A rat model of oral submucous fibrosis induced by bleomycin

Zhang, Shanshan; Gong, Zhaojian; Wang, Xiong; Wang, Xiao; Qian, Min; Luo, Chongdai; Ling, Tianyou

doi:10.1016/j.oooo.2015.07.042

Cited by 14 publications

(16 citation statements)

References 22 publications

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“…We think the solution of chewed betel nut would be similar to the filtered ANE solution but not the centrifuged clear supernatant of the ANE solution. In addition, we found that bleomycin can induce fibrosis in the oral submucosa, which is consistent with the findings of a recent study showing that injection of bleomycin into the buccal mucosa caused pathologic changes similar to those observed in OSMF (Zhang et al, 2016). However, because bleomycin is not an ingredient in natural food, bleomycin-induced OSF is not easy to implicate in the clinical process of OSMF.…”

Section: Discussionsupporting

confidence: 91%

Photobiomodulation therapy inhibits oral submucous fibrosis in mice

et al. 2020

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Objectives Oral submucous fibrosis (OSMF) is a chronic inflammatory disease and a potentially malignant oral disorder. However, the best therapeutic treatment for OSMF remains uncertain. Our previous study showed that photobiomodulation (PBM) therapy and forskolin could reduce arecoline‐induced fibrosis reactions via the cAMP pathway. The present study aimed to establish an animal model of areca nut extract (ANE)‐induced OSMF and to evaluate the therapeutic potential of PBM and forskolin for ANE‐induced OSMF. Subjects and methods The mice were divided into five groups. The buccal tissues were harvested for histomorphological analysis and immunoblotting. Results Our results showed that PBM significantly reduced the development of ANE‐induced OSMF, quantified by changes in submucosal layer thickness and collagen deposition. Additionally, PBM could extensively reduce the protein expression of the fibrotic marker genes alpha‐smooth muscle actin (α‐SMA) and connective tissue growth factor (CTGF) in buccal submucous lesions. However, forskolin treatment significantly decreased the protein expression of fibrotic marker genes but slightly decreased the observed histomorphological changes. Conclusions We established an ANE‐induced OSMF mouse model, which also provided a model for the development of a therapeutic treatment for OSMF. The anti‐fibrotic effects of PBM and forskolin may be useful for clinical interventions.

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Section: Discussionsupporting

confidence: 91%

Photobiomodulation therapy inhibits oral submucous fibrosis in mice

et al. 2020

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“…In the present study, the epithelium of the control group showed hyperplastic epithelium, while the lamina propria of the control group showed few inflammatory cells infiltration, normal appearing of muscle fibers, absence of collagen fibers formation and no vascular changes, the same observations were reported by Zhang S. et al, (2016) who referred these changes to the inflammatory effect of injecting sterile phosphate buffer saline (PBS) (3) .…”

Section: Discussionsupporting

confidence: 89%

“…This study was designed to explain the pathological role of the related proteins TNF-α and K 17 in oral submucous fibrosis in rat model induced by bleomycin. As it was proved before by Zhang S.et al(2016), that OSF of human are similar to OSF of rat model induced by bleomycin in both clinical and pathological features (3) .…”

Section: Discussionsupporting

confidence: 51%

“…It was reported that bleomycin as an anti-carcinogenic antibiotic is dose -dependent pulmonary fibrosis agent and leading to release of alveolar inflammatory cells like macrophages, neutrophils and eosinophils from the alveolar tissue (2) . It was used to induce oral submucous fibrosis (OSF) in rat as in vivo animal model, that mimics to the human OSF clinically and microscopically, within short time (3) .…”

Section: Introductionmentioning

confidence: 99%

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Tumor necrosis factor alpha and keratin 17 expression in oral submucous fibrosis in rat model

Latif

A²

2019

Egyptian Dental Journal

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Background and Objective: Oral submucous fibrosis is an inflammatory and a premalignant lesion as classified by "World Health Organization". Its pathogenesis is related to collagen metabolism. Bleomycin is an anti-carcinogenic drug, but it causes pulmonary fibrosis. This study was carried out to study the role of tumor necrosis factor alpha and keratin 17 in pathogenesis of oral submucous fibrosis.Study Design: Fifty pathologically-free female rats were divided into one control group and four test groups. They were injected by phosphate-buffered saline and Bleomycin into the buccal mucosae daily for 2, 4, 6 and 8 weeks, respectively. The histopathological changes was evaluated by studying the changes within epithelium tissue and lamina propria by (H&E) and the expression of both (tumor necrosis factor alpha and keratin 17) using immunohistochemistry and enzyme linked immunosorbent assay respectively. Results:The buccal mucosae of the test groups in comparison with control showed hyperplastic and hyperatrophic epithelial changes that gradually decreased with the severity of oral submucous fibrosis, with epithelial atrophy and focal dysplastic changes, which increase with severity of oral submucous fibrosis gradually. The lamina propria showed gradual increase in inflammatory cells, collagen formation and closure of the blood vessels. Regarding tumor necrosis factor alpha the area percent of immunoexpression, showed the lowest expression in the control and test groups showed gradually increase after 2, 4, 6,8 weeks within epithelium , on the other hand, the area percent of immunoexpression of tumor necrosis factor alpha within lamina propria showed gradually increase after 2, 4, 6 weeks, then decreased after 8 weeks. Regarding Keratin-17, the lowest value was recorded in control group while it increased gradually from the second week to the 8 th weeks. Conclusion:Both protein molecules tumor necrosis factor alpha and keratin 17 appear to be related in case of oral submucous fibrosis. As tumor necrosis factor alpha and keratin 17 are interdependent regulators, they could be used as diagnostic makers and a prognostic mirror of oral submucous fibrosis cases. Tumor necrosis factor alpha inhibitory drugs can be targeted in new therapeutic agents to improve the prognosis of oral submucous fibrosis.

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“…Epidemiological studies provide overwhelming evidence that areca nut chewing is a major etiological factor for OSF and carcinogenesis [4]. An areca extract-induced oral mucosa fibrosis rat model showed progressive changes in epithelial thickness (ET); this leads to atrophy and cytokine infiltration into the subepithelial layer to promote fibroblast proliferation and collagen formation [5,6]. Recent studies have shown that arecoline, the main areca alkaloid, is cytotoxic to epithelial cells and fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

Role of autophagy and apoptosis in atrophic epithelium in oral submucous fibrosis

et al. 2020

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Oral submucous fibrosis (OSF) is a serious, potentially malignant oral disorder. It is histopathologically characterized by chronic inflammation and atrophic epithelium accompanied by the accumulation of collagen fibers in the lamina propria. The molecular mechanisms leading to atrophic epithelium remain poorly understood. Therefore, the present study investigated the role of autophagy and apoptosis in atrophic epithelium in OSF. The expression of Caspase-3 and autophagy-related proteins (LC3 and P62) in OSF epithelial tissues was quantified by immunohistochemistry. The analysis demonstrated that, compared with normal oral mucosal tissues, autophagy and apoptosis increased with the progression of OSF. Flow cytometry and Western blotting showed that arecoline induces apoptosis in human oral keratinocytes (HOKs) in a time-dependent manner in vitro. Arecoline-induced autophagy was confirmed by transmission electron microscopy and Western blotting. When chloroquine was used as an inhibitor of autophagy, the apoptosis rate and Caspase-3 expression decreased compared with the use of arecoline alone. Thus, autophagy and apoptosis may be involved in atrophic epithelium in OSF, and arecolineinduced autophagy promotes apoptosis in HOKs.

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A rat model of oral submucous fibrosis induced by bleomycin

Cited by 14 publications

References 22 publications

Photobiomodulation therapy inhibits oral submucous fibrosis in mice

Photobiomodulation therapy inhibits oral submucous fibrosis in mice

Tumor necrosis factor alpha and keratin 17 expression in oral submucous fibrosis in rat model

Role of autophagy and apoptosis in atrophic epithelium in oral submucous fibrosis

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