Potential mechanisms of susceptibility to periodontitis in tobacco smokers

Tobacco smoking is probably the most important, controllable environmental risk factor in periodontitis. It results in changes in the vascular, inflam matory, immune and healing responses. The degree of exposure to tobacco smo king can be measured in pack years or by measuring serum cotinine and nicot ine levels. In a previous paper we reported elevated levels of serum solubl e intercellular adhesion molecule-1 (sICAM-1) in smokers, regardless of per iodontal status. Elevated sICAM-1 has been found to be a risk marker for ca rdiovascular disease. In the present paper we report the short-term effects of an episode of smoking on blood how and levels of sICAM-1. Human volunte ers included non-smokers, light smokers and heavy smokers. Relative blood f low was monitored in the gingivae and forehead skin using a laser Doppler f lowmeter and serum levels of sICAM-1, cotinine and nicotine measured before during and up to 60 min following an episode of smoking. We could not prov ide evidence to support the theory that there is localized vasoconstriction within the gingival tissues. In contrast, there was a significant increase in blood flow in the forehead skin of light smokers which was not observed in non-smoking controls or in heavy smokers, suggesting a long-term tolera nce in this latter group. The level of sICAM-1 remained unchanged during th is episode, further suggesting a long-term effect. In a parallel group of s ubjects, we were able to demonstrate a direct significant correlation betwe en sICAM and serum cotinine levels. These observations may be relevant to a etiological mechanisms in periodontitis and other smoking-associated diseas es.