# A study on the association between smoking, periodontal inflammation and alveolar bone resorption in patients with chronic periodontitis based on biomarkers: a meta-analysis

## TL;DR

This study finds that smoking worsens gum inflammation and bone loss in people with chronic periodontitis, based on biomarker analysis.

## Contribution

The study provides a meta-analysis linking smoking to specific biomarkers of periodontal inflammation and bone resorption in chronic periodontitis.

## Key findings

- Smoking increases levels of biomarkers like ICAM-1, HMGB1, and IL-17, indicating heightened inflammation.
- Smoking is associated with higher bone resorption markers such as C-terminal telopeptide and RANKL.
- Smoking reduces osteoprotegerin levels, which may contribute to increased bone loss.

## Abstract

To systematically evaluate the association between smoking and both periodontal inflammation and alveolar bone resorption in patients with chronic periodontitis.

A computerized search was conducted using databases such as PubMed, Embase, Web of Science, and China National Knowledge Infrastructure to identify studies published between January 2005 and January 2023 that examined the relationship between smoking and both periodontal inflammation and alveolar bone resorption in chronic periodontitis. A total of 1,654 articles were initially retrieved. After applying the inclusion and exclusion criteria, 13 studies were included in the final analysis, comprising a total of 1,653 patients—893 in the study group and 760 in the control group. The study group included smoker chronic periodontitis patients, and the control group included non-smoker chronic periodontitis patients. Two independent researchers screened the literature and extracted relevant data. Meta-analysis was performed using RevMan 5.3 software.

Compared with the control group, the study group showed significantly higher levels of intercellular adhesion molecule 1 (mean difference [MD] = 135.93; 95% confidence interval [CI]: 48.91, 222.95; p = 0.002), high-mobility group box 1 (MD = 6.02; 95% CI: 1.30, 10.73; p = 0.01), interleukin-17 (MD = 94.62; 95% CI: 23.34, 165.90; p = 0.009), C-terminal telopeptide of type I collagen (MD = 14.56; 95% CI: 12.03, 17.09; p < 0.00001), receptor activator of nuclear factor kappa-B ligand (MD = 1.49; 95% CI: 0.85, 2.14; p < 0.00001) and matrix metalloproteinase 9 (MD = 27.15; 95% CI: 5.94, 48.37; p = 0.01), as well as lower levels of osteoprotegerin (MD = −1.52; 95% CI: −2.98, −0.06; p = 0.04). There were no significant differences in chitinase-3-like protein 1 levels (MD = 16.40; 95% CI: −3.84, 36.64; p = 0.11), procollagen type I N-terminal propeptide levels (MD = −4.35; 95% CI: −10.71, 2.02; p = 0.18) and N-terminal telopeptide of type I collagen levels (MD = 9.03; 95% CI: −6.75, 24.80; p = 0.26) in the gingival crevicular fluid between the two groups.

Smoking exacerbates periodontal inflammation and promotes alveolar bone resorption in patients with chronic periodontitis.