Predictors of dental implant survival

PURPOSE: To summarize dental implant survival rates under a variety of clinical conditions and identify prognostic variables associated with implant survival. MATERIALS/METHODS: The articles reviewed in this paper were designed as retrospective cohort studies and composed of three subject cohorts having implants placed between 1992 and 2003. The prognostic variables were categorized as demographic/health status, anatomic, implant-specific, prosthetic, and perioperative/operative. The primary outcome variable was duration of implant survival. Kaplan-Meier methods were used to estimate implant survival rates. Multivariate Cox proportional hazards models were used to identify prognostic variables. RESULTS-During the study interval, 921 subjects had 2996 implants placed. Implant survival rates at one year ranged from 90.3 percent for immediate-load implants to 96.2 percent for implants inserted into grafted sinuses. The five-year survivals ranged from 87.9 percent (sinus graft cases) to 91.2 percent (all implants). Frequently cited prognostic variables included tobacco use and implant staging. Other prognostic variables identified included implant length, well size, implant coating, and timing of implant placement relative to tooth extraction. CONCLUSION: Using implants to replace missing teeth is a predictable procedure with five-year survival rates approximating 90 percent. Some of the prognostic variables identified in these studies are under the control, at least to some degree, of the clinician and may be manipulated to enhance implant survival.     

Delta opioid agonists attenuate TAT(1-72)-induced oxidative stress in SK-N-SH cells

Previous reports have indicated that the use of delta agonists may prove to be a viable therapeutic tool as an analgesic agent without conventional opioid side effects. In addition, recent evidence suggests that delta ligands may exert neuroprotective effects under a variety of toxin insults. The aim of the present studies was to assess the ability of delta agonists (peptide: [D-Pen(2,5)] enkephalin (DPDPE), non-peptide: (+)-4-[(aR)-a-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl]-N,N-diethylbenzamide (SNC-80)) and antagonists (naltrindole) to modify dichlorofluorescein (DCFH) fluorescence in the presence of the peroxynitrite generator, 3-morpholinylsydnoneimine chloride (SIN-1) or HIV-protein, TAT(1-72) (TAT) in SK-N-SH cells. Both DPDPE (100 nM) and SNC-80 (250 nM) attenuated (30-50%) the increased oxidative stress in the presence of SIN-1. This effect was partially reversed by addition of naltrindole, suggesting involvement of delta receptors. Peroxynitrite radicals are involved in neurotoxicity associated with TAT. Incubation with TAT (10-250 nM) demonstrated a concentration-dependent increase in oxidative stress up to 200% over control values. Preincubation with delta agonists reduced 50 nM TAT-mediated oxidative stress 15-40%, which was partially reversed by naltrindole. Increasing log-concentrations of DPDPE or SNC-80 (0.01-100 microM) attenuated TAT-mediated oxidative stress up to 50% at 100 microM. In conclusion, these data demonstrate that both peptide and non-peptide delta agonists can partially attenuate intracellular oxidative stress, in part through a receptor-mediated mechanism. This suggests that delta ligands may have therapeutic usefulness in HIV patients beyond analgesia.     

LR11/SorLA expression is reduced in sporadic Alzheimer disease but not in familial Alzheimer disease

LR11 is an ApoE receptor that is enriched in the brain. We have shown that LR11 is markedly downregulated in patients with sporadic Alzheimer disease (AD). This finding led us to explore whether reduced LR11 expression reflects a primary mechanism of disease or merely a secondary consequence of other AD-associated changes. Therefore, LR11 expression was assessed in a transgenic mouse model of AD and familial AD (FAD) brains. Immunohistochemistry and immunoblotting of LR11 in PS1/APP transgenic and wild-type mice indicated that LR11 levels are not affected by genotype or accumulation of amyloid pathology. LR11 expression was also evaluated based on immunoblotting and LR11 immunostaining intensity in human frontal cortex in controls, sporadic AD, and FAD, including cases with presenilin-1 (PS1) and presenilin-2 (PS2) mutations. Although LR11 was reduced in sporadic AD, there was no difference in protein level or staining intensity between control and FAD cases. The finding that LR11 expression is unaffected in both a mouse model of AD and autosomal-dominant forms of AD suggests that LR11 is not regulated by amyloid accumulation or other AD neuropathologic changes. We hypothesize that LR11 loss may be specific to sporadic AD and influence amyloid pathology through mechanisms independent of substrate-enzyme interactions regulated by FAD mutations.     

Stability of Ferruginous Bodies in Human Lung Tissue Following Death,Embalmment, and Burial

The identification of asbestos bodies in tissue sections is an indicator of past exposure to longer asbestos fibers. These structures are formed in lung tissue as a consequence of interactions with pulmonary macrophages resulting in the deposition of a ferroprotein (ferruginous) coating on the fiber. While the process of ferruginous body formation is known to take months in animal tissue, there is no published information on the stability of ferruginous bodies in tissue following death. The material assessed in the present study was obtained from lung material collected from an exhumed body approximately 8½ mo after death, embalmment, and burial. Tissue sections were reviewed for the presence of asbestos bodies. Additional pieces of lung tissue were digested, with the digestate being evaluated by light microscopy for ferruginous bodies and by electron microscopy for uncoated asbestos fibers and core analysis of asbestos bodies. Classical ferruginous (asbestos) bodies were found in abundance in the tissue sections including in areas with fibrosis. The levels of uncoated asbestos fibers and classical appearing ferruginous bodies (asbestos bodies) were consistent with occupational levels of tissue burden. The data from this study indicate that ferruginous bodies remain morphologically stable within the tissue for months following death, embalmment, and burial. Thus the lung tissue from this exhumed individual was usable not only to pathologically confirm asbestosis but also to provide quantitative data of occupational exposure to asbestos.     

Assessment of CPR interruptions from transthoracic impedance during use of the LUCAS™ mechanical chest compression system

BackgroundQuality of cardiopulmonary resuscitation (CPR) is a key determinant of outcome following out-of-hospital cardiac arrest (OHCA). Recent evidence shows manual chest compressions are typically too shallow, interruptions are frequent and prolonged, and incomplete release between compressions is common. Mechanical chest compression systems have been developed as adjuncts for CPR but interruption of CPR during their use is not well documented.AimAnalyze interruptions of CPR during application and use of the LUCAS? chest compression system.Methods54 LUCAS 1 devices operated on compressed air, deployed in 3 major US emergency medical services systems, were used to treat patients with OHCA. Electrocardiogram and transthoracic impedance data from defibrillator/monitors were analyzed to evaluate timing of CPR. Separately, providers estimated their CPR interruption time during application of LUCAS, for comparison to measured application time.ResultsIn the 32 cases analyzed, compressions were paused a median of 32.5 s (IQR 25–61) to apply LUCAS. Providers’ estimates correlated poorly with measured pause length; pauses were often more than twice as long as estimated. The average device compression rate was 104/min (SD 4) and the average compression fraction (percent of time compressions were occurring) during mechanical CPR was 0.88 (SD 0.09).ConclusionsInterruptions in chest compressions to apply LUCAS can be <20 s but are often much longer, and users do not perceive pause time accurately. Therefore, we recommend better training on application technique, and implementation of systems using impedance data to give users objective feedback on their mechanical chest compression device use.