Increased salivary levels of 8-hydroxydeoxyguanosine may be a marker for disease activity for periodontitis


Sezer U., Çiçek Y., ÇANAKÇI C. F.

Disease Markers, vol.32, no.3, pp.165-172, 2012 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 32 Issue: 3
  • Publication Date: 2012
  • Doi Number: 10.3233/dma-2011-0876
  • Journal Name: Disease Markers
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.165-172
  • Keywords: 8-hydroxydeoxyguanosine, clinical attachment level, disease activity, oxidative DNA damage, Periodontitis, saliva
  • Istanbul Gelisim University Affiliated: No

Abstract

Background: 8-hydroxydeoxyguanosine (8-OHdG) is commonly used as a marker to evaluate oxidative DNA damage in disorders including chronic inflammatory diseases such as inflammatory periodontal pathologies. In the current study we hypothesized that the level of 8-OHdG in saliva increases by the periodontal destruction severity determined by clinical parameters as clinical attachment level (CAL). Materials and methods: A cross-sectional study was conducted on a sum of 60 age gender balanced; chronic periodontitis (CP) (n=20), chronic gingivitis (CG) (n=20) and healthy (H) (n=20) individuals. Clinical periodontal parameters and salivary 8-OHdG levels were evaluated. Results: The mean 8-OHdG level in the saliva of the CP group was significantly higher than H and CG groups (p< 0.001). Statistically significant correlation was only observed between the salivary levels of 8-OHdG and age (p< 0.05), probing depth (PD) and CAL (p< 0.001) in CP group. However, when CP patients were classified according to their CAL levels (CAL≥ 3 mm (n=11) and CAL<3 mm (n=9)) statistically significant correlation was only observed between the salivary levels of 8-OHdG and CAL ≥ 3 mm patients (p< 0.001). Conclusion: We suggest that elevated salivary levels of 8-OHdG may be a marker for disease activity and it may reflect indirectly disease severity parameters such as CAL. © 2012-IOS Press and the authors. All rights reserved.