The neurological deterioration associated with Alzheimer’s disease (AD), involving accumulation of amyloid-beta peptides and neurofibrillary tangles, is associated with evident neuroinflammation. This is now seen to be a significant contributor to pathology. Recently the tenet of the privileged status of the brain, regarding microbial compromise, has been questioned, particularly in terms of neurodegenerative diseases. It is now being considered that microbiological incursion into the central nervous system could be either an initiator or significant contributor to these. This is a novel study using 16S ribosomal gene-specific Next generation sequencing (NGS) of extracted brain tissue. A comparison was made of the bacterial species content of both frozen and formaldehyde fixed sections of a small cohort of Alzheimer-affected cases with those of cognitively unimpaired (normal). Our findings suggest an increase in bacterial populations in Alzheimer brain tissue compared with normal.

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Recent data indicate that transforming growth factor-beta1 (TGF-beta1) can act to promote tumour progression in the late stages of carcinogenesis. The mechanism by which this occurs is unknown although a ligand-induced epithelial-mesenchymal transition (EMT) is thought to be important. In this study, we demonstrate that active Ras is required for TGF-beta1-induced EMT in human keratinocytes and that epidermal growth factor (EGF) can substitute for mutant Ras. EMT was reversed by the removal of TGF-beta1. Under conditions of TGF-beta1-induced EMT, cells were growth inhibited by the ligand resulting in G1 arrest. In cells containing normal Ras, TGF-beta1-activated ERK and p38 mitogen-activated protein kinases (MAPKs), and levels of activation were further increased by co-treatment with EGF. Inhibition of MAPK pathways and Smad2/3 signalling blocked the induction of EMT by TGF-beta1. Further, inhibition of the AP-1 transcriptional complex by [6]-Gingerol, or by the ectopic expression of JDP2, blocked TGF-beta1-induced EMT and conversely, stimulation of AP-1 by 12-O-tetradecanoylphorbol 13-acetate (TPA) substituted for EGF in the induction of EMT by TGF-beta1 in cells containing normal Ras. The presence of oncogenic Ras, the treatment of cells with EGF, or the treatment of cells with TPA to activate AP-1, potentiated TGF-beta1-induced Smad-dependent transcription, an effect that was attenuated by the inhibition of MAPKs and AP-1. The results demonstrate that active Ras and TGF-beta1 co-operate to reversibly induce EMT in human keratinocytes by mechanisms that involve MAPKs, Smad2/3 and AP-1. Further we demonstrate that MAPK/AP-1 signalling enhances Smad transcriptional activity under conditions associated with TGF-beta1-induced EMT.

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Because of the difficulties in measuring erosion in vivo, a number of in vitro and in situ models have been developed and validated. These models are flexible and informative, allowing single as well as multiple variables to be examined under specific conditions using accurate measurement techniques over defined timelines, thus yielding useful data without harmful effects on individuals. This information, together with clinical findings, is essential for clinicians advising susceptible patients appropriately regarding the management of their condition. Little guidance is available, however, on the standardisation of in vitro and in situ protocols for erosive tooth wear studies, so it is difficult to make meaningful comparisons between investigations as experimental variables differ widely from study to study. The aim of this review was to collate the available data on models designed to assess erosive challenges which are severe enough to cause tissue loss as opposed to just softening of the surface structure. The different types of models, with their merits and pitfalls, are documented. Test substrates, disinfecting regimens and ethical considerations are discussed. The aims of this paper are to give guidance to the researcher on evidence-based in vitro and in situ erosive tooth wear methodology and to suggest best practice given current knowledge.

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West NX, Seong J, Davies M. Management of dentine hypersensitivity: efficacy of professionally and self-administered agents. J Clin Periodontol 2015; 42 (Suppl. 16): S256-S302. doi: 10.1111/jcpe.12336. Abstract Context:The gold standard treatment modality for dentine hypersensitivity has not yet been established. This review examines the effectiveness of self and professionally applied treatments for the reduction in pain from dentine hypersensitivity. Materials and Methods: Electronic (three databases) and hand searches were performed 14-21 July 2014 to identify randomized controlled trials for the treatment of dentine hypersensitivity. Results: This systematic review provided numerous treatment modalities for dentine hypersensitivity. Eleven agents and 105 Randomized Controlled Trials were robust enough to be included. The studies varied considerably in design, observation period, active agents, formulation of the whole agent, negative and positive controls and comparator products investigated. The stimuli used were predominantly airblast and tactile or thermal. Due to the heterogeneity between the studies and lack of direct comparison between agents there was insufficient data to undertake a meta-analysis to compare agents for meaningful conclusions. Best available evidence for each treatment agent has been documented as a narrative. Conclusions: Treatments including stannous fluoride, arginine, calcium sodium phosphosilicate and strontium toothpaste appear to be clinically effective for the treatment of dentine hypersensitivity compared to comparators and controls. There is limited evidence to confirm the relative effectiveness of individual professionally applied agents.

Dentine hypersensitivity is a common oral pain condition affecting many individuals. The aetiology is multifactorial; however, over recent years the importance of erosion has become more evident. For dentine hypersensitivity to occur, the lesion must first be localised on the tooth surface and then initiated to exposed dentine tubules which are patent to the pulp. The short, sharp pain symptom is thought to be derived from the hydrodynamic pain theory and, although transient, is arresting, affecting quality of life. This episodic pain condition is likely to become a more frequent dental complaint in the future due to the increase in longevity of the dentition and the rise in tooth wear, particularly amongst young adults. Many efficacious treatment regimens are now available, in particular a number of over-the-counter home use products. The basic principles of treatment are altering fluid flow in the dentinal tubules with tubule occlusion or modifying or chemically blocking the pulpal nerve.