William Murray Thomson1, Jiaxu Zeng2, Jonathan M Broadbent1, Lyndie A Foster Page1, Idan Shalev3, Terrie E Moffitt4,5,6, Avshalom Caspi4,5,6, Sheila M Williams2, Antony W Braithwaite7, Stephen P Robertson8, Richie Poulton9. 1. Sir John Walsh Research Institute, School of Dentistry, The University of Otago, Dunedin, New Zealand. 2. Department of Preventive and Social Medicine, Dunedin School of Medicine, The University of Otago, Dunedin, New Zealand. 3. Department of Biobehavioral Health, Pennsylvania State University, University Park, PA, USA. 4. Department of Psychology and Neuroscience, Duke University, Durham, NC, USA. 5. Department of Psychiatry and Behavioral Sciences, Duke University, Durham, NC, USA. 6. Social, Genetic, and Developmental Psychiatry Centre, Institute of Psychiatry, King's College, London, UK. 7. Department of Pathology, School of Medicine, University of Otago, Dunedin, New Zealand. 8. Department of Paediatrics and Child Health, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. 9. Dunedin Multidisciplinary Health and Development Research Unit, Department of Psychology, University of Otago, Dunedin, New Zealand.
Abstract
AIM: The aim of the study was to examine the association between telomere erosion and periodontitis in a long-standing prospective cohort study of New Zealand adults. Specific hypotheses tested were as follows: (i) that exposure to periodontitis at ages 26 and 38 was associated with accelerated leucocyte telomere erosion and (ii) that accelerated leucocyte telomere erosion was associated with higher rates of periodontitis by ages 26 and 38. MATERIALS AND METHODS: Periodontal attachment loss data were collected at ages 26 and 38. Blood samples taken at the same ages were analysed to obtain estimates of leucocyte telomere length and erosion over a 12-year period. RESULTS: Overall, the mean telomere length was reduced by 0.15 T/S ratio (adjusted) from age 26 to 38 among the 661 participants reported on here. During the same period, the mean attachment loss increased by 10%, after adjusting for sex, socio-economic status and smoking. Regression models showed that attachment loss did not predict telomere length, and that telomere erosion did not predict attachment loss. CONCLUSIONS: Although both periodontitis and telomere length are age-dependent, they do not appear to be linked, suggesting that determination of leucocyte telomere length may not be a promising clinical approach at this age for identifying people who are at risk for periodontitis.
AIM: The aim of the study was to examine the association between telomere erosion and periodontitis in a long-standing prospective cohort study of New Zealand adults. Specific hypotheses tested were as follows: (i) that exposure to periodontitis at ages 26 and 38 was associated with accelerated leucocyte telomere erosion and (ii) that accelerated leucocyte telomere erosion was associated with higher rates of periodontitis by ages 26 and 38. MATERIALS AND METHODS: Periodontal attachment loss data were collected at ages 26 and 38. Blood samples taken at the same ages were analysed to obtain estimates of leucocyte telomere length and erosion over a 12-year period. RESULTS: Overall, the mean telomere length was reduced by 0.15 T/S ratio (adjusted) from age 26 to 38 among the 661 participants reported on here. During the same period, the mean attachment loss increased by 10%, after adjusting for sex, socio-economic status and smoking. Regression models showed that attachment loss did not predict telomere length, and that telomere erosion did not predict attachment loss. CONCLUSIONS: Although both periodontitis and telomere length are age-dependent, they do not appear to be linked, suggesting that determination of leucocyte telomere length may not be a promising clinical approach at this age for identifying people who are at risk for periodontitis.
Authors: W Murray Thomson; Gary D Slade; James D Beck; John R Elter; A John Spencer; Jane M Chalmers Journal: J Clin Periodontol Date: 2004-02 Impact factor: 8.728
Authors: Melissa Bateson; Abraham Aviv; Laila Bendix; Athanase Benetos; Yoav Ben-Shlomo; Stig E Bojesen; Cyrus Cooper; Rachel Cooper; Ian J Deary; Sara Hägg; Sarah E Harris; Jeremy D Kark; Florian Kronenberg; Diana Kuh; Carlos Labat; Carmen M Martin-Ruiz; Craig Meyer; Børge G Nordestgaard; Brenda W J H Penninx; Gillian V Pepper; Dóra Révész; M Abdullah Said; John M Starr; Holly Syddall; William Murray Thomson; Pim van der Harst; Mary Whooley; Thomas von Zglinicki; Peter Willeit; Yiqiang Zhan; Daniel Nettle Journal: R Soc Open Sci Date: 2019-06-05 Impact factor: 2.963