Association between nanobacteria and periodontal disease.

Publications Book. 2002;206A. Response We have proposed several potential explanations for the association between oral health and cardiovascular disease, and the activation or release of inflammatory mediators caused by bacteria is one.1–3 However, different measures of oral health, such as the number of remaining teeth, recent tooth loss, and periodontal disease that could reflect different pathways, showed different relationships with 3 the following atherosclerotic diseases: coronary heart disease, stroke, and peripheral arterial disease.1–3 This suggests that the association between oral health and cardiovascular diseases is complex. Antibiotics consistently reduced atherosclerotic vascular disease in four of five small clinical trials with low power, but larger trials testing the relationship between antibiotics and coronary heart disease gave equivocal results.4 A possible explanation consistent with these data may be that infection plays a larger role in atherosclerotic disease such as peripheral arterial disease compared with coronary heart disease, where other factors such as plaque stability may be more important. We therefore agree with Çiftçioğlu et al that 300 species of known bacteria with populations of several hundred billion in the human oral cavity, and even higher among periodontal disease patients, could possibly contribute to development of peripheral arterial disease in particular. Nanobacteria (NB) might be associated with tissue calcifications and hence could increase risk of coronary atherosclerosis. Although NB has been detected in calcified carotid arteries, the evidence to support a causal association with cardiovascular diseases is still limited. Moreover, there is no evidence that NB is associated with periodontal diseases, even though NB has been identified in tooth pulp stone and saliva, as well as in dental plaque.5 We agree that it is important to evaluate specific biological factors that could contribute to these associations, including common genetic factors, microbial factors, cytokines, and other inflammatory mediators. Microorganisms, including bacterial species known to be associated with periodontal disease, are definitely worthy of further study in this context. The qualitative or quantitative differences of NB in specimens from the oral cavity (ie, saliva, dental plaque, or gingival crevicular fluid) between subjects with and without periodontal disease must be documented while considering the role of NB in the relationship between periodontal disease and peripheral artery disease, and we agree that this is worthy of further study. Hsin-Chia Hung, DDS, DrPH Department of Epidemiology Harvard School of Public Health Department of Oral Health Policy and Epidemiology Harvard School of Dental Medicine College of Dental Medicine Boston, Mass Kaohsiung Medical University Taiwan 1 by gest on Jauary 5, 2018 http://ciajournals.org/ D ow nladed from Walter Willett, MD, DrPH Departments of Epidemiology and Nutrition Harvard School of Public Health Channing Laboratory Department of Medicine Harvard Medical School and Brigham and Women’s Hospital Boston, Mass Anwar Merchant, DMD, DrPH Department of Epidemiology Harvard School of Public Health Department of Oral Health Policy and Epidemiology Harvard School of Dental Medicine Boston, Mass Bernard A. Rosner, PhD Department of Biostatistics Harvard School of Public Health Channing Laboratory, Department of Medicine Harvard Medical School and Brigham and Women’s Hospital Boston, Mass Alberto Ascherio, MD, Dr PH Departments of Epidemiology and Nutrition Harvard School of Public Health Boston, Mass Kaumudi J. Joshipura, ScD Department of Epidemiology Harvard School of Public Health Department of Oral Health Policy and Epidemiology Harvard School of Dental Medicine Boston, Mass [email protected] 1. Joshipura KJ, Hung HC, Rimm EB, Willett WC, et al. Periodontal disease, tooth loss, and incidence of ischemic stroke. Stroke. 2003;34: 47–52. 2. Joshipura KJ, Rimm EB, Douglass CW, et al. Poor oral health and coronary heart disease. J Dent Res. 1996;75:1631–1636. 3. Hung HC, Willett W, Merchant A, et al. Oral health and peripheral arterial disease. Circulation. 2003;107:1152–1157. 4. Grayston JT. Antibiotic treatment of atherosclerotic cardiovascular disease. Circulation. 2003;107:1228–1230. 5. Cisar JO, Xu DQ, Thompson J, et al. An alternative interpretation of nanobacteria-induced biomineralization. Proc Natl Acad Sci U S A. 2000; 97:11511–11515. 2 Correspondence by gest on Jauary 5, 2018 http://ciajournals.org/ D ow nladed from Neva Çiftçioglu, David S. McKay and E. Olavi Kajander Association Between Nanobacteria and Periodontal Disease Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2003 American Heart Association, Inc. 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