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Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis

BACKGROUND: Oral submucous fibrosis (OSMF) is an insidious chronic fibrotic condition that involves the oral mucosa and occasionally the pharynx and esophagus. Vascularity in OSMF has always been a matter of debate. The prevailing concept is that epithelial atrophy occurs due to lack of perfusion bu...

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Autores principales: Pandiar, Deepak, Shameena, PM
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196280/
https://www.ncbi.nlm.nih.gov/pubmed/25328292
http://dx.doi.org/10.4103/0973-029X.140718
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author Pandiar, Deepak
Shameena, PM
author_facet Pandiar, Deepak
Shameena, PM
author_sort Pandiar, Deepak
collection PubMed
description BACKGROUND: Oral submucous fibrosis (OSMF) is an insidious chronic fibrotic condition that involves the oral mucosa and occasionally the pharynx and esophagus. Vascularity in OSMF has always been a matter of debate. The prevailing concept is that epithelial atrophy occurs due to lack of perfusion but the recent data challenges this concept. Therefore, the present study was conducted to evaluate the immunoreactivity of CD34 and basic fibroblast growth factor (bFGF) in different histological grades of OSMF. This might further shed light to the role of microvasculature in OSMF, so that the epithelial atrophy and resultant malignant transformation seen in the advanced stages might be elucidated. MATERIALS AND METHODS: A total of 30 cases of OSMF were included in the study and mean vascular density (MVD) was calculated using CD34 and bFGF. Five cases of OSMF with dysplasia and 2 cases of OSMF turning malignant were added during the course of the study. RESULTS: Mean vascular density was found to decrease significantly as the diseases advanced. Furthermore, vascularity increased significantly in cases of OSMF turning towards malignancy. CONCLUSION: Our study supports the concept of epithelial atrophy aftermath of lack of perfusion. There is reduced vascularity as the disease advances and this denies the systemic absorption of carcinogens, which affects the already compromised epithelium. Consequently, liberation of angiogenic factors occurs because of malignant transformation, which explains the neoangiogenesis and increased vascularity in OSMF turning towards malignancy. Further studies are required to identify the mechanism leading to carcinogenesis in the atrophied epithelium aftermath of fibrosis and decreased vascularity.
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spelling pubmed-41962802014-10-17 Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis Pandiar, Deepak Shameena, PM J Oral Maxillofac Pathol Original Article BACKGROUND: Oral submucous fibrosis (OSMF) is an insidious chronic fibrotic condition that involves the oral mucosa and occasionally the pharynx and esophagus. Vascularity in OSMF has always been a matter of debate. The prevailing concept is that epithelial atrophy occurs due to lack of perfusion but the recent data challenges this concept. Therefore, the present study was conducted to evaluate the immunoreactivity of CD34 and basic fibroblast growth factor (bFGF) in different histological grades of OSMF. This might further shed light to the role of microvasculature in OSMF, so that the epithelial atrophy and resultant malignant transformation seen in the advanced stages might be elucidated. MATERIALS AND METHODS: A total of 30 cases of OSMF were included in the study and mean vascular density (MVD) was calculated using CD34 and bFGF. Five cases of OSMF with dysplasia and 2 cases of OSMF turning malignant were added during the course of the study. RESULTS: Mean vascular density was found to decrease significantly as the diseases advanced. Furthermore, vascularity increased significantly in cases of OSMF turning towards malignancy. CONCLUSION: Our study supports the concept of epithelial atrophy aftermath of lack of perfusion. There is reduced vascularity as the disease advances and this denies the systemic absorption of carcinogens, which affects the already compromised epithelium. Consequently, liberation of angiogenic factors occurs because of malignant transformation, which explains the neoangiogenesis and increased vascularity in OSMF turning towards malignancy. Further studies are required to identify the mechanism leading to carcinogenesis in the atrophied epithelium aftermath of fibrosis and decreased vascularity. Medknow Publications & Media Pvt Ltd 2014 /pmc/articles/PMC4196280/ /pubmed/25328292 http://dx.doi.org/10.4103/0973-029X.140718 Text en Copyright: © Journal of Oral and Maxillofacial Pathology http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Pandiar, Deepak
Shameena, PM
Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title_full Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title_fullStr Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title_full_unstemmed Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title_short Immunohistochemical expression of CD34 and basic fibroblast growth factor (bFGF) in oral submucous fibrosis
title_sort immunohistochemical expression of cd34 and basic fibroblast growth factor (bfgf) in oral submucous fibrosis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196280/
https://www.ncbi.nlm.nih.gov/pubmed/25328292
http://dx.doi.org/10.4103/0973-029X.140718
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