Abstract

BackgroundPeriodontal disease is an inflammatory disease in which pathogenic infections trigger a series of inflammatory responses and redox regulation. The hypothesis of this study was that a host’s redox regulation, as modified by genetic polymorphisms, may affect periodontal disease activities (including the plaque index (PlI), bleeding on probing (BOP), and pocket depth (PD)) during periodontal therapy.MethodsIn total, 175 patients diagnosed with periodontitis were recruited from the Department of Periodontology, Taipei Medical University Hospital. Both saliva samples and clinical measurements (PlI, BOP, and PD) were taken at the baseline and at 1 month after completing treatment. Salivary manganese superoxide dismutase (MnSOD) and catalase, and corresponding genetic polymorphisms (MnSOD, T47C, rs4880 and Catalase, C-262 T, rs1001179) were determined. The extent of change (Δ) of MnSOD or catalase was calculated by subtracting the concentration after completing treatment from that at the baseline.ResultsSubjects who carried the Catalase CC genotype had significantly higher salivary MnSOD or catalase levels. The MnSOD genotype had a significant effect on the percentage of PDs of 4~9 mm (p = 0.02), and salivary ΔMnSOD had a significant effect on the PlI (p = 0.03). The Catalase genotype had a significant effect on the PlI (p = 0.01~0.04), but the effect was not found for the mean PlI or PD. There was a significant interaction between the MnSOD genotype and salivary ΔMnSOD on PDs of 4~9 mm. After adjusting for gender, years of schooling, smoking status, and alcohol consumption, subjects with ΔMnSOD of < 0 μg/ml or Δcatalase of < 0 μg/ml had significantly higher 5.58- or 5.17-fold responses to scaling and root planing treatment.ConclusionsThe MnSOD T47C genotype interferes with the phenotype of salivary antioxidant level, alters MnSOD levels, and influences the PD recovery. MnSOD and catalase gene polymorphism associated with phenotype expression and susceptibility in periodontal root planing treatment responses.

Highlights

  • Periodontitis is an inflammatory disease that is initiated by the accumulation of plaque biofilm and its products, with subsequent gingival bleeding, alveolar bone resorption, and periodontal pocket formation [1]

  • There were no significant differences in percentages of the baseline/after treatment for the plaque index (PlI), bleeding on probing (BOP), or pocket depth (PD) in groups stratified be sex, smoking status, and alcohol consumption (Additional file 1: Table S1)

  • After adjusting for gender, smoking status, and alcohol consumption, baseline percentages of BOP and PD of 4~9 mm were significantly associated with years of schooling

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Summary

Introduction

Periodontitis is an inflammatory disease that is initiated by the accumulation of plaque biofilm and its products, with subsequent gingival bleeding, alveolar bone resorption, and periodontal pocket formation [1]. In the decomposition of H2O2, hydroxyl radicals (OH) formed by splitting O-O bonds can cause DNA and protein damage [8,9,10]. Salivary antioxidant activities, such as the total oxidant status, catalase, and SOD, have been useful biomarkers for evaluating the severity of periodontal disease and treatment effectiveness [11, 12]. Periodontal disease is an inflammatory disease in which pathogenic infections trigger a series of inflammatory responses and redox regulation. The hypothesis of this study was that a host’s redox regulation, as modified by genetic polymorphisms, may affect periodontal disease activities (including the plaque index (PlI), bleeding on probing (BOP), and pocket depth (PD)) during periodontal therapy

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