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Abstract
Oral submucous fibrosis (OSF) is an oral potentially malignant disorder and areca quid chewing is the main etiological factor. However, the molecular mechanism underlying OSF remains unclear, partly due to the lack of an appropriate animal model. The present study aimed to establish and characterize an animal model of areca nut extract (ANE)-induced skin fibrosis that mimics OSF. Mice were divided into 4 groups: the control group; the bleomycin group; and the ANE10 and ANE20 groups, which received 10mg/ml and 20mg/ml subcutaneous (SC) injection of ANE, respectively. Skin fibrosis was evaluated by histological analyses. Additionally, the expression levels of the fibrotic marker genes were determined by immunohistochemical staining and immunoblotting. ANE administration significantly increased dermal thickness and collagen deposition compared with the control group. Moreover, ANE induced the expression of the fibrotic marker genes alpha smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) in the skin lesions. The SC injection of ANE successfully induced skin fibrosis, exhibiting characteristics similar to those of OSF. This model may facilitate future studies of the mechanism underlying OSF.
Highlights
Oral submucous fibrosis (OSF) is an oral potentially malignant disorder [1]with a high risk of malignant transformation [1]
To investigate whether SC injection of areca nut extract (ANE) induced dermal fibrosis, mice received different dosages of ANE, and the morphologic changes were analyzed at different time points
Within one week, the ANE treatment groups, i.e., ANE10 (1.45±0.28) and ANE20 (1.5±0.45), exhibited obviously thicker skins compared with the phosphate buffered saline (PBS) group (Fig 1A)
Summary
Oral submucous fibrosis (OSF) is an oral potentially malignant disorder [1]with a high risk of malignant transformation [1]. Several studies have indicated that 7–30% of OSF patients may experience transformation into oral squamous cell carcinoma (OSCC) [2,3,4]. The molecular mechanism of areca nut chewing-induced OSF remains unclear, and the majority of the related information was collected based on clinical and in vitro studies. The possible etiological factors that have been indicated in the development of OSF include vitamin deficiencies, tobacco use, areca nut chewing, and genetic disorders. A number of lines of epidemiological evidence and clinical studies strongly indicate that areca quid chewing is the main etiological factor in the development of OSF [5,6,7,8,9,10,11,12]
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