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The growing interest in oral/systemic links demand new paradigms to understand disease processes. New opportunities for dental research, particularly in the fields of neuroscience and endocrinology will emerge. The role of the hypothalamus portion of the brain cannot be underestimated. Under the influence of nutrition, it plays a significant role in the systemic model of dental caries. Currently, the traditional theory of dental caries considers only the oral environment and does not recognize any significant role for the brain. The healthy tooth, however, has a centrifugal fluid flow to nourish and cleanse it. This is moderated by the hypothalamus/parotid axis which signals the endocrine portion of the parotid glands. High sugar intake creates an increase in reactive oxygen species and oxidative stress in the hypothalamus. When this signaling mechanism halts or reverses the dentinal fluid flow, it renders the tooth vulnerable to oral bacteria, which can now attach to the tooth’s surface. Acid produced by oral bacteria such as Strep Mutans and lactobacillus can now de-mineralize the enamel and irritate the dentin. The acid attack stimulates an inflammatory response which results in dentin breakdown from the body’s own matrix metalloproteinases. Vitamin K2 (K2) has been shown to have an antioxidant potential in the brain and may prove to be a potent way to preserve the endocrine controlled centrifugal dentinal fluid flow. Stress, including oxidative stress, magnifies the body’s inflammatory response. Sugar can not only increase oral bacterial acid production but it can concurrently reduce the tooth’s defenses through endocrine signaling. Saliva production is the exocrine function of the salivary glands. The buffering capacity of saliva is critical to neutralizing the oral environment. This minimizes the de-mineralization of enamel and enhances its re-mineralization. K2, such as that found in fermented cheese, improves salivary buffering through its influence on calcium and inorganic phosphates secreted. Data collected from several selected primitive cultures on the cusp of civilization demonstrated the difference in dental health due to diet. The primitive diet group had few carious lesions compared to the group which consumed a civilized diet high in sugar and refined carbohydrates. The primitives were able to include the fat soluble vitamins, specifically K2, in their diet. More endocrine and neuroscience research is necessary to better understand how nutrition influences the tooth’s defenses through the hypothalamus/parotid axis. It will also link dental caries to other inflammation related degenerative diseases such as diabetes.

The six most dangerous words in evidence-based medicine (EBM) do not directly cause deaths or adverse events. They do not directly cause medical errors or diminutions in quality of care. However, they may indirectly cause these adverse consequences by leading to false inferences for decision making.

Background: Oral health is associated with diabetes, but the chances of experiencing acute or chronic diabetes complications as per this association is unknown in Canada’s most populous province, Ontario. This study assesses the impact of self-reported oral health on the likelihood of experiencing acute and chronic complications among a cohort of previously diagnosed diabetics.

Methods: A retrospective cohort study was conducted of diabetics (n = 5183) who participated in the Canadian Community Health Survey 2003 and 2007-08. Self-reported oral health status was linked to health encounters in electronic medical records until March 31, 2016. Multinomial regression models determined the odds of the first acute or chronic complication after self-report of oral health status.

Results: Thirty-eight percent of diabetics reporting “poor to fair” oral health experienced a diabetes complication, in comparison to 34% of those reporting “good to excellent” oral health. The odds of an acute or chronic complication among participants reporting “poor to fair” oral health status was 10% (OR 1.10; 95% CI 0.81, 1.51) and 34% (OR 1.34; 95% CI 1.11, 1.61) greater respectively, than among participants experiencing no complications and reporting “good to excellent” oral health.

Conclusion: Self-reporting “poor to fair” oral health status is associated with a greater likelihood of chronic complications than acute complications. Further research regarding the underlying causal mechanisms linking oral health and diabetes complications is needed.

It is well established that alterations in phosphate metabolism have a profound effect on hard and soft tissues of the oral cavity. The present-day clinical form of osteonecrosis of the jaw (ONJ) was preceded by phosphorus necrosis of the jaw, ca. 1860. The subsequent removal of yellow phosphorus from matches in the early 20th century saw a parallel decline in “phossy jaw” until the early 2000s, when similar reports of unusual jaw bone necrosis began to appear in the literature describing jaw necrosis in patients undergoing chemotherapy and concomitant steroid and bisphosphonate treatment. Today, the potential side effect of ONJ associated with medications that block osteoclast activity (antiresorptive) is well known, though the mechanism remains unclear and the management and outcomes are often unsatisfactory. Much of the existing literature has focused on the continuing concerns of appropriate use of bisphosphonates and other antiresorptive medications, the incomplete or underdeveloped research on ONJ, and the use of drugs with anabolic potential for treatment of osteoporosis. While recognizing that ONJ is a rare occurrence and ONJ-associated medications play an important role in fracture risk reduction in osteoporotic patients, evidence to date suggests that health care providers can lower the risk further by dental evaluations and care prior to initiating antiresorptive therapies and by monitoring dental health during and after treatment. This review describes the current clinical management guidelines for ONJ, the critical role of dental-medical management in mitigating risks, and the current understanding of the effects of predominantly osteoclast-modulating drugs on bone homeostasis.