| Abstract: | The oral cavities of tobacco smokers and users of smokeless tobacco products are exposed to high concentrations of nicotine. A limited number of animal studies have assessed the effect of nicotine on osseointegration. Results from experimental studies have reported a statistically significant decrease, at 4 weeks of follow‐up, in bone‐to‐implant contact among rats exposed to nicotine compared with unexposed rats. Nicotine increases the production of inflammatory cytokines (such as interleukin‐6 and tumor necrosis factor‐alpha) by osteoblasts. Waterpipe, pipe, and cigarette smokers are at increased risk of developing oral cancer, periodontal disease, and alveolar bone loss. One explanation for this is that smokers (regardless of the type of tobacco product) are exposed to similar chemicals, such as nicotine, tar, oxidants, polyaromatic hydrocarbons, and carbon monoxide. Moreover, raised levels of proinflammatory cytokines have been identified in the gingival crevicular fluid of cigarette smokers with peri‐implant diseases. Therefore, it is hypothesized that nicotine and chemicals in tobacco smoke induce a state of oxidative stress in peri‐implant tissues (gingiva and alveolar bone), thereby increasing the likelihood of peri‐implant disease development via an inflammatory response, which if left uncontrolled, will result in implant failure/loss. In this regard, tobacco smoking (including cigarettes, waterpipe, and pipe) is a significant risk factor for peri‐implant diseases. The impact of vaping electronic cigarettes using nicotine‐containing e‐juices remains unknown. Habitual use of smokeless tobacco products is associated with oral inflammatory conditions, such as oral precancer, cancer, and periodontal disease. However, the effect of habitual use of smokeless tobacco products on the success and survival of dental implants remains undocumented. |
