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.
Highlights
Periodontal disease is one of the most common chronic diseases, with a gradually increasing prevalence worldwide[1]
Baseline plaque index (PI), probing depth (PD) mean or after treatment clinical parameters were similar between those groups which stratified by gender and smoking status
The reduction of PI or bleeding on probing (BOP) was calculated by subtracting the PI or BOP at after completing treatment from that at baseline
Summary
Periodontal disease is one of the most common chronic diseases, with a gradually increasing prevalence worldwide[1]. When ROS are generated, the TRX system is stimulated and transduces redox signals to alter the activities of antioxidant enzymes, such as superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx), to eliminate free radicals. H2O2 is scavenged by catalase, peroxiredoxin-2 (Prx2), and glutathione, by transforms it into H2O and O28 Those antioxidants are induced when oxidative stress is relieved. Salivary oxidative biomarkers, such as the total oxidant status and SOD, have been useful in evaluating the severity of periodontal disease[9]. Associations between salivary oxidative stress, the smoking status, and the effectiveness of periodontal treatment are rarely mentioned. The aim of the present study was to evaluate the associations between cigarette use and salivary oxidative stress biomarkers in subjects undergoing non-surgical periodontal therapy
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