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I am a risk assessment scientist at Oak Ridge Center for Risk Analysis in Oak Ridge, Tennessee. For more than 30 years, I have been involved in the evaluation of exposures, doses, and risks to human health from trace levels of contaminants in the environment, including fluoride, and in the use of uncertainty analysis for environmental and health risk assessment.
2. I was asked to apply risk assessment frameworks used by the Environmental Protection Agency (EPA) to the current scientific literature on fluoride neurotoxicity to determine whether neurotoxicity is a hazard of fluoride exposure, and whether this hazard is a risk at the levels of fluoride added to drinking water for fluoridation (0.7 mg/L).

Chemotherapy usually causes complications affecting several tissues such as oral mucosa. In this case report, a soft palate oral ulcer caused by chemotherapy was treated by ozone gas. This kind of treatment is known for its antimicrobial, regenerative and analgesic proprieties. The results show a complete resolution of the lesion within 2 weeks of treatment. Ozone therapy demonstrates greater effectiveness with respect to this kind of oral lesion compared to traditional therapy. Considering this evidence, ozone therapy should be considered as a useful tool for the adjuvant therapy of oral complications in oncologic patients.

Learning points: Intensive chemotherapy can have side effects, particularly affecting tissue with higher turnover. Therefore, there is a clinical need to prevent or to treat such complications.Ozone therapy could improve oral mucosa healing and have anti-inflammatory, antioxidant and antibacterial effects to prevent suprainfections. To date, there are no reported cases of oral ulcers in oncologic patients being completely resolved using ozone in the literature.Medical and dental doctors should collaborate with regards to complex patients to prevent such types of complications, discovering these clinical cases that are unknown in the literature and treating patients in a more comprehensive way.

Background: To detect annual alveolar bone loss in subjects with cardiovascular disease (CVD) adjusting for associated systemic diseases and risk factors.

Methods: A total number of 132 subjects that reported having CVD from 2008 to 2015 (N = 132). For longitudinal data analysis, 58 subjects eligible for inclusion with at least two exposures of complete mouth set or repeated BW radiographs with at least one-year interval compared with a control group. Alveolar bone level on mesial and distal sites of posterior teeth was measured on bitewing (BW) radiographs available in the electronic health records of each subject.

Results: Subjects who reported having cardiovascular diseases experienced higher annual mean alveolar bone loss (0.062 mm per year) compared to Subjects with no cardiovascular diseases (0.022 mm per year).

Conclusion: Subjects who have reported CVD had higher rate of annual bone loss compared to subjects who did not have any CVD. This observation indicates that targeting high-risk individuals for risk assessment is fundamental to provide the best healthcare possible to those who are the most in need. Periodic examination and assessment of periodontal health is an essential key factor for better oral health, however, it has to be more emphasized and prioritized for individuals that are more prone to the disease.

Background: Topical 0.12% chlorhexidine has been used widely to prevent ventilator-associated pneumonia in patients undergoing mechanical ventilation. However, it is not approved for mucosal application in Japan. The aims of this study were to investigate if topical povidone iodine (i) inhibits bacterial growth and (ii) disrupts the balance of the oral microbiota.

Methods: This randomized controlled clinical trial included 23 patients who underwent mechanical ventilation in the intensive care unit. The patients were divided randomly into two groups: the intervention group (n = 16) and the control group (n = 7). All patients received oral cleaning with 3% hydrogen peroxide, followed by irrigation with tap water. The patients in the intervention group received 10% povidone iodine applied topically to the oral cavity. The concentration of total bacteria in the oropharyngeal fluid were determined before, immediately after, 1 h, 2 h, and 3 h after oral care using the Rapid Oral Bacteria Quantification System, which is based on dielectrophoresis and impedance measurements. The number of streptococci, methicillin-resistant Staphylococcus aureus, Streptococcus pneumoniae, Pseudomonas aeruginosa, Porphyromonas gingivalis, and Candida albicans before, immediately after, 1 h, and 3 h after oral care were estimated based on real-time polymerase chain reaction data.

Results: After irrigation of the oral cavity, the number of bacteria decreased, but increased again at 1 h after oral care in the control group; however, in the intervention group, the concentration of bacteria was significantly lower than that in the control group at 1 hour (p = 0.009), 2 h (p = 0.001), and 3 h (p = 0.001) after oral care. The growth of all bacterial species tested was inhibited in the intervention group at 3 h after oral care, suggesting that povidone iodine did not disturb the balance of the oral microbiota.

Conclusions: Topical application of povidone iodine after cleaning and irrigation of the oral cavity inhibited bacterial growth in the oropharyngeal fluid of patients on mechanical ventilation while not disrupting the balance of the oral microbiota.

Antibacterial photodynamic therapy (aPDT) and antibacterial blue light (aBL) are emerging treatment methods auxiliary to mechanical debridement for periodontitis. APDT provided with near-infrared (NIR) light in conjunction with an indocyanine green (ICG) photosensitizer has shown efficacy in several dental in-office-treatment protocols. In this study, we tested Streptococcus mutans biofilm sensitivity to either aPDT, aBL or their combination dual-light aPDT (simultaneous aPDT and aBL) exposure. Biofilm was cultured by pipetting diluted Streptococcus mutans suspension with growth medium on the bottom of well plates. Either aPDT (810 nm) or aBL (405 nm) or a dual-light aPDT (simultaneous 810 nm aPDT and 405 nm aBL) was applied with an ICG photosensitizer in cases of aPDT or dual-light, while keeping the total given radiant exposure constant at 100 J/cm2. Single-dose light exposures were given after one-day or four-day biofilm incubations. Also, a model of daily treatment was provided by repeating the same light dose daily on four-day and fourteen-day biofilm incubations. Finally, the antibacterial action of the dual-light aPDT with different energy ratios of 810 nm and 405 nm of light were examined on the single-day and four-day biofilm protocols. At the end of each experiment the bacterial viability was assessed by colony-forming unit method. Separate samples were prepared for confocal 3D biofilm imaging. On a one-day biofilm, the dual-light aPDT was significantly more efficient than aBL or aPDT, although all modalities were bactericidal. On a four-day biofilm, a single exposure of aPDT or dual-light aPDT was more efficient than aBL, resulting in a four logarithmic scale reduction in bacterial counts. Surprisingly, when the same amount of aPDT was repeated daily on a four-day or a fourteen-day biofilm, bacterial viability improved significantly. A similar improvement in bacterial viability was observed after repetitive aBL application. This viability improvement was eliminated when dual-light aPDT was applied. By changing the 405 nm to 810 nm radiant exposure ratio in dual-light aPDT, the increase in aBL improved the antibacterial action when the biofilm was older. In conclusion, when aPDT is administered repeatedly to S. mutans biofilm, a single wavelength-based aBL or aPDT leads to a significant biofilm adaptation and increased S. mutans viability. The combined use of aBL light in synchrony with aPDT arrests the adaptation and provides significantly improved and sustained antibacterial efficacy.

Given the widespread lack of access to dental care for many vulnerable Americans, there is a growing realization that integrating dental and primary care may provide comprehensive care. We sought to model the financial impact of integrating dental care provision into a primary care practice. A microsimulation model was used to estimate changes in net revenue per practice by simulating patient visits to a primary dental practice within primary care practices, utilizing national survey and un-identified claims data from a nationwide health insurance plan. The impact of potential changes in utilization rates and payer distributions and hiring additional staff was also evaluated. When dental care services were provided in the primary care setting, annual net revenue changes per practice were -$92,053 (95% CI: -93,054, -91,052) in the first year and $104,626 (95% CI: 103,315, 105,316) in subsequent years. Net revenue per annum after the first year of integration remained positive as long as the overall utilization rates decreased by less than 25%. In settings with a high proportion of publicly insured patients, the net revenue change decreased but was still positive. Integrating primary dental and primary care providers would be financially viable, but this viability depends on demands of dental utilization and payer distributions

Dear Editor
COVID-19 is a novel disease caused by a member of the coronavirus family that originated in Wuhan, Hubei, China in December 2019. Over the last few months, the infection has spread to several countries worldwide. Coronaviruses are described by the World Health Organisation (WHO) as a large family of viruses, which may cause illness in animals or humans (https://www.who.int/news-room/q-a-detail/ q-a-coronaviruses). Although COVID-19 infections in humans most often present with mild symptoms, in a variable percentage of cases, it can cause an acute
respiratory syndrome, which has led to patient fatalities (Phan 2020, Lu et al. 2020). COVID-19 appears to be a particular risk for patient with pre existing medical conditions (such as high blood pressure, heart disease, lung disease, cancer or diabetes; https://www.who.int/news-room/q-a-detail/q-a-coronaviruses).

Background: Various studies, mostly with animals, have provided evidence of adverse impacts of fluoride (F-) on bone density, collagen and microstructure, yet its effects on overall bone quality (strength) has not been clearly or extensively characterized in human populations.

Objective: In this observational study, we assessed variation in an integrated measures of bone quality in a population exposed to wide-ranging F- levels (0.3 to 15.5 mg/L) in drinking water, using a novel application of non-ionizing ultrasonic method.

Method: We collected 871 speed of sound (SOS) measurements from 341 subjects residing in 25 communities, aged 10-70 years (188 males and 153 females). All subjects received scans of the cortical radius and tibia, and adults over the age of 19 received an additional scan of the phalanx. Associations between F- in drinking water and 24-h urine samples, and SOS as a measure of bone quality, were evaluated in bivariate and multivariable regressions adjusting for age, sex, BMI, smoking, and toothpaste use.

Results: We found negative associations between F- exposure and bone quality at all three bones. Adult tibial SOS showed the strongest inverse association with F- exposure, which accounted for 20% of the variance in SOS measures (r = 0.45; n = 199; p < 0.0001). In adjusted analysis, a 1 mg/L increase in F- in drinking water was related to a reduction of 15.8 m/s (95% CI: -21.3 to -10.3), whereas a 1 mg/L increase in 24-h urinary F- (range: 0.04-39.5 mg/L) was linked to a reduction of 8.4 m/s (95% CI: -12.7, -4.12) of adult tibial SOS. Among adolescents, in contrast, weaker and non-significant inverse associations between F- exposure and SOS were found, while age, gender, and BMI were more significant predictors than in adults.

Conclusions: These results are indicative of a fluoride-induced deterioration of bone quality in humans, likely reflecting a combination of factors related to SOS: net bone loss, abnormal mineralization and collagen formation, or altered microarchitecture. The portable and low-cost ultrasound technique appears potentially useful for assessment of bone quality, and should be tested in other locations and for other bone-related disorders, to assess the feasibility of its more extensive diagnostic use in hard-to-reach rural regions.

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.