PURPOSE: This in vitro study was performed to assess the adherence of Porphyromonas gingivalis to a resorbable blast media (RBM) titanium surface pretreated with an ultrasonic scaler or toothbrush and to evaluate the effects of the treatment of the RBM titanium discs on the bacterial removal efficiency of brushing by crystal violet assay and scanning electron microscopy. METHODS: RBM titanium discs were pretreated with one of several ultrasonic scaler tips or cleaned with a toothbrush. Then the titanium discs were incubated with P. gingivalis and the quantity of adherent bacteria was compared. The disc surfaces incubated with bacteria were brushed with a toothbrush with dentifrice. Bacteria remaining on the disc surfaces were quantified. RESULTS: A change in morphology of the surface of the RBM titanium discs after different treatments was noted. There were no significant differences in the adherence of bacteria on the pretreated discs according to the treatment modality. Pretreatment with various instruments did not produce significant differences in the bacterial removal efficiency of brushing with dentifrice. CONCLUSIONS: Within the limits of this study, various types of mechanical instrumentation were shown to cause mechanical changes on the RBM titanium surface but did not show a significant influence on the adherence of bacteria and removal efficiency of brushing.
Bacteria ; Dental Scaling ; Dentifrices ; Gentian Violet ; Microscopy, Electron, Scanning ; Porphyromonas gingivalis ; Surface Properties ; Titanium* ; Toothbrushing ; Ultrasonics*

Alzheimer's Disease (AD) is a progressive neurodegenerative disease, which is pathologically defined by the accumulation of amyloid plaques and hyper-phosphorylated tau aggregates in the brain. Mitochondrial dysfunction is also a prominent feature in AD, and the extracellular Aβ and phosphorylated tau result in the impaired mitochondrial dynamics. In this study, we generated an induced pluripotent stem cell (iPSC) line from an AD patient with amyloid precursor protein (APP) mutation (Val715Met; APP-V715M) for the first time. We demonstrated that both extracellular and intracellular levels of Aβ were dramatically increased in the APP-V715M iPSC-derived neurons. Furthermore, the APP-V715M iPSC-derived neurons exhibited high expression levels of phosphorylated tau (AT8), which was also detected in the soma and neurites by immunocytochemistry. We next investigated mitochondrial dynamics in the iPSC-derived neurons using Mito-tracker, which showed a significant decrease of anterograde and retrograde velocity in the APP-V715M iPSC-derived neurons. We also found that as the Aβ and tau pathology accumulates, fusion-related protein Mfn1 was decreased, whereas fission-related protein DRP1 was increased in the APP-V715M iPSC-derived neurons, compared with the control group. Taken together, we established the first iPSC line derived from an AD patient carrying APP-V715M mutation and showed that this iPSC-derived neurons exhibited typical AD pathological features, including a distinct mitochondrial dysfunction.
Alzheimer Disease ; Amyloid ; Brain ; Carisoprodol ; Humans ; Immunohistochemistry ; Mitochondrial Dynamics ; Neurites ; Neurodegenerative Diseases ; Neurons ; Pathology ; Plaque, Amyloid ; Pluripotent Stem Cells

Disease modeling of Alzheimer's disease (AD) has been hampered by the lack of suitable cellular models while animal models are mainly based on the overexpression of AD-related genes which often results in an overemphasis of certain pathways and is also confounded by aging. In this study, we therefore developed and used induced pluripotent stem cell (iPSC) lines from a middle-aged AD patient with a known presenilin 1 (PSEN1) mutation (Glu120Lys; PS1-E120K) and as a control, an elderly normal subject. Using this approach, we demonstrated that the extracellular accumulation of Aβ was dramatically increased in PS1-E120K iPSC-derived neurons compared with the control iPSC line. PS1-E120K iPSC-derived neurons also exhibited high levels of phosphorylated tau, as well as mitochondrial abnormalities and defective autophagy. Given that the effect of aging is lost with iPSC generation, these abnormal cellular features are therefore indicative of PSEN1-associated AD pathogenesis rather than primary changes associated with aging. Taken together, this iPSC-based approach of AD modeling can now be used to better understand AD pathogenesis as well as a tool for drug discovery.
Aged ; Aging ; Alzheimer Disease* ; Autophagy ; Cerebellar Ataxia* ; Drug Discovery ; Humans ; Models, Animal ; Neurons ; Pluripotent Stem Cells ; Presenilin-1 ; Stem Cells