OBJECTIVES

The study aimed to investigate the relationship between cigarette smoking and macrophage polarization in peri-implantitis (PI) lesions. Additionally, it sought to characterize clinical, radiological, microbiological, and immunological features of PI in smokers and non-smokers.

MATERIALS AND METHODS

A cross-sectional study included 40 patients (20 smokers, ≥ 10 cigarettes/day, and 20 non-smokers) requiring surgical treatment for PI. Samples of peri-implant crevicular fluid (PICF) and granulation tissue were collected during surgery for immunofluorescence and cytokine analyses. Smoking exposure was assessed through cotinine levels. Macrophage polarization (M1/M2) was determined using immunofluorescence. Clinical, radiological, and microbiological parameters were also evaluated.

RESULTS

Smokers showed a significantly higher proportion of M1 macrophages (70.23%) compared to non-smokers (25.09%, p < 0.005). This pro-inflammatory shift correlated positively with cotinine levels (ρ = 0.694; p < 0.005) and pack-years (ρ = 0.81; p < 0.005). No significant differences in M2 macrophage counts, cytokine concentrations, or microbiota diversity were observed between the groups. However, smokers exhibited more severe PI lesions (p = 0.04).

CONCLUSIONS

Smoking is associated with a pro-inflammatory shift at the cellular level due to an increase in M1 macrophage polarization in PI lesions, suggesting a pro-inflammatory response that may exacerbate tissue destruction and hinder treatment outcomes. These findings highlight the need for incorporating smoking cessation into comprehensive peri-implant care strategies to improve disease management and implant prognosis.