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Oxidative Stress and Periodontal Disease in Down Syndrome

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Studies on Periodontal Disease

Abstract

Down syndrome (DS) is caused by a unique metabolic imbalance induced by overexpression of genes on chromosome 21. The enzyme superoxide dismutase (SOD) is responsible for the regulation of reactive oxygen species (ROS) homeostasis. Increased levels or activity of SOD may contribute to neuronal death and disease progression in DS and precede the signature manifestations of the disease by decades. Individuals with DS have a higher prevalence and severity of periodontal disease, which cannot be explained by poor oral hygiene alone and is related to changes in the immune response. Using electron spin resonance (ESR) and spin trapping, we have obtained clear and direct evidence that ROS are generated in the media of cultured gingival cells from DS patients.

A number of findings in the past decade have prompted interest in the diagnostic use of saliva biomarkers. The salivary levels of oxidative stress biomarkers such as 8-hydroxy-2′-deoxyguanosine (8-OHdG) have been shown to be significantly higher in DS patients than in control subjects, suggesting that high oxidative stress may lead to some of the clinical features of DS, especially rapidly progressive periodontal disease associated with premature aging. In the future, analysis of biomarkers such as 8-OHdG in saliva samples could be useful for the assessment and management of periodontal disease with oxidative stress in DS patients.

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Acknowledgments

This research was supported by a Grant-in-Aid for Scientific Research (no. 18592149 to M.L., no. 19592371 to T.K. and M.L., no. 23593049 to T.K., no. 23660047 to M.L.) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.

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Correspondence to Tomoko Komatsu or Masaichi-Chang-Il Lee .

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Komatsu, T., Lee, MCI. (2014). Oxidative Stress and Periodontal Disease in Down Syndrome. In: Ekuni, D., Battino, M., Tomofuji, T., Putnins, E. (eds) Studies on Periodontal Disease. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4614-9557-4_15

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