The oral tissues of smokers are exposed to high nicotine concentrations that negatively affect local cell populations. Gingival crevicular fluid nicotine concentrations can be up to nearly 300 times[47] that of nicotine plasma concentrations in smokers (20 ng/ml).[57] The vasoconstrictive properties of nicotine are hypothesized to impair gingival blood flow; however, studies that have examined the effects of smoking on gingival blood flow in humans have shown either no change or increased flow as measured by laser Doppler flowmetry.[58–60] This may be due to smoking-induced elevation in blood pressure, which overcomes any vasoconstrictive effects of smoking.[60] Smoking has been shown to impair revascularization during soft[61] and hard tissue wound healing,[62] which is critical for periodontal plastic, regenerative, and implant procedures. Nicotine binds to root surface in smokers,[63] and In vitro studies show it can alter fibroblast attachment[64,65] and integrin expression,[66] and decrease collagen production while increasing collagenase production.[67] Root surfaces of teeth extracted from smokers show reduced periodontal ligament (PDL) fibroblast attachment as compared to those from non-smokers.[68] Cultured gingival keratinocytes[69] and fibroblasts[70] exposed to nicotine produce higher amounts of the proinflammatory cytokines IL-1 and IL-6, respectively.