 Aphthous stomatitis is uncommon in people who smoke , and there is also a correlation between habit duration and severity of the condition . Tobacco use is associated with an increase in keratinization of the oral mucosa . In extreme forms , this may manifest as <unk> or stomatitis <unk> ( smoker 's keratosis ) . This increased keratinization may mechanically reinforce the mucosa and reduce the tendency of ulcers to form after minor trauma , or present a more substantial barrier to microbes and antigens , but this is unclear . Nicotine is also known to stimulate production of adrenal steroids and reduce production of TNF @-@ α , interleukin @-@ 1 and interleukin @-@ 6 . <unk> tobacco products also seem to protect against aphthous stomatitis . Cessation of smoking is known to sometimes precede the onset of aphthous stomatitis in people previously unaffected , or exacerbate the condition in those who were already experiencing aphthous ulceration . Despite this correlation , starting smoking again does not usually lessen the condition . 
