Analysis of TIMP-1 expression in leukoplakia and oral squamous cell carcinoma

Susy Carmelita P Nascimento,Liliana Aparecida P Barros,Letícia N G Souza

doi:10.5935/1676-2444.20210025

Susy Carmelita P Nascimento, Liliana Aparecida P Barros + Show 1 more

Open Access

https://doi.org/10.5935/1676-2444.20210025

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Abstract

ABSTRACT Introduction: The current study about transition of oral epithelial dysplasia, present in lesions such as leukoplakia, for squamous cell carcinoma (SCC) involves not only the histopathological aspects, but also the analysis of the presence of biomarkers which influence the microenvironment where cells are embedded. Objective: To evaluate the tissue inhibitor of metalloproteinase-1 (TIMP-1) profile in cases of leukoplakia and SCC classified into different degrees of dysplasia and histological grading, respectively. The immunohistochemical findings were confronted with microscopic features adopted in the classification of each lesion. Material and methods: Cases of leukoplakia and SCC were recovered from files of The Oral Pathological Anatomy Service of the Dental School at the Universidade Federal do Espirito Santo (SAPB-UFES), between the years 2004 and 2010. New slides were obtained and submitted to immunohistochemical assay to determine TIMP-1 expression profile. Parenchyma, as well as the different layers of the epithelium and stroma was evaluated. Results: In all cases the presence of TIMP-1 was detected in the stroma and parenchyma. In mild leukoplakia, the basal layer with hyperplasia showed intense immunolabeling, whereas cells with loss of polarity presented weaker expression. In moderate leukoplakia, all epithelium layers, except the cornea, were labeled. Severe leukoplakia had the spinous layer most intensely labeled, with no variation in areas with pleomorphism. Stage I SCC showed the deepest islands with intense labeling in cells with pleomorphism and mitoses. In the tumor islands, less differentiated cells were weakly labeled, and in keratin pearl, labeling was weak or absent in central cells. In stage II SCC, labeling was observed in basal cell with hyperplasia and in cells of the spinous layer, however, the parabasal layer was not labeled. Also, on tumor islands, less differentiated cells did not express the protein and keratin pearls were not labeled. Conclusion: It was possible to detect TIMP-1 immunolabeling in all specimens, ranging in intensity and location. The absence of expression in less differentiated cell suggests that more aggressive lesions present reduced enzyme expression. The microenvironment is important for the various cellular activities, and TIMP is an enzyme that participates in matrix remodeling, therefore changes in its expression can be a valuable tool in the better understanding oral carcinogenesis.

Highlights

The history of muscle biopsy dates back to 1860, when Duchenne first performed a biopsy on a patient with symptoms of myopathy[1]
The twenty-first century has brought in a new spectacular progress in the utility of muscle biopsy with the commencement of molecular methods
The molecular era was made possible by the development of molecular biology and its application to muscle diseases

Summary

Introduction

The history of muscle biopsy dates back to 1860, when Duchenne first performed a biopsy on a patient with symptoms of myopathy[1]. The introduction of enzyme histochemical methods by Victor Dubowitz, in 1970, revolutionized the role of muscle biopsy in the diagnosis of various primary and secondary muscle diseases[2]. The adaptation of histo- and cytochemical techniques to the study of muscle biopsies improved diagnostic accuracy and enabled the identification of new changes and structures[3, 4].

Results

Conclusion