In this section of our web site we hope to increase your knowledge and understanding of some of the ways your general health and oral health are intimately connected.

Firstly, it is important to understand that your body is a complex machine made of complex systems that all interrelate. No part of your body operates like an island. If you have systemic health conditions that plague one system, there is a good chance that this will have a role in creating an imbalance in other systems. This is the case with your oral health too!

If you have diabetes, gastro-intestinal problems, smoke, take medication for high-blood pressure or suffer from immune system deficiencies, we will commonly see evidence of that in your mouth. The converse is true as well...... if you have poor oral health, it can greatly effect your general health.

Recently, much attention has been paid to the discovery that there is a link between gum disease and heart disease. There is also a demonstrated connection between poorly controlled Type II diabetes and gum disease. We know that there is a link between gum disease and pre-mature births as well. The mechanisms of these connections are not clear, but the list of systemic "links" is growing every year.

In the last half-century, dentists and physicians have thought that gum disease was a focused infection and that, as such, it was NOT a factor in your general health. More recent evidence, however, has indicated that patients with gum disease (periodontitis) have increased levels of blood components that are associated with the whole body's immune response.

Please refer to the sub-categories on the left side of this page for information of a more specific nature. We hope that whether you are a layperson or another healthcare provider, this part of our web site will help you to help yourself and others live longer, healthier lives.

If you are a health professional and want more information, you may be interested to know.....

People with chronic periodontal disease have increased serum levels of CRP, hyper-fibrinogenemia, moderate leukocytosis, as well as increased serum levels of IL-1 and IL-6 when compared with unaffected control populations (Kweider et al., 1993; Ebersole et al., 1997; Loos et al., 2000; Slade et al., 2000, 2003; Hutter et al., 2001). Furthermore, in periodontitis patients, elevated serum CRP is associated with high levels of infection with periodontal pathogens (Noack et al., 2001).

Support for the hypothesis that periodontitis-driven inflammatory responses are of significance for otherwise healthy individuals is at least three-fold: (i) Periodontitis has been associated with increased odds of cardiovascular events (Genco et al., 2002; Joshipura et al., 2003), of delivering pre-term low-birthweight babies (Offenbacher et al., 1996), and of having sub-optimal control of type II diabetes (Grossi and Genco, 1998); (ii) the strength of association between periodontitis or other chronic infections and cardiovascular events seems to be of similar magnitude (Danesh, 1999); and (iii) experimental pre-clinical models have indicated that chronic infection with periodontal pathogens leads to thickening of the carotid intima (Li et al., 2002) and to fetal growth restriction (Collins et al., 1994).

Independently of the underlying mechanism(s), systemic inflammation seems to be central for explaining the nature of the link between chronic infections and atherosclerosis (Ridker et al., 1997; Danesh, 1999; Ross, 1999; Libby et al., 2002; Pearson et al., 2003). Within this context, CRP represents an emerging and reliable marker of the acute phase response to infectious burdens and/or inflammation. As a consequence of its kinetics, it best describes the inflammatory status of the individual (de Maat and Kluft, 2001). CRP hepatic production is usually elicited by an inflammatory stimulus and mediated through a complex network of cytokines (mainly IL-6) (Ablij and Meinders, 2002). CRP has also assumed a significant role as a predictor for future coronary events in healthy populations (Blake and Ridker, 2002).