Laser-assisted treatment of peri-implantitis: a retrospective cohort study.

The intent of this study was to provide a retrospective analysis of the clinical outcomes of 222 consecutive patients with 437 implants diagnosed with peri-implantitis and treated with the LAPIP protocol. All patients treated with LAPIP therapy at this practice were included. The primary outcome variable studied was probing depth (PD), and secondary variables were erythema, bleeding on probing, and suppuration. The significance of reductions in PD and clinical signs was assessed using repeated-measures analysis of variance. Complete data for both baseline and follow-up visits were available for 116 patients with a total of 224 treated implants. The rate of successful treatments-defined as follow-up PD ≤ 4.0 mm and elimination of clinical signs-was 90%. The reduction in PD from 5.4 mm at baseline to 3.4 mm at a median of 7.6 months was statistically significant (P ≤ 0.001). The reduction in the frequency of clinical signs was also statistically significant (P ≤ 0.001). Among 138 patients who had follow-up visits but not necessarily complete PD data, 15 implants were recorded as failed and 249 were recorded as intact at the median longest follow-up time of 13.1 months, resulting in a survival rate of 94%. In this single clinical practice, use of the minimally invasive LAPIP protocol for the treatment of peri-implantitis provided effective and predictable clinical outcomes. Future randomized controlled trials are indicated.

The prototypical ranitidine analog JWS-USC-75-IX improves information processing and cognitive function in animal models.

This study was designed to evaluate further a prototypical ranitidine analog, JWS-USC-75-IX, [(3-[[[2-[[(5-dimethylaminomethyl)-2-furanyl]methyl]thio]ethyl]amino]-4-nitropyridazine, JWS], for neuropharmacologic properties that would theoretically be useful for treating cognitive and noncognitive behavioral symptoms of neuropsychiatric disorders. JWS was previously found to inhibit acetylcholinesterase (AChE) activity, serve as a potent ligand at muscarinic M2 acetylcholine receptors, and elicit positive effects on spatial learning, passive avoidance, and working memory in rodents. In the current study, JWS was evaluated for binding activity at more than 60 neurotransmitter receptors, transporters, and ion channels, as well as for inhibitory activity at AChE and butyrylcholinesterase (BChE). The results indicate that JWS inhibits AChE and BChE at low (micromolar) concentrations and that it is a functional antagonist at M2 receptors (K(B) = 320 nM). JWS was subsequently evaluated orally across additional behavioral assays in rodents (dose range, 0.03-10.0 mg/kg) as well as nonhuman primates (dose range, 0.05-2.0 mg/kg). In rats, JWS improved prepulse inhibition (PPI) of the acoustic startle response in nonimpaired rats and attenuated PPI deficits in three pharmacologic impairment models. JWS also attenuated scopolamine and (-)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801)-related impairments in a spontaneous novel object recognition task and a five-choice serial reaction time task, respectively. In monkeys, JWS elicited dose-dependent improvements of a delayed match-to-sample task as well as an attention-related version of the task where randomly presented (task-relevant) distractors were presented. Thus, JWS (potentially via effects at several drug targets) improves information processing, attention, and memory in animal models and could potentially treat the cognitive and behavioral symptoms of some neuropsychiatric illnesses.