Treatment of periodontal disease and control of diabetes

Treatment of periodontal disease and control of diabetes: an assessment of the evidence and need for future research.
Grossi SG.
Source

Periodontal Disease Research Center, Department of Oral Biology, School of Dental Medicine, The University at Buffalo, Buffalo, New York, USA. grossi@acsu.buffalo.edu
Abstract

Evidence points to an increased cytokine response in type 2 diabetes, especially the proinflammatory cytokines interleukin (IL)-1 beta, IL-6, and tumor necrosis factor (TNF)-alpha. Genetics, age, and, nutrition are important signals for this increased response and as reported more recently, infections and inflammation. Persistent elevation of IL-1 beta, IL-6, and TNF-alpha in the diabetic state have an effect on the liver, stimulate the release of acute-phase proteins, produce the characteristic dysregulation of lipid metabolism associated with type 2 diabetes, and have effects on pancreatic beta cells as well. In addition, TNF-alpha, a potent inhibitor of the tyrosine kinase activity of the insulin receptor, has been implicated as an etiologic factor for insulin resistance. Collectively, the evidence supports a role for cytokine elevation in the pathophysiology and metabolic abnormalities associated with diabetes. Periodontitis is an infection that is twice as prevalent in diabetic individuals compared to non-diabetics. Porphyromonas gingivalis, one of the microorganisms responsible for this infection, is able to invade endothelial cells and is a potent signal for monocyte and macrophage activation. Thus, once established in the diabetic host, this chronic infection complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications. Unlike treatment of acute infections, modalities of treatment for chronic infections are a matter of debate. Evidence indicates that mechanical removal of subgingival infection does not result in complete elimination of periodontal infection and consequently there is no effect on diabetes control measured as reduction in glycated hemoglobin. On the other hand, studies incorporating systemic antibiotics as adjuncts to mechanical debridement result in a reduction of P. gingivalis to nondetectable levels and a concomitant reduction in glycated hemoglobin, independent of the hypoglycemic effects of diabetes drugs or insulin. The evidence supports the notion that treatment of chronic periodontal infection is essential in the diabetic patient. Assessment of infection status in diabetic patients is fundamental for appropriate treatment decisions.

rdkml wrote:A good quote from author The Silent Saboteurs

"We have been monitoring our very old patients for the last 5 years and found that our very old population who are healthy with no chronic illnesses have no spirochetes. Our in house study is up to over 100 patients who have no chronic illnesses. These folks have not had diabetes, heart disease, or signs of alzheimers. They have no oral spirochetes! Why? We do not know why some persons are not infected with spirochetes but we are seeing that those who are not have no other chronic illnesses as well. These persons are remarkable"

https://www.youtube.com/user/implantdrdm#p/u/17/xnZ8KylZneM

Bet they also don't have blocked VDR receptors (Vitamin D receptors)... which if you take D3 supplement helps with above conditions including diabetes but as I've mentioned in the past isn't the solution and actually part of the problem.

Effect of Periodontitis on Insulin Resistance and the Onset of Type 2 Diabetes Mellitus in Zucker Diabetic Fatty Rats.

Journal of periodontology 2008 Jul 1; 79(7):1208-1216

Link to PubMed abstract

Watanabe K, Petro B BJ, Shlimon A AE, Unterman T TG

* Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago, IL., dagger Department of Medicine, College of Medicine, University of Illinois at Chicago., double dagger Department of Physiology and Biophysics, College of

Background: Studies indicate that an association exists between periodontitis and type 2 diabetes mellitus (T2DM) and/or obesity, with chronic inflammation hypothesized as the common denominator. The purpose of this study was to determine the causal effect of periodontitis and the concomitant impact of diet on the onset of insulin resistance (IR) and T2DM using a rat model system that simulates human obesity and T2DM. Methods: Twenty-eight, 5-week-old female Zucker diabetic fatty (ZDF, fa/fa) rats were divided into four groups of seven animals: high-fat fed-periodontitis (HF/P), high-fat fed-no periodontitis (HF/C), low-fat fed-periodontitis (LF/P), and low-fat fed-no periodontitis (LF/C). Periodontitis was induced by ligature placement. Fasting plasma insulin and glucose levels were measured, and glucose tolerance tests were performed to assess glucose homeostasis, IR, and the onset of T2DM. The level of tumor necrosis factor-alpha (TNF-alpha), leptin, triglycerides, and free fatty acids were determined in week 13 at sacrifice. Results: HF/P rats developed more severe IR compared to HF/C rats (P <0.01) and LF/P or LF/C rats (P <0.001) as measured by fasting insulin levels and homeostasis model assessment analysis. The onset of severe IR occurred approximately 3 weeks earlier in HF/P rats compared to HF/C rats. HF/P rats developed impaired (110 to 125 mg/dl) and frank fasting hyperglycemia (>125 mg/dl) 2 weeks earlier than HF/C rats. There was no difference in the severity and onset of IR and T2DM between LF/P and LF/C rats. The level of TNF-alpha was significantly higher in HF/P rats compared to HF/C rats (P <0.01). Conclusion: Periodontitis accelerated the onset of severe IR and impaired glucose homeostasis in high-fat fed ZDF rats.