The impact of smoking on peri-implant microbiota: A systematic review

Dental implants have been widely used as an alternative to fixed and removable partial dentures. Despite their high survival rates of 96.4% over a 10-year follow-up period [1], dental implants are prone to clinical inflammatory conditions, such as peri‑implant mucositis and peri‑implantitis [2]. Peri-implant mucositis, characterized by bleeding on probing and clinical signs of inflammation, is caused by the accumulation of bacterial plaque around peri‑implant tissue [3]. Peri-implantitis, characterized by visual inflammation in addition to alveolar bone destruction and increased probing depth, has been associated with poor plaque control and a history of severe periodontitis [3]. Similar to periodontal microorganisms in healthy gingiva, the microorganisms in peri‑implant tissues of healthy implants are predominantly Gram-positive cocci and rod microorganisms [4]. The microbiota in diseased peri‑implant sites is comprised of Gram-negative anaerobic periodontitis-associated pathogens and opportunistic microorganisms, and is frequently associated with non-saccharolytic anaerobic Gram-positive rods [5]. Data show that the detectable periodontitis-associated pathogens are Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia [6,7], suggesting that peri‑implantitis could be a polymicrobial anaerobic infection [8], [9], [10]; however, the specificity of the microbiota causing peri‑implantitis remains unclear [8].

Smoking is a remarkable risk factor for periodontitis [11]. Smoking changes the subgingival bacterial profile by depleting the beneficial commensal and increasing the periodontitis-associated pathogenic bacteria in gingiva tissue [12]. Colonization by the so-called keystone periodontal pathogen (i.e., P. gingivalis), which is enhanced by community-associated oral streptococci, such as Streptococcus gordonii, leads to dysbiotic microbial communities and chronic inflammation in gingival tissue [13]. These changes contribute to the emergence of a dysregulated host immune response and may lead to periodontitis in a susceptible host [13]. Most importantly, the data show that dysbiosis is present in the periodontal microbiota of smokers, regardless of their periodontal condition (healthy, gingivitis, or periodontitis), and remains significant in smokers even after treating the disease [14].

Smoking may affect the microbiota profile in peri‑implant tissue as well. However, there is limited understanding of the effects of smoking on peri‑implant microbiota. Thus, this review aimed to assess the evidence from the literature to ascertain if smoking affects the peri‑implant microbiota, by answering the following questions: 1) Are there differences in the microbiota of healthy peri‑implant tissue between smokers and nonsmokers? 2) Are there differences in the microbiota of diseased peri‑implant tissue between smokers and nonsmokers? 3) Does smoking affect the transition of the microbiome from a healthy to a diseased status? After applying selection criteria for study inclusion and quality assessment, we investigated the impact of smoking on peri‑implant microbiota.

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