Abstract
Recurrent aphthous stomatitis (RAS) is one of the most common ulcers affecting the oral cavity. Though it is known that RAS affects only the lining (non-keratinized) mucosa sparing the masticatory (keratinized) mucosa and is unlikely to be seen in smokers, no concrete explanations have been put forward. A hypothesis is proposed that the keratin layer blocks the ingress of antigens and prevents the occurrence of RAS on masticatory mucosa. Similarly, combustible products of smoking are known to cause keratinization and therefore have a similar effect on the lining mucosa and inhibit its occurrence. In addition, nicotine or its metabolites can result in decrease of pro-inflammatory cytokines like tumor necrosis factor-α, interleukins 1 and 6, and increase of anti-inflammatory cytokine interleukin-10. Consequently, there is reduced susceptibility to RAS due to immunosuppression and/or reduction in inflammatory response.