Cigarette smoking has been shown to alter an individual’s response to various forms of periodontal therapy. In vitro and in vivo studies have indicated that smoking and the use of smokeless tobacco products may significantly contribute to the development and progression of inflammatory periodontal disease. The enhanced periodontal destruction observed in smokers may be caused by an alteration of the host response such as the reduced function of oral and peripheral neutrophils, and the decreased levels of salivary and serum antibodies. Similar effects have been observed at higher concentrations of various tobacco components such as nicotine, acroleine, and cyanide. Another hypothesis regarding the contribution of tobacco, and especially nicotine, to the etiology of periodontitis is that the reparative and regenerative potential of periodontal cells may be affected. It has been documented that nicotine can suppress the growth of osteoblast-like cells in vitro. Additionally, nicotine may be stored in and then released from periodontal fibroblasts. However, most of this cytotoxic substance remains within the fibroblasts, resulting in alterations of the cellular metabolism or various functions. Nicotine is a potent component of tobacco smoke. Nicotinic receptors are widespread and are heterogeneous groups comprised of multiple sub-units. The exact importance of individual receptor sub-units is currently not fully understood. However, this may explain in part the wide variety of physio-