Type 2 diabetes mellitus (diabetes) is a growing public health problem. Chronic infections have been suggested as a potential risk factor for diabetes and there is a known association between periodontal infections and diabetes. Although it is generally believed that periodontal infections are a consequence of existing diabetes, there is growing support for the hypothesis that periodontal infections might contribute tq diabetogenesis, although research on this topic is limited. The evidence supporting the role of periodontal infections as a risk factor for a number of other systemic diseases (i.e., cardiovascular disease and pregnancy outcomes) continues to grow and further supports the rationale for. the current research proposal. Furthermore, recent reports implicate inflammation as a strong risk factor for incident diabetes. Since the inflammatory response is a central aspect of periodontal pathology, it is of interest to explore whether or not inflammation might mediate the association between periodontal disease and diabetes, or simply be an underlying contributor to both disease processes. The current proposal aims to test the hypothesis that periodontal infection is an etiologic factor in the development of diabetes. Baseline exposure to known periodontal pathogens will be assessed to see if elevated infectious exposure is associated with accelerated progression of fasting glucose and insulin levels. This will be achieved using a longitudinal cohort design among n=300 participants in a population of men and women aged 25 - 55 years at baseline enrollment. The proposed design will carefully control for potential confounders such as baseline levels of fasting glucose, insulin, lipids, obesity, diet, age, smoking, ethnicity and gender.
The proposed research can advance the-scientific knowledge regarding the well-known association between periodontal infection and diabetes through its provision of a powerful study design appropriate for addressing temporarily (i.e., do periodontal infections precede the onset of diabetes pathology), hi addition, data on the independent contribution of infections to the underlying pathology of diabetes can be addressed for the first time using a population based, chronic infection model
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