MMP‐8 and ‐9 expression in polymorphonuclear neutrophils in the extracellular area and these MMPs correlated positively with each other. Osteoclasts lining bone margins and multinuclear giant cells expressed MMP‐9. Neither MMP‐8 nor MMP‐9 immunoexpression could be detected in ameloblastoma cells. MMP‐7 expression was seen in some apoptotic cells. Conclusion The fact that E‐cadherin immunoexpression was weaker in maxillary compared to mandibular ameloblastomas might associate to earlier recurrences. It promotes the idea of mandibular and maxillary ameloblastoma exerting differences in their biologies. We detected MMP‐8 and ‐9 in polymorphonuclear neutrophils which relates to these MMPs participating in extracellular remodeling through a mild inflammatory process. Bone degradation around ameloblastoma may be due to MMP‐9 in osteoclasts but this phenomenon might be an independent process and needs further investigations.

Objectives We aimed to investigate BRAF V600E percentage immunohistochemically in ameloblastomas of a single institute cohort. We were interested if age, location, histological properties, or tumor recurrence depend on the BRAF status. Subjects, materials and methods We had 36 formalin‐fixed, paraffin‐embedded ameloblastoma tissue samples of patients treated at the Helsinki University Hospital between the years 1983–2016. Tissue sections underwent immunohistochemistry by Ventana BenchMark XT immunostainer using Ms Anti‐Braf V600E (VE1) MAB. We used R 3.4.2 and RStudio 1.1.383 to conduct statistical analysis for BRAF positivity and earlier onset as well as tumor location. We used chi‐squared tests and 2‐by‐2 table functions to determine connections between BRAF positivity and recurrence, growth pattern, and type. Results BRAF‐positive tumors occurred in younger patients compared to BRAF‐negative tumors (p = 0.015) and they located mostly to the mandible (p < 0.001). Growth patterns were limited to two in BRAF‐negative tumors when BRAF‐positive tumors presented with one to four growth patterns (p = 0.02). None of the maxillary tumors showed BRAF positivity and of these, 72.2% recurred. Conclusions An immunohistochemical BRAF marker could be a beneficial tool to predict the outcome of patients with this aggressive, easily recurring tumor.

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