Cigarette Smoking Aggravates the Activity of Periodontal Disease by Disrupting Redox Homeostasis- An Observational Study

Abstract

The aim of this study was to evaluate the associations between cigarette use and five salivary oxidative stress biomarkers, copper-zinc superoxide dismutase (Cu/Zn SOD), manganese superoxide dismutase (MnSOD), catalase, thioredoxin-1 (TRX1), and peroxiredoxin-2 (PRX2), to assess the effectiveness of non-surgical periodontal therapy. Materials and Methods: This is an observational study,167 patients diagnosed with periodontitis were recruited. Both saliva samples and clinical measurements (plaque index (PI), bleeding on probing (BOP), and pocket depth (PD)) were taken at baseline and after completing non-surgical periodontal therapy. The Levels of salivary biomarkers were determined using a MILLIPLEX® MAP Human Oxidative Stress Magnetic Bead Panel kit. The overall reductions in PI and BOP were 31.56% and 42.16%, respectively. BOP reduction after treatment in female or male non-smokers was significantly higher than in male former smokers (p < 0.05). After completing non-surgical periodontal therapy, Cu/ZnSOD, MnSOD, catalase, and Prx2 significantly decreased. There was a significant interaction between smoking status and ΔCu/ZnSOD on PI and a significant interaction between smoking status and ΔCatalase on BOP. Conclusions: Cigarette smoking interferes with redox homeostasis in the body, alters antioxidants levels, and influences the periodontal disease activity.

Longitudinal assessment of clinical and radiographic periimplant status around narrow and regular diameter implants placed in cigarette‐smokers and nonsmokers

“…There is growing indication that smoking tobacco is a well-recognized component cause of both periodontal and periimplant inflammatory disorders and is the second well-known of the modifiable risk factors after microbial dental plaque. [1][2][3] It is indicated that tobacco smoking is associated with a substantial risk for soft tissue destruction and alveolar bone loss, depending mainly on the dosage, frequency, and level of disease severity. 4 Smoking has been shown to impair several features of the innate and adaptive host immune responses as exhaustively documented in numerous laboratory-based studies of tobaccorelated soft tissue destruction.…”

“…There is growing indication that smoking tobacco is a well‐recognized component cause of both periodontal and periimplant inflammatory disorders and is the second well‐known of the modifiable risk factors after microbial dental plaque . It is indicated that tobacco smoking is associated with a substantial risk for soft tissue destruction and alveolar bone loss, depending mainly on the dosage, frequency, and level of disease severity .…”

Soft tissue status and crestal bone loss around conventionally‐loaded dental implants placed in cigarette‐ and waterpipe (narghile) smokers: 8‐years' follow‐up results

“…Studies [1][2][3][4] have shown that tobacco-smoking is a prospect of periodontal and peri-implant diseases, such as periodontitis and periimplantitis, respectively. Furthermore, outcomes of oral surgical interventions are undermined in tobacco smoking users compared to nonsmokers.…”

Periodontitis is associated with an increased risk for proximal colorectal neoplasms

“…Molecular studies have demonstrated a definitive link between smoking and colorectal carcinogenesis such as MSI, CIMP, and a serrated pathway, which occur most often in the proximal colon 48,49 . Meanwhile, smoking increases the abundance of periodontal pathogen including Fusobacterium and Bacteroides , as well as the severity of periodontitis 28,51,52 , which might explain another mechanism that smoking affects the development of proximal CRNs via periodontal pathogen related gut dysbiosis 26,47 .…”