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Does smoking really protect from recurrent aphthous stomatitis?

PURPOSE: To study the effect of smoking on the prevalence of recurrent aphthous stomatitis (RAS) and to examine whether intensity and duration of smoking influence RAS lesions. SUBJECTS AND METHODS: A cross-sectional survey was conducted on a random sample of 1000 students of The University of Jorda...

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Detalles Bibliográficos
Autor principal: Sawair, Faleh A
Formato: Texto
Lenguaje:English
Publicado: Dove Medical Press 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2999509/
https://www.ncbi.nlm.nih.gov/pubmed/21151626
http://dx.doi.org/10.2147/TCRM.S15145
Descripción
Sumario:PURPOSE: To study the effect of smoking on the prevalence of recurrent aphthous stomatitis (RAS) and to examine whether intensity and duration of smoking influence RAS lesions. SUBJECTS AND METHODS: A cross-sectional survey was conducted on a random sample of 1000 students of The University of Jordan, Amman, between May and September 2008. Sociodemographic factors and details about smoking habits and RAS in last 12 months were collected. RESULTS: Annual prevalence (AP) of RAS was 37.1%. Tobacco use was common among students: 30.2% were current smokers and 2.8% were exsmokers. AP was not significantly influenced by students’ age, gender, marital status, college, and household income but was significantly affected by place of living (P = 0.02) and presence of chronic diseases (P = 0.03). No significant difference in AP of RAS was found between smokers and nonsmokers. Cigarette smokers who smoked heavily and for a longer period of time had significantly less AP of RAS when compared to moderate smokers and those who smoked for a shorter period of time. The protective effect of smoking was only noticed when there was heavy cigarette smoking (>20 cigarettes/day) (P = 0.021) or smoking for long periods of time (>5 years) (P = 0.009). Nevertheless, no significant associations were found between intensity or duration of smoking and clinical severity of RAS lesions. CONCLUSION: The “protective effect” of smoking on RAS was dose- and time-dependent. When lesions are present, smoking had no effect on RAS severity.