Periodontal Health and Total Antioxidant Capacity for Jordanian Smokers at Dental Teaching Clinic

TL;DR

This study shows that smoking worsens periodontitis by increasing oxidative stress and damaging liver and kidney function in Jordanian patients.

Contribution

The study is the first to simultaneously assess systemic antioxidant capacity, organ function, and hematological indices in smokers with periodontitis.

Findings

Smokers with periodontitis had higher oxidative stress markers (TBARS) in serum and saliva.

Smokers showed reduced antioxidant enzyme levels (GSH, GPX, SOD, TAOA) and elevated liver enzymes (ALT, AST).

Smoking was linked to higher BUN and creatinine levels, indicating kidney dysfunction and systemic inflammation.

Abstract

Background: Smoking exacerbates oxidative stress and inflammation, both of which contribute to periodontitis. However, few studies have simultaneously assessed/systemic antioxidant capacity, organ function, and hematological indices in smokers with periodontitis. This study aimed to examine antioxidant enzymes, hepatic and renal function, and hematological profiles, offering a comprehensive perspective on smoking-related periodontal damage.

Methods: A total of 47 participants were divided into three groups: smokers with periodontitis (n = 18), nonsmokers with periodontitis (n = 17), and healthy nonsmoking controls without periodontitis (n = 12). Salivary and blood samples were collected, and oxidative stress biomarkers, including thiobarbituric acid reactive substances (TBARS) and antioxidant enzymes, such as glutathione (GSH), GSH peroxidase (GPX), superoxide dismutase (SOD), and total antioxidant activity (TAOA), were measured. Additionally, liver function (ALT, AST, GGT, Total bilirubin), kidney function (BUN, creatinine), and hematological parameters were assessed and compared among the three groups.

Results: Smokers with periodontitis illustrate significant elevation in TBARS levels in both serum and saliva (p  < 0.05), indicating increased oxidative stress compared to nonsmokers and controls. Serum antioxidant enzyme levels (GSH, GPX, SOD, and TAOA) were significantly decreased in the smokers with periodontitis groups (p  < 0.05). ALT and AST levels were significantly elevated in the smoking and periodontitis group (44.45 ± 19.64 and 28.27 ± 7.77 U/L), respectively, suggesting significant liver impairment among smokers (p  < 0.05). Kidney function was also affected; the BUN and creatinine levels were noticeably higher in smokers compared to the healthy controls and nonsmokers (p  < 0.05). Hematological findings exhibit a significant increase in WBCs among smokers-periodontitis patients, indicating an increase in systemic inflammation.

Conclusion: The imbalance between oxidative stress and antioxidant capacity may play a role in the pathogenesis of periodontal disease. Smoking is highly linked to oxidative stress-antioxidant (redox) imbalance, which exacerbates the impact of periodontitis. This leads to significant oxidative damage, noticeable liver and kidney dysfunction, and elevated systemic inflammation.

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