title: New evidence of premature oxidative DNA damage: mitochondrial DNA deletion in gingival tissue of patients with periodontitis.
abstract: BACKGROUND
  Overproduction of reactive oxygen species (ROS) causes increased oxidative stress in gingival tissue. It has been generally accepted that increased oxidative stress might contribute to additional damage of lipids, proteins, and DNA molecules. The mitochondrial DNA (mtDNA) mutation is a superb biomarker of oxidative damage. The aim of the present study was to investigate the mtDNA deletions in the gingival tissue of patients with periodontitis and to explain the correlations between mtDNA deletion in gingival tissue and clinical parameters of periodontitis and age.
  
  
  METHODS
  Gingival tissue and blood samples were collected from 30 patients with chronic periodontitis (CP group) and 30 healthy control subjects (H group). To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level, and probing depth were measured. Using the polymerase chain reaction (PCR) method, we examined the 7.4- and 5-kbp mtDNA deletions in tissue and blood samples. Three different pairs of PCR primers were used in this study.
  
  
  RESULTS
  In this study, we did not detect any deletions in blood DNA samples in either the CP or H group. Also, the 7.4-kbp mtDNA deletion was not detected in gingival tissues of subjects. However, the 5-kbp mtDNA deletion was detected in 24 of the 30 subjects (80%) in the CP group and was not detected in the H group (0%). Significant correlations were found between the occurrence of the 5-kbp mtDNA deletion and all clinical parameters (P <0.01). A similar correlation was found between the occurrence of the 5-kbp mtDNA deletion and age (P <0.05).
  
  
  CONCLUSIONS
  The overproduction of ROS by activated polymorphonuclear leukocytes in chronic inflammation may lead to premature oxidative damage of the mtDNA. In this study, the occurrence of the 5-kbp mtDNA deletion in 24 periodontitis subjects may be evidence of premature oxidative DNA damage.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, Ataturk University, Erzurum, Turkey. cfcanakci@yahoo.com
authors.forename: Cenk Fatih
authors.initials: CF
authors.lastname: Canakçi
authors.forename: Abdulgani
authors.initials: A
authors.lastname: Tatar
authors.forename: Varol
authors.initials: V
authors.lastname: Canakçi
authors.forename: Yasin
authors.initials: Y
authors.lastname: Cicek
authors.forename: Sitki
authors.initials: S
authors.lastname: Oztas
authors.forename: Recep
authors.initials: R
authors.lastname: Orbak
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D016022:Case-Control Studies; D002908:Chronic Disease; D004249:DNA Damage; D004272:DNA, Mitochondrial / Q000235:genetics*; D005260:Female; D005881:Gingiva / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism; D018384:Oxidative Stress / Q000235:genetics*; D010512:Periodontal Index; D010518:Periodontitis / Q000097:blood / Q000235:genetics* / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism; D017384:Sequence Deletion; D018709:Statistics, Nonparametric
chemical_list: D004272:DNA, Mitochondrial; D017382:Reactive Oxygen Species