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Mercury is one of the most toxic elements and causes a multitude of health problems. It is ten times more toxic to neurons than lead. This study was created to determine if mercury could be causing Alzheimer’s disease (AD) by cross referencing the effects of mercury with 70 factors associated with AD. The results found that all these factors could be attributed to mercury. The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss-all changes that can be caused by mercury. Neurotransmitters such as acetylcholine, serotonin, dopamine, glutamate, and norepinephrine are inhibited in patients with Alzheimer’s disease, with the same inhibition occurring in mercury toxicity. Enzyme dysfunction in patients with Alzheimer’s disease include BACE 1, gamma secretase, cyclooxygenase-2, cytochrome-c-oxidase, protein kinases, monoamine oxidase, nitric oxide synthetase, acetyl choline transferase, and caspases, all which can be explained by mercury toxicity. Immune and inflammatory responses seen in patients with Alzheimer’s disease also occur when cells are exposed to mercury, including complement activation, cytokine expression, production of glial fibrillary acid protein antibodies and interleukin-1, transforming growth factor, beta 2 microglobulins, and phosphodiesterase 4 stimulation. Genetic factors in patients with Alzheimer’s disease are also associated with mercury. Apolipoprotein E 4 allele increases the toxicity of mercury. Mercury can inhibit DNA synthesis in the hippocampus, and has been associated with genetic mutations of presenilin 1 and 2, found in AD. The abnormalities of minerals and vitamins, specifically aluminum, calcium, copper, iron, magnesium, selenium, zinc, and vitamins B1, B12, E, and C, that occur in patients with Alzheimer’s disease, also occur in mercury toxicity. Aluminum has been found to increase mercury’s toxicity. Likewise, similar biochemical factors in AD are affected by mercury, including changes in blood levels of homocysteine, arachidonic acid, DHEA sulfate, glutathione, hydrogen peroxide, glycosamine glycans, acetyl-L carnitine, melatonin, and HDL. Other factors seen in Alzheimer’s disease, such as increased platelet activation, poor odor identification, hypertension, depression, increased incidences of herpes virus and chlamydia infections, also occur in mercury exposure. In addition, patients diagnosed with Alzheimer’s disease exhibit higher levels of brain mercury, blood mercury, and tissue mercury in some studies. The greatest exogenous sources of brain mercury come from dental amalgams. Conclusion: This review of the literature strongly suggests that mercury can be a cause of Alzheimer’s Disease.

Periodontal diseases are caused by bacterial infection and may progress to chronic dental disease; severe inflammation may result in bone loss. Therefore, it is necessary to prevent bacterial infection or control inflammation. Periodontal ligament fibroblasts (PDLFs) are responsible for the maintenance of tissue integrity and immune and inflammatory events in periodontal diseases. The formation of bacterial complexes by Fusobacterium nucleatum and Porphyromonas gingivalis is crucial in the pathogenesis of periodontal disease. F. nucleatum is a facultative anaerobic species, considered to be a key mediator of dental plaque maturation and aggregation of other oral bacteria. P. gingivalis is an obligate anaerobic species that induces gingival inflammation by secreting virulence factors. In this study, we investigated whether Osmunda japonica extract exerted anti-inflammatory effects in primary PDLFs stimulated by oral pathogens. PDLFs were stimulated with F. nucleatum or P. gingivalis. We showed that pro-inflammatory cytokine (IL-6 and IL-8) expression was induced by LPS or bacterial infection but decreased by treatment with O. japonica extract following bacterial infection. We found that the activation of NF-κB, a transcription factor for pro-inflammatory cytokines, was modulated by O. japonica extract. Thus, O. japonica extract has immunomodulatory activity that can be harnessed to control inflammation.

Background: Malnutrition is the main risk factor for most common communicable diseases. The aim of this study is to determine the relationship between country-level prevalence of early childhood caries (ECC), malnutrition and anemia in infants and preschool children.

Methods: Matched country-level ECC, malnutrition and anemia prevalence were generated from databases covering the period 2000 to 2017. Multivariate general linear models were developed to assess the relationship between outcome variables (prevalence of stunting, wasting, overweight, and anemia) and the explanatory variable (ECC prevalence) adjusted for gross national income per capita. Adjusted regression coefficients (B) and partial eta squared were computed.

Results: The mean (standard deviation (SD)) ECC prevalence was 23.8 (14.8)% for 0-2 year-olds and 57.3 (22.4)% for 3-5-year-olds. The mean (SD) prevalence of wasting was 6.3 (4.8)%, overweight 7.2 (4.9)%, stunting 24.3 (13.5)%, and anemia 37.8 (18.1)%. For 0-2-year-olds, the strongest and only significant association was between the prevalence of ECC and overweight (η2 = 0.21): 1 % higher ECC prevalence was associated with 0.12% higher prevalence of overweight (B = 0.12, P = 0.03). In 3-5-year-olds, the strongest and only significant association was between the prevalence of ECC and anemia (η2 = 0.08): 1 % higher prevalence of ECC was associated with 0.14% lower prevalence of anemia (B = – 0.14, P = 0.048).

Conclusion: Country-level prevalence of ECC was associated with malnutrition in 0-2-year-olds and with anemia in 3-5-year-olds. The pathway for the direct relationship between ECC and overweight may be diet related. The pathway for the inverse relationship between ECC and anemia is less clear and needs further investigations.

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.

Introduction: Metallic implants are integral to the practice of orthopedic surgery. Delayed-onset T-cell-mediated metal hypersensitivity (diagnosed by patch testing) is reported in 10% to 17% of the general population. Inconclusive evidence exists about the role of metal hypersensitivity in persistently painful or aseptic loosening of arthroplasties. Literature suggests that preoperative patch testing may influence surgical practice.

Objective: To determine the incidence of metal hypersensitivity in orthopedic surgical patients who self-report hypersensitivity and to characterize which metals are most commonly implicated.

Methods: A retrospective chart review of patients from a single surgeon’s practice was conducted during a 1-year period. All patients were questioned about metal hypersensitivity history; all patients who responded affirmatively were sent for patch testing for specific metals.

Results: Only 41 (4.9%) of 840 patients self-reported any metal hypersensitivity. Of these, 34 (83%) were patch-test positive to 1 or more metals. There were 27 whose test results were positive for nickel, 4 each to cobalt or gold thiosulfate, and 1 each to tin or titanium. Seven patients had positive results to multiple metals, all of whom were also nickel hypersensitive. Six patients had metal orthopedic implants before patch testing, and 4 (67%) tested positively to a metal in their implant.

Conclusion: Metal hypersensitivity can be concerning for treating surgeons and patients. Greater awareness of a history to hypersensitivity may prevent patient exposure to implants containing metals that may cause hypersensitivity. Non-metal-containing or nonreactive metal implants are an option for patients in whom metal hypersensitivity is suspected or confirmed.

Vitamin D (VD) levels have been gaining growing attention in Oral Health. During growth and adulthood, VD deficiency (VDD) is associated with a wide variety of oral health disorders, and impaired VD synthesis may expedite some of these conditions. In children, severe VDD can induce defective tooth mineralization, resulting in dentin and enamel defects. As a consequence, these defects may increase the risk of the onset and progression of dental caries. Further, VDD has been associated with higher prevalence of periodontitis and gingival inflammation, and several recent preclinical and clinical studies have unveiled potential pathways through which Vitamin D may interact with the periodontium. VDD correction through supplementation may contribute to a successful treatment of periodontitis; however, alveolar bone regeneration procedures performed in baseline VDD patients seem more prone to failure. Vitamin D may also be linked with some oral pathology entities such as certain oral cancers and events of osteonecrosis of the jaw. This review aims to provide comprehensive evidence of how VD levels should be considered to promote good oral health, and to summarize how VDD may hamper oral development and its role in certain oral conditions.

The erbium-doped yttrium aluminum garnet (Er:YAG) laser is used to treat periodontal disease; however, its effectiveness at killing oral bacteria is not well known. Furthermore, the compounding effect of the combination of a laser treatment and irrigation methods with antimicrobials on bacterial viability is yet to be determined. The purpose of this in vitro study was to evaluate the effect of the Er:YAG laser with irrigation using chlorhexidine (CHX), hydrogen peroxide (H2O2), or sodium hypochlorite (NaOCl) on the viability of oral bacteria. Three bacterial species were used in our study: Streptococcus gordonii, Fusobacterium nucleatum, and Porphyromonas gingivalis. Bacteria were grown in an anaerobic chamber in brain heart infusion broth and incubated at 37 °C. Bacterial samples with an OD of 0.5 were irradiated with the Er:YAG laser at 2940 nm using a 400-µm Varian tip. The experiment was repeated four times using these parameters: 40 mJ, 40 Hz, and 1.6 W for 20 seconds with the 300 µs short pulse duration in contact mode. Treatment groups consisted of the following: (1) no treatment, (2) 0.5% H2O2 alone, (3) 0.5% NaOCl alone, (4) 0.03% CHX alone, (5) Er:YAG irradiation alone, (6) Er:YAG irradiation with 0.5% H2O2, (7) Er:YAG irradiation with 0.5% NaOCl, and (8) Er:YAG irradiation with 0.03% CHX. Microbial viability was determined through plating and colony counts and calculated into CFU/ml. Statistical analysis was done using a two-tailed paired t-test. The use of the Er:YAG laser alone failed to show statistically significant antibacterial activity against any of bacteria. The most effective mono-treatment with irrigation solutions for all three bacteria were 0.5% H2O2 and 0.5% NaOCl (p < 0.001 for each solution). Irrigation with 0.03% CHX was most effective against F. nucleatum (p < 0.01) and less against P. gingivalis and S. gordonii and showed the least antibacterial action alone but improved significantly in combination therapy (p < 0.05). The combined treatment with the Er:YAG showed the greatest and most significant improvement in the reduction of bacterial viability compared to any other treatment group (p < 0.05 for each combined treatment). Irradiation with the Er:YAG laser with the addition of 0.5% H2O2, 0.5% NaOCl, or 0.03% CHX under a short working time (20 s) resulted in a significant reduction of bacterial viability for all three bacterial species compared with any single treatment option. The combination of irradiation with the Er:YAG laser with the addition of 0.5% H2O2, 0.5% NaOCl, or 0.03% CHX resulted in a larger reduction of bacterial survival when compared to monotherapies with antimicrobial solutions or laser. The combination of the Er:YAG laser with a low concentration irrigant solution of 0.5% H2O2, 0.5% NaOCl, or 0.03% CHX could be an effective treatment protocol for the reduction of periodontal pathogens and thus suitable treatment for non-surgical periodontal therapy.