Original ContributionOxidative stress, chronic inflammation, and telomere length in patients with periodontitis
Section snippets
Study groups
In a case–control design, a total of 563 participants were recruited among subjects referred to the UCL Eastman Dental Institute in London between 2002 and 2006. For all participants a complete medical history was obtained via interview (including smoking history and current or previous use of medications). Subjects with any medical disorder, including cancer, type 2 diabetes, hypertension, and major cardiovascular/endocrine diseases, were excluded from the study. All subjects currently taking
Results
The characteristics of the study population are summarized in Table 1. Periodontal patients had higher serum levels of CRP (P < 0.001) and leukocyte counts (P < 0.001) compared to controls. Further, greater total cholesterol (P = 0.003) and LDL cholesterol (P < 0.001) levels, as well as lower HDL cholesterol (P < 0.001), were observed. Cases exhibited higher levels of reactive oxygen metabolites (P < 0.001) and lower antioxidant potential (P < 0.001) as assessed by D-ROM and BAP tests, respectively (Table 1
Discussion
This is the first report to describe an association between shorter LTL and periodontitis. Patients with periodontitis presented shorter LTL, higher systemic inflammation, and higher oxidative stress compared to controls. Furthermore, LTL was negatively correlated with total levels of reactive oxidative metabolites detected by D-ROM test and severity of periodontitis. These associations were independent of age, gender, ethnicity, and smoking differences. In subgroup analyses of periodontal
Conclusions
In conclusion our data suggest that chronic inflammation could be the main driver of shorter LTL in patients with periodontitis and that the local and systemic effects of oxidative stress could be considered the main predictor of the LTL attrition. Moreover, the evidence of shorter LTL detected in individuals with chronic periodontitis could provide a possible biological explanation for the reported higher mortality rate in these patients compared to the general population. Further research and
Acknowledgments
This work was undertaken at UCLH/UCL, which received a proportion of funding from the Department of Health's NIHR Biomedical Research Centres funding scheme. S.E.H. and K.D.S. are funded by the British Heart Foundation (RG2008/08 and FS/06/053). F.D. holds a Clinical Senior Lectureship Award supported by the UK Clinical Research Collaboration. We thank Prof. Eugenio Iorio for his assistance with the laboratory oxidative stress analyses.
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2021, Environmental ResearchCitation Excerpt :Some mechanisms, including oxidative stress and systemic inflammation, have been postulated to underlie the relationship of exposure to PAHs and molecular changes (DNA and proteins). Both increased inflammation and oxidative stress have been suggested to play a main role in the shorting of the TL (Houben et al., 2008; Masi et al., 2011). PAHs metabolites are detoxified through P450 enzymes such as glutathione S-transferase M1 (GSTM1) (Seidegård and Ekström, 1997), but their high and continuous exposure has the potential to generate oxygen radicals, which, in turn, could result in the formation of 8-hydro-20-deoxyguanosine (8-OHdG) and DNA damage (Asami et al., 1997).
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These authors equally contributed to this work.