Hyperplasia of Wistar rat tongue mucosa due to exposure to cigarette side-stream smoke
Downloads
Background: Hyperplasia, a condition whereby an excessive number of cells are produced due to their uncontrolled division, represents a common symptom of carcinogenesis. Cancer is a physical manifestation of cell malignancy resulting from abnormal proliferation. Globally, oral cancer currently constitutes the sixth largest lethal form of the condition. The most common etiology of oral cancer is tobacco of which cigarettes are the most popular related product. The health risks associated with cigarette smoke not only affect active smokers but also individuals who ingest it passively. Sidestream smoke comes from the lighted end of a burning tobacco product such as a cigarette, pipe or cigar and contains nicotine and many harmful cancer-causing chemicals. Inhaling sidestream smoke increases the risk of lung and other types of cancer. Purpose: The purpose of this study was to understand how sidestream cigarette smoke initiates precancerous changes, in this case hyperplasia, in the oral mucosa epithelium of Wistar rats. Methods: The subjects were divided into three groups, a 4-weektreatment group (P1), an 8-week treatment group (P2), and a control group (K), each consisting of tensubjects. Thesubjects were exposed to a daily two-cigarette dose of smoke. The experiment used a post-test only control group design. All samples were sacrificedduring the fourth and eighth weeks. Haematoxylin-eosin staining was performed on the tongues of theWistar rats to establish the presence of hyperplasia.Data was analyzed using aone-way ANOVA test.Results: After the Wistar rats had been exposed to cigarette smoke, an increaseddegree of epithelial cell proliferation (hyperplasia) showed a significant difference with a p-value <0.05 during the eighth week. Conclusion: Exposure to cigarette sidestream smoke induces increased epithelial cell proliferation (hyperplasia) in Wistar rats.
Downloads
Bisen PS, Khan Z, Bundela S. Biology of oral cancer: key apoptosis regulators. Boca Raton: CRC Press; 2014. p. 1–6, 21–22, 37–46, 49–195.
Sembulingam K, Sembulingam P. Essential of Medical physiology. 6th ed. New Delhi: Jaypee Brothers Medical Publishers; 2012. p. 20, 351–6.
Tanaka T, Ishigamori R. Understanding carcinogenesis for fighting oral cancer. J Oncol. 2011; 2011: 1–10.
Watanabe N, Ohkubo T, Shimizu M, Tanaka T. Preneoplasia and carcinogenesis of the oral cavity. Oncol Discov. 2015; 3(1): 1–12.
Kuriakose MA. Contemporary oral oncology. New York: Springer; 2016. p. 31–6.
Behera SN, Xian H, Balasubramanian R. Human health risk associated with exposure to toxic elements in mainstream and sidestream cigarette smoke. Sci Total Environ. 2014; 472: 947–56.
Fujimoto H, Tsuji H, Okubo C, Fukuda I, Nishino T, Lee KM, Renne R, Yoshimura H. Biological responses in rats exposed to mainstream smoke from a heated cigarette compared to a conventional reference cigarette. Inhal Toxicol. 2015; 27(4): 224–36.
Kusuma ARP. Pengaruh Merokok Terhadap Kesehatan Gigi Dan Rongga Mulut. Maj Ilm Sultan Agung. 2011; 49(124): 1–8.
Oral Health Foundation. Mouth cancer risk factors. Available from: https://www.dentalhealth.org/mouth-cancer-risk-factors. Accessed 2018 Aug 25.
Glick M. Burket's oral medicine. Sheffield: People's Medical Publishing House; 2015. p. 173–201.
Arifa Beegom A. Passive smoking and oral cancer risk: a case report. Kerala Med J. 2014; 7(3): 74–8.
Ibuki Y, Toyooka T, Zhao X, Yoshida I. Cigarette sidestream smoke induces histone H3 phosphorylation via JNK and PI3K/Akt pathways, leading to the expression of proto-oncogenes. Carcinogenesis. 2014; 35(6): 1228–37.
Travers M, Nayak N, Annigeri V, Billava N. Indoor air quality due to secondhand smoke: Signals from selected hospitality locations in rural and urban areas of Bangalore and Dharwad districts in Karnataka, India. Indian J Cancer. 2015; 52(4): 708–13.
Teague S V., Pinkerton KE, Goldsmith M, Gebremichael A, Chang S, Jenkins RA, Moneyhun JH. Sidestream cigarette smoke generation and exposure system for environmental tobacco smoke studies. Inhal Toxicol. 1994; 6(1): 79–93.
Thirion-delalande C, Gervais F. Comparative analysis of the oral mucosae from rodents and non-rodents: application to the nonclinical evaluation of sublingual immunotherapy products. PLoS One. 2017; 12(9): 1–18.
de Oliveira Semenzati G, de Souza Salgado B, Rocha NS, Michelin Matheus SM, de Carvalho LR, Garcia Martins RH. Histological and immunohistochemical study of the expression of p53 and ki-67 proteins in the mucosa of the tongue, pharynx and larynx of rats exposed to cigarette smoke. Inhal Toxicol. 2012; 24(11): 723–31.
Husein A. Pengaruh rokok terhadap peningkatan frekuensi pembentukan mikronukleus pada mukosa mulut. Thesis. Universitas Diponegoro: Semarang; 2013. p. 8–15.
Alharbi I. Study the effects of cigarette smoke on gingival epithelial cell growth and the expression of keratins. Thesis. Université Laval: Québec; 2015. p. 22–24, 42.
Wee P, Wang Z. Epidermal growth factor receptor cell proliferation signaling pathways. Cancers (Basel). 2017; 9(5): 1–45.
Ackers I, Malgor R. Interrelationship of canonical and non-canonical Wnt signalling pathways in chronic metabolic diseases. Diabetes Vasc Dis Res. 2018; 15(1): 3–13.
Chen YT, Gallup M, Nikulina K, Lazarev S, Zlock L, Finkbeiner W, McNamara N. Cigarette smoke induces epidermal growth factor receptor-dependent redistribution of apical MUC1 and junctional β-catenin in polarized human airway epithelial cells. Am J Pathol. 2010; 177(3): 1255–64.
Dwivedi N, Chandra S, Kashyap B, Raj V, Agarwal A. Suprabasal expression of Ki-67 as a marker for the severity of oral epithelial dysplasia and oral squamous cell carcinoma. Contemp Clin Dent. 2013; 4(1): 7–12.
Lee J, Taneja V, Vassallo R. Cigarette smoking and inflammation: Cellular and molecular mechanisms. J Dent Res. 2012; 91(2): 142–9.
Fitria F, Triandini R, Mangimbulude JC, Karwur FF. Merokok dan oksidasi DNA. Sains Med. 2014; 5(2): 121–7.
Alharbi IA, Rouabhia M. Repeated exposure to whole cigarette smoke promotes primary human gingival epithelial cell growth and modulates keratin expression. J Periodontal Res. 2016; 51(5): 630–8.
Geng H, Zhao L, Liang Z, Zhang Z, Xie D, Bi L, Wang Y, Zhang T, Cheng L, Yu D, Zhong C. Cigarette smoke extract-induced proliferation of normal human urothelial cells via the MAPK/AP-1 pathway. Oncol Lett. 2017; 13(1): 469–75.
- Every manuscript submitted to must observe the policy and terms set by the Dental Journal (Majalah Kedokteran Gigi).
- Publication rights to manuscript content published by the Dental Journal (Majalah Kedokteran Gigi) is owned by the journal with the consent and approval of the author(s) concerned.
- Full texts of electronically published manuscripts can be accessed free of charge and used according to the license shown below.
- The Dental Journal (Majalah Kedokteran Gigi) is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License