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30 August 2021

Periodontal parameters and biomarkers in progression of periodontitis in smokers: e-cigarettes vs traditional cigarettes

Lara Figini

Tobacco smoke is an established risk factor for the impoverishment of oral health and is associated with various oral inflammatory diseases including oral cancer, aphthous stomatitis and periodontitis. Several literature studies reported that cigarette smoking has deleterious effects on periodontal tissues by inducing a state of oxidative stress. Furthermore, the nicotine from tobacco smoke is associated with an increase in the expression of the final products of accumulated glycation (AGE) in the soft and hard periodontal tissues and this deteriorates the support of the teeth. Research studies have also shown that even the aerosols of electronic cigarettes cause cytotoxicity to oral keratinocytes in vitro, due to the state of oxidative stress induced by the toxic substances released by nicotine. Furthermore, it is believed that the aldehydes in the aerosols of electronic cigarettes cause the carbonylation of proteins that could predispose to lesions of the bone tissue, generating or worsening the state of periodontitis.

Materials and Methods
In a longitudinal split-mouth study, to be published in the Journal of Dentistry June 2021, the authors evaluated periodontal parameters and analyzed samples of gingival crevicular fluid (GCF) from diseased and healthy sites in cigarette and e-cigarette smokers (ecig) using Raman spectroscopy. They also sought to determine whether biomarkers such as metallo-proteinase matrix (MMP-8) and cross-linked C-terminal type I collagen telopeptide (CTX) could be predictors for attachment loss at periodontal sites. Sixty periodontally healthy and 60 periodontally diseased sites from 30 e-cigarette smokers and 30 traditional cigarette smokers were monitored at baseline, 3-month and 6-month time. GCF was sampled to study MMP-8 and CTX concentrations using the enzyme-linked immunosorbent assay. The infrared absorption spectra of GCF were acquired for each time interval and processed to identify key functional groups.

Significantly increased loss of clinical attachment was observed at 6 months for both groups of smokers compared to baseline time 0 (p <0.01). This difference was significantly higher for traditional cigarette smokers than for e-cigarette users. The MMP-8, CTX biomarkers were significantly correlated with probing depth and clinical attachment loss among both e-cigarette and traditional cigarette smokers. For MMP-8 and CTX, sites with periodontitis showed a statistically significant difference between e-cigarette and traditional cigarette smokers at both 3 and 6 months of follow-up. From baseline time to 6 months of follow-up, the periodontitis sites of both groups showed higher spectral band intensities with deconvulations and Raman shifts for the Amide I and Amide II peaks.

From the results of this study, which must be confirmed in other similar studies, it can be concluded that traditional cigarette smokers develop more periodontal worsening than e-cigarette smokers. Smoking, MMP-8, CTX are prognostic factors for the loss of clinical attack in both traditional and e-cigarette smokers.

Clinical implications
This type of analysis can be a valuable diagnostic and prognosis tool for periodontal disease, as smoking, MMP-8 and CTX biomarkers are prognostic factors for clinical attack loss in both traditional and e-cigarette smokers.

For additional information: Longitudinal evaluation of clinical, spectral and tissue degradation biomarkers in progression of periodontitis among cigarette and electronic cigarette smokers

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