Conflict of interest statement: In Australia, these studies were supported by the NHMRC of Australia, the Australian Dental Research Fund, and unrestricted grants from Colgate Oral Care Australia and Colgate-Palmolive USA. In Japan, they were supported by grants from the Ministry of Education, Science, Sports and Culture (13470462, 14657553, 14771219), grants for the promotion of Niigata University Research Projects, and the Fund for Scientific Promotion of Tanaka Industries Co., Ltd, Niigata Japan.
Relationship between periodontal infections and systemic disease
Article first published online: 17 AUG 2007
Clinical Microbiology and Infection
Volume 13, Issue Supplement s4, pages 3–10, October 2007
How to Cite
Seymour, G. J., Ford, P. J., Cullinan, M. P., Leishman, S. and Yamazaki, K. (2007), Relationship between periodontal infections and systemic disease. Clinical Microbiology and Infection, 13: 3–10. doi: 10.1111/j.1469-0691.2007.01798.x
- Issue published online: 17 AUG 2007
- Article first published online: 17 AUG 2007
- Molecular mimicry;
- oral disease;
- systemic disease
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.