Smoking by altering the peri-implant microbial community structure compromises the responsiveness to treatment.

Abstract

Smoking is an essential risk factor for peri-implant diseases. It also hampers the clinical outcomes of peri-implant therapies. Nonetheless, the effect of smoking can go undetected until the emergence of clinical signs. Bacterial-induced inflammation is responsible for the initiation and progression of peri-implant diseases. We hypothesize that smoking impacts the peri-implant microbiome even in status of clinical health, putting it into a sub-healthy condition that responds poorly to peri-implant treatments. To validate this, peri-implant plaque samples from 18 participants including 10 smokers (S) and 8 non-smokers (NS), who had received implant prostheses were analyzed using metagenomic shotgun sequencing. The results showed that in addition to taxonomical and functional differences, the local stability in the S group was also shown to be much higher than that in the NS group, indicating greater stubbornness of the peri-implant microbiome associated with smoking. Besides, the topological structures were also distinct between the two groups. The highly connected species interacted more preferentially with each other in the S group (eigenvector centralization, 0.0273 in S and 0.0183 in NS), resulting in a greater tendency of forming small-world modules (modularity, 0.714 in S and 0.582 in NS). While in the NS group, inter-species correlations were more evenly distributed (clustering coefficient, 0.532 in S and 0.666 in NS). These alterations overall explained the greater stubbornness of the peri-implant microbiome associated with smoking, which may cause poor responsiveness to peri-implant therapies. From a microbial perspective, this may be a potential reason why smoking impacts negatively on the outcome of peri-implant treatments.