Implant failure : etiology and complications

The possible occurrence of implant failure is a major concern for implantologists and knowledge in such unavoidable fact is clinically essential. Periimplantitis is an inflammatory response in which there is a loss of the bony support of the implant. Diagnosis is based on the clinical signs of infection such as hyperplastic soft tissues, suppuration, colour changes of the marginal peri-implant tissues and gradual bone loss. This site-specific infection may have many features in common with chronic adult periodontitis. Surgical trauma, micromotion and overload are also considered to be associated with implant failures. The lack of osseointegration is generally distinguished by implant mobility and radiological radiolucency. Here, the implant is considered to be failed . Progressive marginal bone loss without marked mobility is referring to a failing implant. The purpose of this concise review was to discuss the implant complications and failure by highlighting the major etiologic factors as well as the parameters used for evaluating such failure

Third molar removal and orofacial pain : a population-based survey

Peer reviewedPublisher PD

A longitudinal observational study of home-based conversations for detecting early dementia:protocol for the CUBOId TV task

INTRODUCTION: Limitations in effective dementia therapies mean that early diagnosis and monitoring are critical for disease management, but current clinical tools are impractical and/or unreliable, and disregard short-term symptom variability. Behavioural biomarkers of cognitive decline, such as speech, sleep and activity patterns, can manifest prodromal pathological changes. They can be continuously measured at home with smart sensing technologies, and permit leveraging of interpersonal interactions for optimising diagnostic and prognostic performance. Here we describe the ContinUous behavioural Biomarkers Of cognitive Impairment (CUBOId) study, which explores the feasibility of multimodal data fusion for in-home monitoring of mild cognitive impairment (MCI) and early Alzheimer’s disease (AD). The report focuses on a subset of CUBOId participants who perform a novel speech task, the ‘TV task’, designed to track changes in ecologically valid conversations with disease progression. METHODS AND ANALYSIS: CUBOId is a longitudinal observational study. Participants have diagnoses of MCI or AD, and controls are their live-in partners with no such diagnosis. Multimodal activity data were passively acquired from wearables and in-home fixed sensors over timespans of 8–25 months. At two time points participants completed the TV task over 5 days by recording audio of their conversations as they watched a favourite TV programme, with further testing to be completed after removal of the sensor installations. Behavioural testing is supported by neuropsychological assessment for deriving ground truths on cognitive status. Deep learning will be used to generate fused multimodal activity-speech embeddings for optimisation of diagnostic and predictive performance from speech alone. ETHICS AND DISSEMINATION: CUBOId was approved by an NHS Research Ethics Committee (Wales REC; ref: 18/WA/0158) and is sponsored by University of Bristol. It is supported by the National Institute for Health Research Clinical Research Network West of England. Results will be reported at conferences and in peer-reviewed scientific journals

Protocol for a double-blind placebo-controlled randomised controlled trial assessing the impact of oral semaglutide in amyloid positivity (ISAP) in community dwelling UK adults

Introduction: Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), currently marketed for type 2 diabetes and obesity, may offer novel mechanisms to delay or prevent neurotoxicity associated with Alzheimer’s disease (AD). The impact of semaglutide in amyloid positivity (ISAP) trial is investigating whether the GLP-1 RA semaglutide reduces accumulation in the brain of cortical tau protein and neuroinflammation in individuals with preclinical/prodromal AD. Methods and analysis: ISAP is an investigator-led, randomised, double-blind, superiority trial of oral semaglutide compared with placebo. Up to 88 individuals aged ≥55 years with brain amyloid positivity as assessed by positron emission tomography (PET) or cerebrospinal fluid, and no or mild cognitive impairment, will be randomised. People with the low-affinity binding variant of the rs6971 allele of the Translocator Protein 18 kDa (TSPO) gene, which can interfere with interpreting TSPO PET scans (a measure of neuroinflammation), will be excluded. At baseline, participants undergo tau, TSPO PET and MRI scanning, and provide data on physical activity and cognition. Eligible individuals are randomised in a 1:1 ratio to once-daily oral semaglutide or placebo, starting at 3 mg and up-titrating to 14 mg over 8 weeks. They will attend safety visits and provide blood samples to measure AD biomarkers at weeks 4, 8, 26 and 39. All cognitive assessments are repeated at week 26. The last study visit will be at week 52, when all baseline measurements will be repeated. The primary end point is the 1-year change in tau PET signal. Ethics and dissemination: The study was approved by the West Midlands—Edgbaston Research Ethics Committee (22/WM/0013). The results of the study will be disseminated through scientific presentations and peer-reviewed publications. Trial registration number: ISRCTN71283871

Treatment seeking for alcohol and drug use disorders by immigrants to the Netherlands: Retrospective, population-based, cohort study

Background We compared risks of first contact with services for an alcohol use disorder (AUD) or drug use disorder (DUD) between the largest immigrant groups to the Netherlands and Dutch nationals. We tested the hypothesis that the ethnic pattern for DUD is similar to the previously demonstrated pattern for schizophrenia. Methods Retrospective, population-based cohort study of First Admissions to Dutch psychiatric hospitals during the period 1990-1996 (national data) and First Contacts with inpatient or outpatient centres in Rotterdam for treatment of AUD or DUD during the period 1992-2001 (Rotterdam data). Results In both datasets the risk of service contact for AUD was significantly lower in immigrants from Surinam, Turkey and Morocco than in Dutch nationals. The risk was lower or moderately higher in immigrants from western countries. Analysis of the national data showed that, compared with Dutch males, the risk of first hospital admission for DUD was higher for male immigrants from the Dutch Antilles (RR = 4.6; 95% CI: 4.0-5.3), Surinam (RR = 4.3; 3.94.7) and Morocco (RR = 23; 2.0-2.6), but not for male immigrants from Turkey (RR = 0.9; 0.7-1.1). A similar pattern was found with the Rotterdam data. Female immigrants from Surinam and the Dutch Antilles had a higher risk for DUD according to the national data, but a lower risk according to the Rotterdam data. Female immigrants from Turkey and Morocco had a lower risk (both datasets). Immigrants from western countries had a higher risk for DUD, but many had developed the disorder before emigrating. Conclusion Those immigrant groups in the Netherlands that are at increased risk of schizophrenia appear also at increased risk of developing DUD, but not AUD

Association of Liver Injury From Specific Drugs, or Groups of Drugs, With Polymorphisms in HLA and Other Genes in a Genome-Wide Association Study

BACKGROUND & AIMS: We performed a genome-wide association study (GWAS) to identify genetic risk factors for drug-induced liver injury (DILI) from licensed drugs without previously reported genetic risk factors. METHODS: We performed a GWAS of 862 persons with DILI and 10,588 population-matched controls. The first set of cases was recruited before May 2009 in Europe (n = 137) and the United States (n = 274). The second set of cases were identified from May 2009 through May 2013 from international collaborative studies performed in Europe, the United States, and South America. For the GWAS, we included only cases with patients of European ancestry associated with a particular drug (but not flucloxacillin or amoxicillin-clavulanate). We used DNA samples from all subjects to analyze HLA genes and single nucleotide polymorphisms. After the discovery analysis was concluded, we validated our findings using data from 283 European patients with diagnosis of DILI associated with various drugs. RESULTS: We associated DILI with rs114577328 (a proxy for A*33:01 a HLA class I allele; odds ratio [OR], 2.7; 95% confidence interval [CI], 1.9-3.8; P = 2.4 × 10-8) and with rs72631567 on chromosome 2 (OR, 2.0; 95% CI, 1.6-2.5; P = 9.7 × 10-9). The association with A*33:01 was mediated by large effects for terbinafine-, fenofibrate-, and ticlopidine-related DILI. The variant on chromosome 2 was associated with DILI from a variety of drugs. Further phenotypic analysis indicated that the association between DILI and A*33:01 was significant genome wide for cholestatic and mixed DILI, but not for hepatocellular DILI; the polymorphism on chromosome 2 was associated with cholestatic and mixed DILI as well as hepatocellular DILI. We identified an association between rs28521457 (within the lipopolysaccharide-responsive vesicle trafficking, beach and anchor containing gene) and only hepatocellular DILI (OR, 2.1; 95% CI, 1.6-2.7; P = 4.8 × 10-9). We did not associate any specific drug classes with genetic polymorphisms, except for statin-associated DILI, which was associated with rs116561224 on chromosome 18 (OR, 5.4; 95% CI, 3.0-9.5; P = 7.1 × 10-9). We validated the association between A*33:01 terbinafine- and sertraline-induced DILI. We could not validate the association between DILI and rs72631567, rs28521457, or rs116561224. CONCLUSIONS: In a GWAS of persons of European descent with DILI, we associated HLA-A*33:01 with DILI due to terbinafine and possibly fenofibrate and ticlopidine. We identified polymorphisms that appear to be associated with DILI from statins, as well as 2 non-drug-specific risk factors