Open AccessTransforming growth factor beta 1 in oral submucous fibrosis: An immunohistochemical study - Understanding the pathogenesis
Author(s) -
Venkatesh V Kamath,
Krishnanand Satelur,
Komali Rajkumar,
Shruti Krishnamurthy
Publication year - 2014
Publication title -
journal of dental research and reviews
Language(s) - English
Resource type - Journals
eISSN - 2348-3172
pISSN - 2348-2915
DOI - 10.4103/2348-2915.133942
Subject(s) - oral submucous fibrosis , pathology , immunohistochemistry , submucosa , fibrosis , pathogenesis , medicine , oral mucosa , areca , extracellular matrix , staining , transforming growth factor , epithelium , chemistry , biochemistry , structural engineering , nut , engineering
Background: The development of fibrosis is pathognomic in the potentially malignant oral disorder, oral submucous fibrosis (OSF). Strong evidence exists to implicate the chewing of areca nut in the pathogenesis of the lesion. The constituents of areca nut activate several pro-fibrotic cytokines, chiefly transforming growth factor beta 1 (TGF-β1), which leads to an increased deposition and decreased degradation of extracellular matrix and collagen. TGF-β1 probably represents the major pathway in the deposition of collagen fibers in this condition. The present study aims to identify and correlate the expressions of TGF-β1 immunohistochemically on paraffin sections of various stages of OSF. Materials and Methods: The expression of TGF-β1 antibody was detected immunohistochemically using the anti-TGF-β1 mouse monoclonal antibodies (8A11-NovusBio USA) on paraffin sections of 58 cases of OSF, 10 cases of normal buccal mucosa tissue and 5 cases of scar tissue. The site, extent, and intensity of expression and quantification of TGF-β1 were noted and a comparative evaluation between various grades of OSF. Scar tissue and normal oral mucosa was made using image analysis software (Jenoptik optical system-ProReg ® Capture Pro 2.8.8 software [2011]). Results: Cells of spinous layer of the epithelium showed more intense staining in all grades of OSF, Grade II showed the highest percentage of expression, same as that of keloid (17%) but less than that of normal mucosa (12%). Positive staining was seen around blood vessels, muscles, fibers in the submucosa and perimuscle fibers. Highest expression was in the muscle in Grade III (80%) compared with normal oral mucosa (37%). Conclusion: These results suggest that the pathogenesis of OSF and scar/keloid could be linked through the TGF-β1 pathway. Interventions directed at the TGF-beta pathway may hold the key in the future management of this oral potentially malignant condition