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Bidirectional Associations between Oral Conditions, Glucose Abnormalities and Potential Nutrition-Related Mediators

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 9986

Special Issue Editor

Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA 02115, USA
Interests: epidemiology; health promotion; non-communicable disease; nutrition

Special Issue Information

Dear Colleagues,

Periodontitis is one of the potential complications of diabetes. Conversely, periodontitis could lead to tooth loss, which in turn could detrimentally impact dietary intake and lead to chronic disease like diabetes. Potential mediators include dietary and nutritional factors, dyslipidemia, markers of inflammation and endothelial dysfunction, and advanced glycation end-products. Other components of oral health such as the microbiome may also play an important role in both disease and in its associations, and very few studies have evaluated “omics” in this context.

Numerous studies have shown associations between periodontitis and diabetes, but the majority are cross-sectional, which limits causal interpretation. In addition to diabetes, several glucose abnormalities such as insulin resistance, impaired glucose tolerance, and pre-diabetes have been evaluated in a few studies in this context, and findings are inconsistent. Longitudinal studies relating periodontitis and glucose abnormalities show inconsistent results in both directions. The causal interpretations of these associations are further complicated by numerous common risk factors that may confound the associations. More research is needed to better understand these associations, the reasons for inconsistencies, causal interpretation, and understanding pathways for these associations. This Special Issue welcomes original manuscripts and review articles that provide insight or new data to better understand these associations. 

Prof. Dr. Kaumudi J. Joshipura
Guest Editor

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Keywords

  • diabetes
  • glucose abnormalities
  • oral health
  • periodontitis
  • nutrition

Published Papers (2 papers)

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Research

16 pages, 952 KiB  
Article
How a Nutritional Deficiency Became Treated with Fluoride
by Philippe P. Hujoel
Nutrients 2021, 13(12), 4361; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13124361 - 03 Dec 2021
Cited by 1 | Viewed by 6256
Abstract
Ignoring evidence on causes of disease such as smoking can harm public health. This report explores how public health experts started to ignore evidence that pediatric vitamin D deficiencies are associated with dental caries. Historical analyses show that an organization of clinical specialists, [...] Read more.
Ignoring evidence on causes of disease such as smoking can harm public health. This report explores how public health experts started to ignore evidence that pediatric vitamin D deficiencies are associated with dental caries. Historical analyses show that an organization of clinical specialists, the American Dental Association (ADA), initiated this view. The ADA was a world-leading organization and its governing bodies worked through political channels to make fluoride a global standard of care for a disease which at the time was viewed as an indicator of vitamin D deficiencies. The ADA scientific council was enlisted in this endeavor and authorized the statement saying that “claims for vitamin D as a factor in tooth decay are not acceptable”. This statement was ghost-written, the opposite of what the ADA scientific council had endorsed for 15 years, and the opposite of what the National Academy of Sciences concluded. Internal ADA documents are informative on the origin of this scientific conundrum; the ADA scientific council had ignored their scientific rules and was assisting ADA governing bodies in conflicts with the medical profession on advertising policies. The evidence presented here suggests that professional organizations of clinical specialists have the power to create standards of care which ignore key evidence and consequently can harm public health. Full article
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18 pages, 10090 KiB  
Article
Astaxanthin Inhibits Diabetes-Triggered Periodontal Destruction, Ameliorates Oxidative Complications in STZ-Injected Mice, and Recovers Nrf2-Dependent Antioxidant System
by Govinda Bhattarai, Han-Sol So, Thi Thu Trang Kieu, Sung-Ho Kook, Jeong-Chae Lee and Young-Mi Jeon
Nutrients 2021, 13(10), 3575; https://0-doi-org.brum.beds.ac.uk/10.3390/nu13103575 - 12 Oct 2021
Cited by 9 | Viewed by 3155
Abstract
Numerous studies highlight that astaxanthin (ASTX) ameliorates hyperglycemic condition and hyperglycemia-associated chronic complications. While periodontitis and periodontic tissue degradation are also triggered under chronic hyperglycemia, the roles of ASTX on diabetes-associated periodontal destruction and the related mechanisms therein are not yet fully understood. [...] Read more.
Numerous studies highlight that astaxanthin (ASTX) ameliorates hyperglycemic condition and hyperglycemia-associated chronic complications. While periodontitis and periodontic tissue degradation are also triggered under chronic hyperglycemia, the roles of ASTX on diabetes-associated periodontal destruction and the related mechanisms therein are not yet fully understood. Here, we explored the impacts of supplemental ASTX on periodontal destruction and systemic complications in type I diabetic mice. To induce diabetes, C57BL/6 mice received a single intraperitoneal injection of streptozotocin (STZ; 150 mg/kg), and the hyperglycemic mice were orally administered with ASTX (12.5 mg/kg) (STZ+ASTX group) or vehicle only (STZ group) daily for 60 days. Supplemental ASTX did not improve hyperglycemic condition, but ameliorated excessive water and feed consumptions and lethality in STZ-induced diabetic mice. Compared with the non-diabetic and STZ+ASTX groups, the STZ group exhibited severe periodontal destruction. Oral gavage with ASTX inhibited osteoclastic formation and the expression of receptor activator of nuclear factor (NF)-κB ligand, 8-OHdG, γ-H2AX, cyclooxygenase 2, and interleukin-1β in the periodontium of STZ-injected mice. Supplemental ASTX not only increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and osteogenic transcription factors in the periodontium, but also recovered circulating lymphocytes and endogenous antioxidant enzyme activity in the blood of STZ-injected mice. Furthermore, the addition of ASTX blocked advanced glycation end products-induced oxidative stress and growth inhibition in human-derived periodontal ligament cells by upregulating the Nrf2 pathway. Together, our results suggest that ASTX does not directly improve hyperglycemia, but ameliorates hyperglycemia-triggered periodontal destruction and oxidative systemic complications in type I diabetes. Full article
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