A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä

MMP-7, -8, -9, E-cadherin, and beta-catenin expression in 34 ameloblastoma cases




TekijätKelppe Jetta, Thoren Hanna, Haglund Caj, Sorsa Timo, Hagström Jaana

KustantajaWILEY

Julkaisuvuosi2021

JournalClinical and Experimental Dental Research

Tietokannassa oleva lehden nimiCLINICAL AND EXPERIMENTAL DENTAL RESEARCH

Lehden akronyymiCLIN EXP DENT RES

Vuosikerta7

Numero1

Aloitussivu63

Lopetussivu69

Sivujen määrä7

ISSN2057-4347

eISSN2057-4347

DOIhttps://doi.org/10.1002/cre2.331

Verkko-osoitehttps://doi.org/10.1002/cre2.331

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/50117167


Tiivistelmä

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.


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