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Potentiated action on the progression of OSMF by hypoxia mediated signaling pathway by the epithelial mesenchymal transition and angiogenic apparatus

 Department of Oral and Maxillofacial Pathology and Microbiology, I.T.S. Center for Dental Studies and Research, Ghaziabad, Uttar Pradesh, India

Correspondence Address:
Nikita Gulati,
Department of Oral and Maxillofacial Pathology and Microbiology, I.T.S. Center for Dental Studies and Research, Muradnagar, Ghaziabad - 201 206, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jcrt.jcrt_502_21

Background: Epithelial–mesenchymal transition (EMT) is a complex process, in which epithelial cells acquire the characteristics of invasive mesenchymal cells. EMT has been implicated in cancer progression and metastasis as well as the formation of many tissues and organs during development. Aim: The aim of the study was to ascertain the role of hypoxia-mediated signaling pathways influencing EMT and angiogenesis in progression of oral submucous fibrosis (OSMF). Materials and Methods: Evaluation of the immunoexpression of alpha-smooth muscle actin (α-SMA), E-cadherin, vimentin, and factor VIII receptor antigen in OSMF and oral squamous cell carcinoma (OSCC) arising from OSMF was done. Differences between the different variables were analyzed using ANOVA test and Pearson's Chi-square test, and Mann–Whitney test was also calculated. Results: The mean α-SMA positive myofibroblasts increased from Group 1 (OSMF) to Group 2 (OSCC), especially those in the deeper connective tissue stroma. The mean labeling index of vimentin and mean vessel density immunoexpression was more in Group 2 (OSCC) as compared to Group 1 (OSMF). Mean α-SMA correlated negatively with E-cadherin expression and positively with vimentin and factor VIII immunoexpression. E-cadherin expression correlated negatively with factor VIII and positively with Vimentin expression. Conclusions: The molecular mechanisms responsible for the development of OSCC in patients with OSMF require unification of multiple progressive pathogenetic mechanisms involved in the progression of the disease.

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