According to a study published this August 9th, periodontal inflammation in rodents with diabetes is derived from caries and not from periodontal disease.
Through fluoride administration, Yutaka Nakahara from the Setsunan University in Osaka, Japan, and colleagues applied to diabetic animal models prevented carious inflammation and yet confirmed the presence of periodontal disease. Tap water and tap water with fluoride was administered to F344 rats injected with a type 1 diabetes model and db/db mice or type 2 diabetes model.
The study showed the cariostatic effect of fluoride in the diabetic animal models, which not only prevented dental caries but also diminished periodontal inflammation. However, the research also demonstrated the lack of Periodontitis in the periodontal tissue that surrounds the normal molars with fluoride treatment; on the other hand, the teeth that were enveloped with persistent periodontitis, showed clearly the caries-forming process.
These results, prove that although long-term hyperglycemia naturally induces dental caries, t does not cause periodontal disease in neither type 2 or type 1 diabetic rodents. Nevertheless, diabetes does cause a shift in the oral microbiome that fosters periodontitis.
In another study -led by University of Pennsylvania–, the research showed how this shift in the oral microbiome -caused by diabetes– makes for a more inflammatory environment and promotes bone loss, which are typical characteristics of periodontitis gum disease. The study was published in the journal Cell Host & Microbe this week, and it states and confirms that not only the oral microbiome of diabetic mice shifted but that these changes were directly associated with an increase in inflammation and bone loss.
Before this research was conducted, there was no definitive evidence that confirmed the fact that diabetes affects the oral microbiome but according to Dana Graves, vice dean of scholarship and research at Penn’s School of Dental Medicine and senior author of the new study, the studies previously conducted were not very rigorous.
Four years ago, the American Academy of Periodontology and the European Federation of Periodontology issued a report which didn’t offer any compelling evidence that showed diabetes is related directly to the changes in the oral microbiome. However, Graves and her colleagues were skeptical about the results and henceforth, decided to embark on this research, using a mouse model that mimics Type 2 diabetes.
Graves’ argument was based on the idea that appropriate studies haven’t been done. Graves co-authored the study with Kyle Bittinger of the Children’s Hospital of Philadelphia, he assisted with microbiome analysis, whilst E Xiao from Peking University -first author of the study– and a group of co-authors from the University of São Paulo, Sichuan University, the Federal University of Minas Gerais and the University of Capinas, consulted with Daniel Beiting of Penn Vet’s Center for Host-Microbial Interactions and performed the bone-loss measurements at the Penn Center for Musculoskeletal Diseases.
They showed that before developing high blood sugar levels, or hyperglycemia, the diabetic mice had oral microbiome rather similar to their healthy counterparts. However, once the diabetic mice were hyperglycemic, the microbiome became different from that of their normal littermates. The diabetic mice also displayed periodontitis, including a loss of bone supporting the teeth as well as increased levels of IL-17, a signaling molecule important in immune response and inflammation. Graves stated that the diabetic mice display a behaviour very similar to the one of humans with periodontal where bone loss and increased IL-17 caused by a genetic disease.
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