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So far Wade WG. has created 991 blog entries.

The oral microbiome in health and disease.

The human mouth harbours one of the most diverse microbiomes in the human body, including viruses, fungi, protozoa, archaea and bacteria. The bacteria are responsible for the two commonest bacterial diseases of man: dental caries (tooth decay) and the periodontal (gum) diseases. Archaea are restricted to a small number of species of methanogens while around 1000 bacterial species have been found, with representatives from the phyla Actinobacteria, Bacteroidetes, Firmicutes, Proteobacteria, Spirochaetes, Synergistetes and Tenericutes and the uncultured divisions GN02, SR1 and TM7. Around half of oral bacteria are as yet uncultured and culture-independent methods have been successfully used to comprehensively describe the oral bacterial community. The human oral microbiome database (HOMD, www.homd.org) provides a comprehensive resource consisting of descriptions of oral bacterial taxa, a 16S rRNA identification tool and a repository of oral bacterial genome sequences. Individuals’ oral microbiomes are highly specific at the species level, although overall the human oral microbiome shows few geographical differences. Although caries and periodontitis are clearly bacterial diseases, they are not infectious diseases in the classical sense because they result from a complex interaction between the commensal microbiota, host susceptibility and environmental factors such as diet and smoking. Periodontitis, in particular, appears to result from an inappropriate inflammatory reaction to the normal microbiota, exacerbated by the presence of some disease-associated bacterial species. In functional terms, there appears to considerable redundancy among the oral microbiota and a focus on functional rather than phylogenetic diversity may be required in order to fully understand host-microbiome interactions.

By |2019-06-02T01:16:07+00:00January 1st, 2013|Other|

RANTES and fibroblast growth factor 2 in jawbone cavitations: triggers for systemic disease?

BACKGROUND:

Jawbone cavitations (JC) are hollow dead spaces in jawbones with dying or dead bone marrow. These areas are defined as fatty degenerative osteonecrosis of the jawbone or neuralgia-inducing cavitational osteonecrosis and may produce facial pain. These afflictions have been linked to the immune system and chronic illnesses. Surgical debridement of JC is reported to lead to an improvement in immunological complaints, such as rheumatic, allergic, and other inflammatory diseases (ID). Little is known about the underlying cause/effect relationship.

OBJECTIVES:

JC bone samples were analyzed to assess the expression and quantification of immune modulators that can play a role in the pathogenesis of IDs. The study supports a potential mechanism where JC is a mediating link in IDs.

MATERIALS AND METHODS:

Samples of fatty softened bone taken from JCs were extracted from 31 patients. The specimens were analyzed by bead-based multiplex technology and tested for seven immune messengers.

RESULTS:

Regulated upon activation, normal T-cell expressed, and secreted (RANTES) and fibroblast growth factor (FGF)-2 were found at high levels in the JCs tested. Other cytokines could not be detected at excessive levels.

DISCUSSION:

The study confirms that JC is able to produce inflammatory messengers, primarily RANTES, and, secondarily, FGF-2. Both are implicated in many serious illnesses. The excessive levels of RANTES/FGF-2 in JC patients with amyotrophic lateral sclerosis, multiple sclerosis, rheumatoid arthritis, and breast cancer are compared to levels published in medical journals. Levels detected in JCs are higher than in the serum and cerebrospinal fluid of amyotrophic lateral sclerosis and multiple sclerosis patients and four-fold higher than in breast cancer tissue.

CONCLUSION:

This study suggests that JC might serve as a fundamental cause of IDs, through RANTES/FGF-2 production. Thus, JC and implicated immune messengers represent an integrative aspect of IDs and serve as a possible cause. Removing JCs may be a key to reversing IDs. There is a need to raise awareness about JC throughout medicine and dentistry.

By |2019-11-23T01:02:47+00:00January 1st, 2013|Other|

Total fluoride intake and excretion in children up to 4 years of age living in fluoridated and non‐fluoridated areas.

Fractional fluoride retention is important during the early years of life when considering the risk of development of dental fluorosis. This study aimed to measure fractional fluoride retention in young children. The objectives were to investigate the relationships between fractional fluoride retention and total daily fluoride intake, age, and body mass index (BMI). Twenty-nine healthy children, up to 4 yr of age, participated; 14 lived in a fluoridated area (0.64 μg ml(-1) of fluoride in drinking water) and 15 lived in a non-fluoridated area (0.04 μg ml(-1) of fluoride in drinking water). The total daily fluoride intake of each child was calculated from the daily dietary fluoride intake and toothpaste ingestion (if fluoride toothpaste was used). Total daily fluoride excretion was measured by collecting voided urine and faeces over a 24-h period, and fractional fluoride retention was calculated by dividing the amount of fluoride retained in the body (total daily fluoride intake minus total daily fluoride excretion) by the total daily fluoride intake. Nine children were excluded from data analysis because of suspected invalid samples. Mean (range) fractional fluoride retention for the remaining 20 children was 0.61 (0.06-0.98). There were no statistically significant correlations between fractional fluoride retention and either age or BMI. However, fractional fluoride retention was correlated with total daily fluoride intake: fractional fluoride retention = 1 – exp (-C × total daily fluoride intake), where C = 28.75 (95% CI = 19.75-37.75). The wide variation in fluoride retention in young children could have important implications when recommendations for fluoride use are being considered.

Mercury biogeochemical cycling in the ocean and policy implications.

Anthropogenic activities have enriched mercury in the biosphere by at least a factor of three, leading to increases in total mercury (Hg) in the surface ocean. However, the impacts on ocean fish and associated trends in human exposure as a result of such changes are less clear. Here we review our understanding of global mass budgets for both inorganic and methylated Hg species in ocean seawater. We consider external inputs from atmospheric deposition and rivers as well as internal production of monomethylmercury (CH₃Hg) and dimethylmercury ((CH₃)₂Hg). Impacts of large-scale ocean circulation and vertical transport processes on Hg distribution throughout the water column and how this influences bioaccumulation into ocean food chains are also discussed. Our analysis suggests that while atmospheric deposition is the main source of inorganic Hg to open ocean systems, most of the CH₃Hg accumulating in ocean fish is derived from in situ production within the upper waters (<1000 m). An analysis of the available data suggests that concentrations in the various ocean basins are changing at different rates due to differences in atmospheric loading and that the deeper waters of the oceans are responding slowly to changes in atmospheric Hg inputs. Most biological exposures occur in the upper ocean and therefore should respond over years to decades to changes in atmospheric mercury inputs achieved by regulatory control strategies. Migratory pelagic fish such as tuna and swordfish are an important component of CH₃Hg exposure for many human populations and therefore any reduction in anthropogenic releases of Hg and associated deposition to the ocean will result in a decline in human exposure and risk.

Occupational Exposure to Elemental Mercury in Odontology/Dentistry

This report reviews the literature, describes the use of mercury in odontology, and raises issues of concern for human health. In odontology and dental clinics,1 mercury may be found in dental amalgam and measuring devices such as thermometers and blood pres-sure cuffs (sphygmomanometers, tensiometers). Studies have shown elevated concentra-tions of mercury in the ambient air in dental settings. This mercury vapor may enter the body through inhalation and be transported to different organs throughout the body where it can accumulate. This report recommends developing a program to minimize the use of mercury, lessen  the potential for exposure, and control mercury waste. This will benefit dental workers by decreasing their exposure to this toxic material and will reduce environmental impacts from mercury in solid waste, in the air, and in wastewater.

By |2018-08-06T23:42:22+00:00January 1st, 2012|Mercury|

Systemic affliction of oral focal sepsis.

Multitude of etiologies can cause diseases in various systems. One important etiology is focal sepsis in the oral cavity which has been hypothesized till now to cause various diseases. This hypothesis has now been proved beyond doubt.

By |2019-06-06T23:08:47+00:00January 1st, 2012|Other|

Molecular mechanisms of cytotoxicity and apoptosis induced by inorganic fluoride.

Fluoride (F) is ubiquitous natural substance and widespread industrial pollutant. Although low fluoride concentrations are beneficial for normal tooth and bone development, acute or chronic exposure to high fluoride doses results in adverse health effects. The molecular mechanisms underlying fluoride toxicity are different by nature. Fluoride is able to stimulate G-proteins with subsequent activation of downstream signal transduction pathways such as PKA-, PKC-, PI3-kinase-, Ca2+-, and MAPK-dependent systems. G-protein-independent routes include tyrosine phosphorylation and protein phosphatase inhibition. Along with other toxic effects, fluoride was shown to induce oxidative stress leading to excessive generation of ROS, lipid peroxidation, decrease in the GSH/GSSH ratio, and alterations in activities of antioxidant enzymes, as well as to inhibit glycolysis thus causing the depletion of cellular ATP and disturbances in cellular metabolism. Fluoride triggers the disruption of mitochondria outer membrane and release of cytochrome c into cytosol, what activates caspases-9 and -3 (intrinsic) apoptotic pathway. Extrinsic (death receptor) Fas/FasL-caspase-8 and -3 pathway was also described to be implicated in fluoride-induced apoptosis. Fluoride decreases the ratio of antiapoptotic/proapoptotic Bcl-2 family proteins and upregulates the expression of p53 protein. Finally, fluoride changes the expression profile of apoptosis-related genes and causes endoplasmic reticulum stress leading to inhibition of protein synthesis.

By |2018-07-18T15:46:06+00:00January 1st, 2012|Fluoride|

Heavy metal toxicity and the environment.

Heavy metals are naturally occurring elements that have a high atomic weight and a density at least 5 times greater than that of water. Their multiple industrial, domestic, agricultural, medical and technological applications have led to their wide distribution in the environment; raising concerns over their potential effects on human health and the environment. Their toxicity depends on several factors including the dose, route of exposure, and chemical species, as well as the age, gender, genetics, and nutritional status of exposed individuals. Because of their high degree of toxicity, arsenic, cadmium, chromium, lead, and mercury rank among the priority metals that are of public health significance. These metallic elements are considered systemic toxicants that are known to induce multiple organ damage, even at lower levels of exposure. They are also classified as human carcinogens (known or probable) according to the U.S. Environmental Protection Agency, and the International Agency for Research on Cancer. This review provides an analysis of their environmental occurrence, production and use, potential for human exposure, and molecular mechanisms of toxicity, genotoxicity, and carcinogenicity.

By |2018-08-02T21:27:12+00:00January 1st, 2012|Mercury|

The toxicology of mercury and its compounds.

A concentrated review on the toxicology of inorganic mercury together with an extensive review on the neurotoxicology of methylmercury is presented. The challenges of using inorganic mercury in dental amalgam are reviewed both regarding the occupational exposure and the possible health problems for the dental patients. The two remaining “mysteries” of methylmercury neurotoxicology are also being reviewed; the cellular selectivity and the delayed onset of symptoms. The relevant literature on these aspects has been discussed and some suggestions towards explaining these observations have been presented.

By |2018-08-02T21:10:57+00:00January 1st, 2012|Mercury|
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