Relationship between periodontal infections and systemic disease
Relationship between periodontal infections and systemic disease
Clinical Microbiology and Infection 13 (s4), 3–10.
doi:10.1111/j.1469-0691.2007.01798.x
Oral conditions such as gingivitis and chronic periodontitis are found worldwide and are among the most prevalent microbial diseases of mankind. The cause of these common inflammatory conditions is the complex microbiota found as dental plaque, a complex microbial biofilm. Despite 3000 years of history demonstrating the influence of oral status on general health, it is only in recent decades that the association between periodontal diseases and systemic conditions such as coronary heart disease and stroke, and a higher risk of preterm low birth-weight babies, has been realised. Similarly, recognition of the threats posed by periodontal diseases to individuals with chronic diseases such as diabetes, respiratory diseases and osteoporosis is relatively recent. Despite these epidemiological associations, the mechanisms for the various relationships remain unknown.
Nevertheless, a number of hypotheses have been postulated, including common susceptibility, systemic inflammation with increased circulating cytokines and mediators, direct infection and cross-reactivity or molecular mimicry between bacterial antigens and self-antigens. With respect to the latter, cross-reactive antibodies and T-cells between self heat-shock proteins (HSPs) and Porphyromonas gingivalis GroEL have been demonstrated in the peripheral blood of patients with atherosclerosis as well as in the atherosclerotic plaques themselves. In addition, P. gingivalis infection has been shown to enhance the development and progression of atherosclerosis in apoE-deficient mice. From these data, it is clear that oral infection may represent a significant risk-factor for systemic diseases, and hence the control of oral disease is essential in the prevention and management of these systemic conditions.
• G. J. Seymour1,21Faculty of Dentistry, University of Otago, Dunedin, New Zealand2Oral Biology and Pathology, The University of Queensland, Brisbane, Queensland, Australia,
• P. J. Ford22Oral Biology and Pathology, The University of Queensland, Brisbane, Queensland, Australia,
• M. P. Cullinan1,21Faculty of Dentistry, University of Otago, Dunedin, New Zealand2Oral Biology and Pathology, The University of Queensland, Brisbane, Queensland, Australia,
• S. Leishman22Oral Biology and Pathology, The University of Queensland, Brisbane, Queensland, Australia, and
• K. Yamazaki33Laboratory of Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Niigata, Japan
• 1Faculty of Dentistry, University of Otago, Dunedin, New Zealand, 2Oral Biology and Pathology, The University of Queensland, Brisbane, Queensland, Australia and 3Laboratory of Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Niigata, Japan
Corresponding author and reprint requests: G. J. Seymour, Faculty of Dentistry, University of Otago, 310 Great King Street, PO Box 647, Dunedin 9054, New Zealand
E-mail: gregory.seymour@dent.otago.ac.nz
