Smoking negatively impacts the clinical, microbiological, and immunological treatment response of young adults with Grade C periodontitis

Abstract

Objective This study aimed to investigate the influence of smoking on clinical, microbiological and immunological parameters in young adult with stage III‐IV Grade C periodontitis after full‐mouth ultrasonic debridement (FMUD) associated with Amoxicillin and Metronidazole (AMX + MTZ), comparing smokers (PerioC‐Y‐Smk) with non‐smokers (PerioC‐Y‐NSmk). Materials and Methods Fifteen PerioC‐Y‐NSmk and 14 PerioC‐Y‐Smk patients underwent FMUD associated with AMX + MTZ for 10 days. All parameters were collected at baseline and 3 and 6 months after treatment. Plaque index (PI), bleeding on probing (BoP), probing depth (PD), clinical attachment level (CAL)‐ the primary variable‐, and gingival recession (GR) were clinically assessed. The impact of PI on CAL change at 6‐month was verified by a regression analysis. Samples of the subgingival biofilm was collected for detection of levels of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P.gingivalis), Tannerella forsythia (T. forsythia), and Fusobacterium nucleatum ssp (F. nucleatum), and were analyzed by real‐time qPCR; gingival crevicular fluid was collected for detection of levels of interleukin (IL)‐1β, IL‐4, IL‐6, IL‐10, tumor necrosis factor (TNF)‐α, and interferon (IFN)‐γ, which were analyzed using an enzyme immunoassay. Results PerioC‐Y‐Smk had significantly higher PI, BOP, and GR at baseline compared to non‐smokers (p < .05). PerioC‐Y‐Smk presented higher PD, CAL, and GR at 3 and 6 months (p < .05) compared with PerioC‐Y‐NSmk in the same periods; PI negatively affected CAL gain in PerioC‐Y‐NSmk at 6‐month follow‐up (p = .052) and did not impact on clinical response in PerioC‐Y‐Smk (p = .882). Lower levels of IFN‐γ, IL1‐β, and IL‐4 were observed at 3 months in the PerioC‐Y‐NSmk (p < .05) compared with PerioC‐Y‐Smk. Lower proportions of P. gingivalis were observed in PerioC‐Y‐NSmk at baseline and at 3 months (p < .05) and lower proportions of F. nucleatum were observed at 6 months, in the PerioC‐Y‐NSmk (p < .05). Conclusions PerioC‐Y‐Smk presents an unfavorable clinical, microbiological, and immunological response after 3 and 6 months after FMUD associated with AMX + MTZ. Clinical Relevance Smoking worsens periodontal condition of young treated adults presenting stage III/IV Grade C periodontitis.

Expression of tight junction proteins in smokers and non‐smokers with generalized Stage III periodontitis

“…In our study, we observed that smoking was associated with decreased levels of all biomarkers in GCF. This finding contradicts some existing literature which suggests that smoking actually increases TNF‐α expression 44–46 . However, Fredrikson et al conducted a study in which they did not find a statistically significant difference in TNF‐α levels released in response to bacterial stimulation between smoking and non‐smoking groups 47 .…”

“…This finding contradicts some existing literature which suggests that smoking actually increases TNFα expression. [44][45][46] However, Fredrikson et al conducted a study in which they did not find a statistically significant difference in TNFα levels released in response to bacterial stimulation between smoking and non-smoking groups. 47 They attributed this to the low sensitivity of peripheral lymphocytes to stimuli.…”

Factors Associated with Periodontitis in Younger Individuals: A Scoping Review

“…Other risk identified factors were "gums bleeding" and "low bone density" [37,38]. Compared to non-smokers, smoking tobacco caused greater gingival recession and gingival pocket depths and a decrease in tissue repair and immune response [39].…”

“…Among the studies, smoking and being overweight or obese were identified as significant risk factors associated with periodontitis in younger adults. Da Silva et al [39] examined the influence of smoking on periodontal health and inflammatory markers in patients who received full-mouth ultrasonic debridement coupled with the use of amoxicillin and metronidazole. Their findings revealed a significant association between smoking and higher probing depth, bleeding on probing, and gingival recession compared to nonsmokers after treatment.…”

“…A cascade of events sets the stage for a slew of adverse consequences, including periodontal tissue damage, the formation of pathological pockets around the teeth, and ultimately, the unsettling loosening and loss of teeth [48]. De Silva et al [39] found fewer pathogenic bacterial species, Porphyromonas gingivalis and Fusobacterium nucleatum, in non-smokers, suggesting a potential mechanism for how smoking exacerbates periodontitis. It implies that smoking may create a more hospitable environment for these pathogenic bacteria to flourish, perpetuating the destructive cycle of periodontal disease.…”