Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease

Chang Yu Lee, Chia Huang Chang, Nai Chia Teng, Hung Ming Chang, Wan Ting Huang, Yung Kai Huang

Research output: Contribution to journalArticle

Abstract

Background: 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. Methods: In 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. Results: Subjects 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. Conclusions: The 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.

Original languageEnglish
Article number201
JournalBMC Oral Health
Volume19
Issue number1
DOIs
Publication statusPublished - Aug 30 2019

Fingerprint

Genetic Association Studies
Periodontal Diseases
Catalase
Superoxide Dismutase
Genotype
Root Planing
Genetic Polymorphisms
Oxidation-Reduction
Hemorrhage
Phenotype
Periodontitis
Therapeutics
Saliva
Alcohol Drinking
Antioxidants
Smoking

Keywords

  • Biomarker
  • Genetic polymorphism
  • Oxidative stress
  • Phenotype

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease. / Lee, Chang Yu; Chang, Chia Huang; Teng, Nai Chia; Chang, Hung Ming; Huang, Wan Ting; Huang, Yung Kai.

In: BMC Oral Health, Vol. 19, No. 1, 201, 30.08.2019.

Research output: Contribution to journalArticle

@article{25a78d432dca4b778c3b704ee2ccf910,
title = "Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease",
abstract = "Background: 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. Methods: In 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. Results: Subjects 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. Conclusions: The 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.",
keywords = "Biomarker, Genetic polymorphism, Oxidative stress, Phenotype",
author = "Lee, {Chang Yu} and Chang, {Chia Huang} and Teng, {Nai Chia} and Chang, {Hung Ming} and Huang, {Wan Ting} and Huang, {Yung Kai}",
year = "2019",
month = "8",
day = "30",
doi = "10.1186/s12903-019-0877-3",
language = "English",
volume = "19",
journal = "BMC Oral Health",
issn = "1472-6831",
publisher = "BioMed Central",
number = "1",

}

TY - JOUR

T1 - Associations between the phenotype and genotype of MnSOD and catalase in periodontal disease

AU - Lee, Chang Yu

AU - Chang, Chia Huang

AU - Teng, Nai Chia

AU - Chang, Hung Ming

AU - Huang, Wan Ting

AU - Huang, Yung Kai

PY - 2019/8/30

Y1 - 2019/8/30

N2 - Background: 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. Methods: In 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. Results: Subjects 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. Conclusions: The 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.

AB - Background: 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. Methods: In 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. Results: Subjects 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. Conclusions: The 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.

KW - Biomarker

KW - Genetic polymorphism

KW - Oxidative stress

KW - Phenotype

UR - http://www.scopus.com/inward/record.url?scp=85071773292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85071773292&partnerID=8YFLogxK

U2 - 10.1186/s12903-019-0877-3

DO - 10.1186/s12903-019-0877-3

M3 - Article

C2 - 31470840

AN - SCOPUS:85071773292

VL - 19

JO - BMC Oral Health

JF - BMC Oral Health

SN - 1472-6831

IS - 1

M1 - 201

ER -