Over the past few years, genetic findings have changed our views on the molecular pathogenesis of Parkinson disease (PD), as mutations in a growing number of genes have been found to cause monogenic ...forms of the disorder. These mutations cause neuronal dysfunction and neurodegeneration either by a toxic gain of function, as in the case of the dominant forms of monogenic PD caused by mutations in the genes for alpha-synuclein or LRRK2, or by a loss of an intrinsic protective function, as is likely for the recessive PD genes parkin (PRKN), PINK1 and DJ-1. Evidence is emerging that at least some of the pathways uncovered in the rare monogenic forms of PD may play a direct role in the aetiology of the common sporadic disorder and that variants of the respective genes contribute to the risk of developing the disease. These findings will allow the search for new treatment strategies that focus on the underlying molecular pathophysiology, rather than simply on ameliorating symptoms.
The etiology of Parkinson’s disease (PD) is complex and most likely involves numerous environmental and heritable risk factors. Interestingly, many genetic variants, which have been linked to ...familial forms of PD or identified as strong risk factors, also play a critical role in modulating inflammatory responses. There has been considerable debate in the field as to whether inflammation is a driving force in neurodegeneration or simply represents a response to neuronal death. One emerging hypothesis is that inflammation plays a critical role in the early phases of neurodegeneration. In this review, we will discuss emerging aspects of both innate and adaptive immunity in the context of the pathogenesis of PD. We will highlight recent data from genetic and functional studies that strongly support the theory that genetic susceptibility plays an important role in modulating immune pathways and inflammatory reactions, which may precede and initiate neuronal dysfunction and subsequent neurodegeneration. A detailed understanding of such cellular and molecular inflammatory pathways is crucial to uncover pathogenic mechanisms linking sporadic and hereditary PD and devise tailored neuroprotective interventions.
Summary The dystonias are a heterogeneous group of hyperkinetic movement disorders characterised by involuntary sustained muscle contractions that lead to abnormal postures and repetitive movements. ...Dystonia syndromes represent common movement disorders and yet are often misdiagnosed or unrecognised. In recent years, there have been substantial advances in the understanding of the spectrum of clinical features that encompass dystonia syndromes, from severe generalised childhood dystonia that is often genetic in origin, to adult-onset focal dystonias and rarer forms of secondary dystonias, to dystonia as a feature of other types of CNS dysfunction. There has also been a rationalisation of the classification of dystonia and a greater understanding of the causes of dystonic movements from the study of genetics, neurophysiology, and functional imaging in the most prevalent form of dystonia syndrome, primary dystonia.
Aim
To assess mid‐term clinical, radiographic and profilometric outcomes at implant sites, previously grafted with a volume‐stable collagen matrix (VCMX) or an autogenous subepithelial connective ...tissue graft (SCTG).
Methods
VCMX or SCTG were randomly applied to single implant sites in 20 patients. Following abutment connection and insertion of final reconstructions (baseline), patients were re‐examined at 6 months (6M), at 1 year (FU‐1) and at 3 years (FU‐3). Measurements included the following: clinical data, radiographic measurement of first bone to implant contact (fBIC), soft tissue thickness and volumetric outcomes. Non‐parametric tests and estimates were applied for the statistical analysis.
Results
The median buccal mucosal thickness increased by 0.5 mm (Q1: ‐0.5; Q3: 1.25) (VCMX) (p = .281) and by 0.8 mm (Q1: 0.0; Q3: 2.5) (SCTG) (p = .047) between BL and FU‐3 (intergroup p = .303). The profilometric changes of the buccal soft tissues demonstrated a median decrease between BL and FU‐3 of −0.2 mm (Q1: −0.5; Q3: −0.1) (p = .039) for VCMX and a decrease of −0.1 mm (Q1: −0.8; Q3: 0.1) (p = .020) for SCTG, respectively (intergroup p = .596). Peri‐implant soft tissues and bone levels remained healthy throughout the entire study period. PROMs did not show any significant differences between the groups nor significant changes over time.
Conclusion
Minimal changes of the peri‐implant tissue contour as well as of the soft tissue thickness were observed at implant sites previously grafted with VCMX or SCTG.
The aim of this study was to compare patient‐reported outcome measures (PROMs) of soft tissue substitutes versus autogenous grafts for soft tissue augmentation procedures at implant sites. ...Comprehensive and systematic literature searches were performed until December 2021. A focused question was formulated based on the Population, Intervention, Comparison and Outcome criteria (PICO): In patients with dental implants undergoing soft tissue augmentation (P), do soft tissue substitutes (I) compared to autogenous soft tissue graft (SCTG subepithelial connective tissue graft) (C) limit the post‐operative morbidity and other patient reported‐outcomes measures (O). Randomized controlled clinical trials, prospective‐, retrospective‐ and case‐series studies were included. Meta‐analyses were performed whenever possible and the results were expressed as weighted mean differences (WMD). A total of 29 clinical studies were included. For mucosal thickness gain, soft tissue substitutes significantly reduced the pain perception compared to SCTG (n = 4; WMD = 14.91 Visual Analog Scale VAS units; 95% confidence interval CI 6.42‐23.40; P < .0006) based on a 0‐100 VAS scale. Based on a 0‐10 VAS scale, a borderline significance of pain reduction was found when soft tissue substitutes were applied (n = 4; WMD = 1.62 VAS units; 95% CI 0.01‐3.23; P = .05). For keratinized tissue gain, soft tissue substitutes significantly reduced the pain perception after keratinized tissue augmentation compared to SCTG based on a 0‐100 VAS scale (n = 2; WMD = 21.43 VAS units; 95% CI 12.58‐30.28; P < .0001). Based on the 0‐10 VAS scale, soft tissue substitutes significantly reduced the pain as compared to SCTG (n = 4; WMD = 1.65 VAS units; 95% CI 0.66‐2.64; P = .001). Regarding pain medication, soft tissue substitutes required less painkillers (n = 6; WMD = 1.56 tablets; 95% CI 1.22‐1.91; P < .00001) after soft tissue augmentation. The surgery time was significantly reduced when soft tissue substitutes were used (n = 5; WMD = 10.9 minutes; 95% CI 4.60‐17.19; P < .00001). There were no significant differences in satisfaction, aesthetics, and quality of life (OHIP‐14) between soft tissue substitutes and autogenous grafts following soft tissue augmentation at implants sites. Soft tissue substitutes, compared to autogenous grafts, significantly improve PROMs following soft tissue augmentation at implant sites. Soft tissue substitutes can reduce pain perception, amounts of painkillers and surgery time while achieving similar levels of patient´s satisfaction as autogenous grafts without impairing the clinical outcomes. The current evidence indicates that they constitute a valid and reliable alternative to minimize the invasiveness in soft tissue augmentation procedures at implant sites.
Objectives
This study aimed to retrospectively evaluate clinical and radiographic outcomes of partial pulpotomy performed in permanent teeth with carious pulp exposure.
Materials and methods
Records ...of patients undergoing treatment at an undergraduate dental clinic between 2010 and 2019 were screened for partial pulpotomies in teeth with a presumptive diagnosis of normal pulp or reversible pulpitis. The follow-up had to be ≥ 1 year. Patient data were retrieved and analyzed using Mantel-Cox chi square tests and Kaplan–Meier statistics. The level of significance was set at α = 0.05.
Results
Partial pulpotomy was performed in 111 cases, of which 64 (58%) fulfilled the eligibility criteria. At the time of partial pulpotomy, the mean age was 37.3 (± 13.5) years (age range 18–85). The mean observation period was 3.1 (± 2.0) years. Two early failures (3.1%) and five late failures (7.7%) were recorded. The overall success rate of maintaining pulp vitality was 89.1%, with 98.4% tooth survival. The cumulative pulp survival rates of partial pulpotomy in patients aged < 30 years, between 30 and 40 years, and > 40 years were 100%, 75.5%, and 90.5%, respectively, with no significant difference between the age groups (p = 0.225). At follow-up, narrowing of the pulp canal space and tooth discoloration were observed in 10.9% and 3.1% of cases, respectively.
Conclusions
Across age groups, partial pulpotomy achieved favorable short and medium-term outcomes in teeth with carious pulp exposure.
Clinical relevance
Adequate case selection provided, partial pulpotomy is a viable operative approach to treat permanent teeth with deep carious lesions irrespective of patients’ age.
Summary Background Intraoperative MRI is increasingly used in neurosurgery, although there is little evidence for its use. We aimed to assess efficacy of intraoperative MRI guidance on extent of ...resection in patients with glioma. Methods In our prospective, randomised, parallel-group trial, we enrolled adults (≥18 years) with contrast enhancing gliomas amenable to radiologically complete resection who presented to Goethe University (Frankfurt, Germany). We randomly assigned patients (1:1) with computer-generated blocks of four and a sealed-envelope design to undergo intraoperative MRI-guided surgery or conventional microsurgery (control group). Surgeons and patients were unmasked to treatment group allocation, but an independent neuroradiologist was masked during analysis of all preoperative and postoperative imaging data. The primary endpoint was rate of complete resections as established by early postoperative high-field MRI (1·5 T or 3·0 T). Analysis was done per protocol. This study is registered with ClinicalTrials.gov , number NCT01394692. Findings We enrolled 58 patients between Oct 1, 2007, and July 1, 2010. 24 (83%) of 29 patients randomly allocated to the intraoperative MRI group and 25 (86%) of 29 controls were eligible for analysis (four patients in each group had metastasis and one patient in the intraoperative MRI group withdrew consent after randomisation). More patients in the intraoperative MRI group had complete tumour resection (23 96% of 24 patients) than did in the control group (17 68% of 25, p=0·023). Postoperative rates of new neurological deficits did not differ between patients in the intraoperative MRI group (three 13% of 24) and controls (two 8% of 25, p=1·0). No patient for whom use of intraoperative MRI led to continued resection of residual tumour had neurological deterioration. One patient in the control group died before 6 months. Interpretation Our study provides evidence for the use of intraoperative MRI guidance in glioma surgery: such imaging helps surgeons provide the optimum extent of resection. Funding None.
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