Periodontal disease and Dawei Chen

Trends of Diabetes up to 2010 in the U.S.

Diabetes overview As of 2014: Total:29.1 million people or 9.3% of the population have diabetes. Diagnosed:21.0 million people. Undiagnosed:8.1 million people (27.8% of people with diabetes are undiagnosed). In Connecticut: the rate (of 100) of diagnosed diabetes has increased from 4.8 to 8.2 According to the CDC, 86 million people (1 out of three adults) have prediabetes

What is Diabetes? A disease associated with impaired glucose metabolism which can lead to abnormal blood glucose levels and symptoms such as polydipsia, polyuria, and polyphagia. Divided into two types: Type I- insulin-dependent; autoimmune destruction of beta cells in the pancreas, preventing insulin production and elevated blood and urine glucose levels. Type II- noninsulin-dependent; relatively lower insulin levels and insulin resistance.

Complications Associated with Diabetes Nephropathy- decreased sensation, Encephalopathy- decline and cognition leading to increased risk of dementia. Nephropathy Retinopathy- poor blood flow in the retina leading to vision loss Vascular disease Coronary artery disease leading to myocardial infarctions And recently…..

Periodontal disease Since the early 90s, there has been extensive research on possible ways of attenuating glycemic control by periodontal treatment. It has been discovered that both diabetes and periodontal disease run parallel with each other. The appearance or existence of one tends to promote the other Also, there is a possibility that proper management of one may be beneficial in the treatment of the other

What is Periodontal Disease? Characterized by invasion of biofilms (otherwise known as plaque) around the periodontal ligament leading to infection. Two stages: Gingivitis- treatable and reversible. Periodontal disease- destruction of periodontal ligament and pocket formation; irreversible.

Gingivitis Inflammatory response from the presence of the oral pathogens. Neutrophils can phagocytize the bacteria and cause lysis. The complement system can also lead to increase in antibody production to increase efficacy of pathogen removal In this case, gingivitis can be resolved by the inflammatory response and the infection will not be propagated to other sites around the area.

Periodontal Infections Mucosal pathogens can be recognized by innate dendritic cells of the mucosa which can lead to antigen presenting and processing, ultimately leading to cytokine release and T cell differentiation This local activation can also lead to alveolar bone resorption Jeffrey L. Ebersole, Dolphus R. Dawson, and Octavio A. Gonzaléz

A Tale of Two Diseases What is the Connection? Patients with both diseases show increased levels of cytokines such as IL-1 and TNF-alpha In Diabetes, there are two major proposed mechanisms Polyol Pathway AGE (Advanced Glycosylation End) production

Polyol Pathway Access glucose in the bloodstream leads to increase production of sorbtiol, which requires NADPH to breakdown into fructose. NAD+ depletion due to this access usage can cause a glutathione deficiency and lead to oxidative stress from ROS buildup

AGE production Elevated glucose can react with proteins, lipids and nucleic acids to produce AGEs. Can lead to numerous complications.

AGE production RAGEs, or AGE receptors, have been found in phagocytic cells, attenuating their function and causing larger buildup of pathogens in periodontal disease. RAGEs were also found in fibroblasts, which directly contribute to collagen production, i.e. periodontal tissue. Increases in collagenases and further periodontium degradation.