Effect of length, diameter, intraoral location on implant stability.

OBJECTIVES: To quantitatively compare stability of dental implants with varying lengths, diameters, and intraoral locations. STUDY DESIGN: Retrospectively, 200 consecutive NobelReplace Tapered Groovy implants of varying lengths and diameters were evaluated via implant stability quotient readings at placement (T1) and follow-up (T2). Data were analyzed by analysis of variance and simple linear regression tests. RESULTS: Intraoral location was statistically significant at T1 and T2. Although implant diameter was not statistically significant, implant length resulted in T1 (P = .08) and T2 (P = .09), which may have a clinically relevant effect on implant stability. An overall implant survival rate of 98% was achieved. Gender and age did not seem to affect implant stability quotient values at placement, follow-up, or implant survival. CONCLUSIONS: Intraoral location is an important factor in implant stability, with implants placed in the mandible being more stable than implants placed in the maxilla both at T1 and T2. Length may have a clinically relevant effect on implant stability.

Mechanical versus biological stability of immediate and delayed implant placement using resonance frequency analysis.

PURPOSE: The purpose was to objectively measure the stability of immediately placed implants compared with implants placed at healed sites using implant stability quotient (ISQ) values obtained by resonance frequency analysis. MATERIALS AND METHODS: Data were collected from 137 Nobel Replace Tapered Groovy Implants placed in 85 patients 19 to 93 years old. All implants were placed by the same surgeon from May 2007 to October 2011. Forty-one implants were placed immediately after extraction with MasterGraft bone grafting material and 96 were placed in healed sites with no grafting material. ISQ values obtained by the Osstell ISQ System were recorded at the time of implant placement and at a subsequent follow-up appointment (T2). T2 was split into 2- to 3-month and 4- to 6-month groups depending on when their follow-up ISQ values were obtained. Data were analyzed using simple linear regression. RESULTS: Implants placed in healed sites had higher average ISQ values at implant placement compared with immediately placed implants; however, mean ISQ values in the 2 immediate implant groups exceeded the ISQ threshold of 65. Immediately placed implants in the 2- to 3-month and 4- to 6-month groups had average ISQ values of 65.60 and 68.65, respectively, whereas implants placed in healed sites had averages of 76.73 (2- to 3-month group) and 71.23 (4- to 6-month group). These differences were statistically significant (P < .05). At subsequent follow-up appointments, implants placed in healed sites had higher mean ISQ values. Implants in healed sites had ISQ averages of 79.58 (2- to 3-month group) and 77.31 (4- to 6-month group), whereas immediately placed implants had averages of 73.88 and 70.14. These differences were statistically significant (P < .05). Moreover, these mean ISQ values in immediate implants exceeded the ISQ threshold of 65. CONCLUSION: Although mean ISQ values of immediately placed implants are lower than those of delayed implants at implant placement and follow-up appointments, immediate implant mean ISQ values consistently remain higher than the clinically successful ISQ threshold of 65 throughout the osseointegration process. These results support the immediate placement of implants in extraction sockets under favorable conditions.

Electrostimulation to reduce synaptic scaling driven progression of Alzheimer's disease.

Cell death and synapse dysfunction are two likely causes of cognitive decline in AD. As cells die and synapses lose their drive, remaining cells suffer an initial decrease in activity. Neuronal homeostatic synaptic scaling then provides a feedback mechanism to restore activity. This homeostatic mechanism is believed to sense levels of activity-dependent cytosolic calcium within the cell and to adjust neuronal firing activity by increasing the density of AMPA synapses at remaining synapses to achieve balance. The scaling mechanism increases the firing rates of remaining cells in the network to compensate for decreases in network activity. However, this effect can itself become a pathology, as it produces increased imbalance between excitatory and inhibitory circuits, leading to greater susceptibility to further cell loss via calcium-mediated excitotoxicity. Here, we present a mechanistic explanation of how directed brain stimulation might be expected to slow AD progression based on computational simulations in a 470-neuron biomimetic model of a neocortical column. The simulations demonstrate that the addition of low-intensity electrostimulation (neuroprosthesis) to a network undergoing AD-like cell death can raise global activity and break this homeostatic-excitotoxic cascade. The increase in activity within the remaining cells in the column results in lower scaling-driven AMPAR upregulation, reduced imbalances in excitatory and inhibitory circuits, and lower susceptibility to ongoing damage.

Information-selectivity of Beta-amyloid pathology in an associative memory model.

This work models the progression of beta-amyloid pathology according to Small's synaptic scaling theory in an updated version of Ruppin and Reggia's associative neural network model of Alzheimer's disease, leading to a self-reinforcing cascade of damage. Using an information theoretic approach, it is shown that the simulated beta-amyloid pathology initially selectively targets neurons with low informational contribution to the overall performance of the network, but that it targets neurons with increasingly higher significance to the network as the disease progresses. The results additionally provide a possible explanation for the apparent low correlation between amyloid plaque density and cognitive decline in the early stages of Alzheimer's disease.

The utility of the new generation of humanized mice to study HIV-1 infection: transmission, prevention, pathogenesis, and treatment.

Substantial improvements have been made in recent years in the ability to engraft human cells and tissues into immunodeficient mice. The use of human hematopoietic stem cells (HSCs) leads to multi-lineage human hematopoiesis accompanied by production of a variety of human immune cell types. Population of murine primary and secondary lymphoid organs with human cells occurs, and long-term engraftment has been achieved. Engrafted cells are capable of producing human innate and adaptive immune responses, making these models the most physiologically relevant humanized animal models to date. New models have been successfully infected by a variety of strains of Human Immunodeficiency Virus Type 1 (HIV-1), accompanied by virus replication in lymphoid and non-lymphoid organs, including the gut-associated lymphoid tissue, the male and female reproductive tracts, and the brain. Multiple forms of virus-induced pathogenesis are present, and human T cell and antibody responses to HIV-1 are detected. These humanized mice are susceptible to a high rate of rectal and vaginal transmission of HIV-1 across an intact epithelium, indicating the potential to study vaccines and microbicides. Antiviral drugs, siRNAs, and hematopoietic stem cell gene therapy strategies have all been shown to be effective at reducing viral load and preventing or reversing helper T cell loss in humanized mice, indicating that they will serve as an important preclinical model to study new therapeutic modalities. HIV-1 has also been shown to evolve in response to selective pressures in humanized mice, thus showing that the model will be useful to study and/or predict viral evolution in response to drug or immune pressures. The purpose of this review is to summarize the findings reported to date on all new humanized mouse models (those transplanted with human HSCs) in regards to HIV-1 sexual transmission, pathogenesis, anti-HIV-1 immune responses, viral evolution, pre- and post-exposure prophylaxis, and gene therapeutic strategies.