-
Journal of Oral Rehabilitation May 2022Osseoperception is defined as the ability to perceive tactile sensation via mechanoreception in the peri-implant environment. The objective was to systematically review... (Review)
Review
OBJECTIVES
Osseoperception is defined as the ability to perceive tactile sensation via mechanoreception in the peri-implant environment. The objective was to systematically review the available literature on the osseoperception phenomenon following dental implant placement and to explore potential factors which might improve the perception capacity.
MATERIAL AND METHODS
A literature search was performed using PubMed, Cochrane, Embase, and Web of Science databases up to June 2021. Both human and animal studies assessing sensory capacity or innervation following implant placement were included in this review. Two reviewers independently performed the study selection, data extraction and quality assessment of the included studies. The methodological quality of the included papers was assessed using Cochrane risk of bias for human studies and SYRCLE's risk of bias tool for animal studies.
RESULTS
The electronic search of databases yielded 1667 results. Following removal of duplicates, title and abstract screening and full-text reading, 22 publications were eligible to be included in the review. Psychophysical evidence from 14 studies indicated a lower tactile function of implants, where active and passive threshold levels were found to be 5 and 50 times higher for implants compared to natural teeth, respectively. The neurophysiological evidence from three studies indicated cortical plasticity following dental implant placement, measured via trigeminal nerve evoked potentials and functional magnetic resonance imaging. Histological evidence from five studies demonstrated the presence of myelinated nerve fibres in the peri-implant tissues. Additionally, immediate implant placement and loading showed beneficial effect on peri-implant tissue (re)innervation; however, no other biological or physiological factors could be identified influencing osseoperception.
CONCLUSIONS
The reported evidence supported the existence of so-called osseoperception phenomenon for restoring the sensory feedback pathway following oral implant rehabilitation. Further studies are required to identify factors that might further assist physiological integration of the oral implants in the human body as such to approach natural oral function.
Topics: Animals; Dental Implantation, Endosseous; Dental Implants; Humans; Mouth, Edentulous; Touch
PubMed: 34911146
DOI: 10.1111/joor.13296 -
Frontiers in Neuroscience 2023Perivascular spaces have been involved in neuroinflammatory and neurodegenerative diseases. Upon a certain size, these spaces can become visible on magnetic resonance...
OBJECTIVES
Perivascular spaces have been involved in neuroinflammatory and neurodegenerative diseases. Upon a certain size, these spaces can become visible on magnetic resonance imaging (MRI), referred to as enlarged perivascular spaces (EPVS) or MRI-visible perivascular spaces (MVPVS). However, the lack of systematic evidence on etiology and temporal dynamics of MVPVS hampers their diagnostic utility as MRI biomarker. Thus, the goal of this systematic review was to summarize potential etiologies and evolution of MVPVS.
METHODS
In a comprehensive literature search, out of 1,488 unique publications, 140 records assessing etiopathogenesis and dynamics of MVPVS were eligible for a qualitative summary. 6 records were included in a meta-analysis to assess the association between MVPVS and brain atrophy.
RESULTS
Four overarching and partly overlapping etiologies of MVPVS have been proposed: (1) Impairment of interstitial fluid circulation, (2) Spiral elongation of arteries, (3) Brain atrophy and/or perivascular myelin loss, and (4) Immune cell accumulation in the perivascular space. The meta-analysis in patients with neuroinflammatory diseases did not support an association between MVPVS and brain volume measures [R: -0.15 (95%-CI -0.40-0.11)]. Based on few and mostly small studies in tumefactive MVPVS and in vascular and neuroinflammatory diseases, temporal evolution of MVPVS is slow.
CONCLUSION
Collectively, this study provides high-grade evidence for MVPVS etiopathogenesis and temporal dynamics. Although several potential etiologies for MVPVS emergence have been proposed, they are only partially supported by data. Advanced MRI methods should be employed to further dissect etiopathogenesis and evolution of MVPVS. This can benefit their implementation as an imaging biomarker.
SYSTEMATIC REVIEW REGISTRATION
https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=346564, identifier CRD42022346564.
PubMed: 37065926
DOI: 10.3389/fnins.2023.1038011 -
Acta Histochemica Jan 2023Epithelial membrane protein 2 (EMP2) is a cell surface protein composed of approximately 160 amino acids and encoded by the growth arrest-specific 3 (GAS3)/peripheral... (Review)
Review
OBJECTIVES
Epithelial membrane protein 2 (EMP2) is a cell surface protein composed of approximately 160 amino acids and encoded by the growth arrest-specific 3 (GAS3)/peripheral myelin protein 22 kDa (PMP22) gene family. Although EMP2 expression has been investigated in several diseases, much remains unknown regarding its mechanism of action and the extent of its role in pathogenesis. Our aim was to perform a systematic review on the involvement of EMP2 in disease processes and the current usage of anti-EMP2 therapies.
METHODS
A Boolean search of the English-language medical literature was performed. PubMed, Scopus, Cochrane, and Web of Science were used to identify relevant citations. This study followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.
RESULTS
52 studies met the inclusion criteria for qualitative analysis. Of those, 28 (53.8%) were human-only studies, 11 (21.2%) were animal-only studies, and 13 (25%) studies included both human and animal models. Furthermore, 34 (65.4%) studies focused on EMP2's role in neoplasms, while the remaining 18 (34.6%) articles evaluated its role in other pathologies.
CONCLUSION
Overall, the evidence suggests the mechanisms of action of EMP2 are context dependent. Promising results have been produced by utilizing EMP2 as a biomarker and therapeutic target. More studies are warranted to better understand the mechanism and comprehend the role of EMP2 in the pathogenesis of diseases.
Topics: Animals; Humans; Membrane Glycoproteins; Membrane Proteins
PubMed: 36455339
DOI: 10.1016/j.acthis.2022.151976 -
NeuroImage Apr 2021Recent years have seen an increased understanding of the importance of myelination in healthy brain function and neuropsychiatric diseases. Non-invasive microstructural... (Meta-Analysis)
Meta-Analysis
Recent years have seen an increased understanding of the importance of myelination in healthy brain function and neuropsychiatric diseases. Non-invasive microstructural magnetic resonance imaging (MRI) holds the potential to expand and translate these insights to basic and clinical human research, but the sensitivity and specificity of different MR markers to myelination is a subject of debate. To consolidate current knowledge on the topic, we perform a systematic review and meta-analysis of studies that validate microstructural imaging by combining it with myelin histology. We find meta-analytic evidence for correlations between various myelin histology metrics and markers from different MRI modalities, including fractional anisotropy, radial diffusivity, macromolecular pool, magnetization transfer ratio, susceptibility and longitudinal relaxation rate, but not mean diffusivity. Meta-analytic correlation effect sizes range widely, between R = 0.26 and R = 0.82. However, formal comparisons between MRI-based myelin markers are limited by methodological variability, inconsistent reporting and potential for publication bias, thus preventing the establishment of a single most sensitive strategy to measure myelin with MRI. To facilitate further progress, we provide a detailed characterisation of the evaluated studies as an online resource. We also share a set of 12 recommendations for future studies validating putative MR-based myelin markers and deploying them in vivo in humans.
Topics: Brain; Humans; Magnetic Resonance Imaging; Myelin Proteins; Myelin Sheath; Qualitative Research; Reproducibility of Results
PubMed: 33524576
DOI: 10.1016/j.neuroimage.2021.117744 -
Lupus Mar 2021Myelin oligodendrocyte glycoprotein (MOG) is a nervous system protein expressed by oligodendrocytes to constitute the myelin sheath. Autoantibodies against MOG have been...
INTRODUCTION
Myelin oligodendrocyte glycoprotein (MOG) is a nervous system protein expressed by oligodendrocytes to constitute the myelin sheath. Autoantibodies against MOG have been widely described in neurological and autoimmune diseases such as MOG-IgG-associated disorder (MOGAD).Although underlying mechanisms have not yet been understood, an overlap of MOGAD and Systemic Lupus Erythematosus (SLE) has been shown in the literature.
OBJECTIVES
The aim of this systematic review was to assess the possible correlations between MOGAD and SLE based on reported features found in the literature that support the association of the two.
METHODS
A keyword-based literature search was conducted, applying a ten-year filter and using the following key-words: "MOG autoantibody-associated disease and Systemic Lupus Erythematosus"; "MOG and Systemic Lupus Erythematosus" "Anti-MOG and Lupus"; "MOG and SLE"; "MOG and LUPUS" on MEDLINE/PUBMED, ScienceDirect, SciELO, LILACS and Cochrane; and "MOG antibody-associated disease and SLE" on Google Scholar.
RESULTS
Eleven publications reporting on the MOGAD and SLE correlation were included in qualitative synthesis: animal experiment (1), cross-sectional (3), prospective (2), retrospective (1), non-systematic review (3), and case report (1) studies.
CONCLUSION
Not much is known about the connection between MOG-IgG-associated disorder and SLE. Unfortunately, only observational studies have been conducted in humans so far, providing us with limited data. While MOGAD features have been reported to develop in SLE patients, this is not an universal finding. In fact, many different issues impair these results, making it difficult to match the findings of different studies.
Topics: Animals; Aquaporin 4; Autoantibodies; Humans; Immunoglobulin G; Lupus Erythematosus, Systemic; Myelin-Oligodendrocyte Glycoprotein; Neuromyelitis Optica; Observational Studies as Topic
PubMed: 33290135
DOI: 10.1177/0961203320978514 -
Multiple Sclerosis and Related Disorders Jul 2020Recent reports have suggested that seizures may be a component of the clinical presentation in myelin oligodendrocyte glycoprotein antibody (MOG-Ab)-associated disease.... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
Recent reports have suggested that seizures may be a component of the clinical presentation in myelin oligodendrocyte glycoprotein antibody (MOG-Ab)-associated disease. We aimed to conduct a systematic review and meta-analysis to comprehensively evaluate the occurrence of epileptic seizures in the disease.
METHODS
We searched PubMed, MEDLINE and EMBASE for studies reporting the occurrence of acute symptomatic seizures in MOG-Ab-associated disease. Fixed or random effects model was used to pool results across studies with a meta-analysis.
RESULTS
A total of 14 studies met the inclusion criteria. Overall, acute symptomatic seizures were observed in 20.5% (95% confidence interval [CI] 13.7%-30.7%, I=60.6%) patients with MOG-Ab-associated disease, and in a similar proportion of children respectively (20.0%; 95% CI 14.3%-27.8%, I=7.0%). The pooled probability of seizure occurrence in males was 30.1% (95% CI 17.5%-52%, I=0.0%) while that in females was much lower (12.0%; 95% CI 5.5%-26.4%, I=0.0%). Furthermore, when we focused on those with acute disseminated encephalomyelitis-like phenotype, 37.3% patients experienced seizures (95% CI 21.0%-66.3%, I=55.8%).
CONCLUSIONS
Our study suggested that epileptic seizures were common in MOG-Ab-associated disease and offered insight into associated factors that contribute to the occurrence of seizures. Future studies with explicit evaluation are required.
Topics: Autoantibodies; Child; Encephalomyelitis, Acute Disseminated; Epilepsy; Female; Humans; Male; Myelin-Oligodendrocyte Glycoprotein; Seizures
PubMed: 32222694
DOI: 10.1016/j.msard.2020.102057 -
Journal of Neurology Feb 2023Retina thickness has been studied in patients with neuromyelitis optica spectrum disorders (NMOSD) without distinguishing serostatus and limited data are available in... (Meta-Analysis)
Meta-Analysis Review
Retina thickness in clinically affected and unaffected eyes in patients with aquaporin-4 immunoglobulin G antibody seropositive neuromyelitis optica spectrum disorders: a systematic review and meta-analysis.
BACKGROUND AND PURPOSE
Retina thickness has been studied in patients with neuromyelitis optica spectrum disorders (NMOSD) without distinguishing serostatus and limited data are available in unaffected eyes. We aimed to investigate retina thickness in eyes of aquaporin-4 immunoglobulin G antibody seropositive (AQP4-IgG) NMOSD patients with optic neuritis (AQP4-ON) and without (AQP4-NON).
METHODS
Eligible studies were identified by searching PubMed and Embase. Mean difference (MD, μm) with corresponding 95% confidence interval (CI) was pooled with random-effect models. The primary measures were average thickness of peripapillar retinal nerve fiber layer (pRNFL) centered on optic disc and the combination of ganglion cell layer and inner plexiform layer (GCIPL) at macula.
RESULTS
We included 21 studies enrolling 787 AQP4-IgG NMOSD patients. Compared with healthy control, pRNFL was thinner in eyes of AQP4-ON (- 32.78, 95% CI [- 36.24, - 29.33]) and AQP4-NON (- 2.76, 95% CI [- 3.94, - 1.58]), so was GICPL in AQP4-ON (-21.38, 95% CI [- 24.01, - 18.74]) and AQP4-NON (95% CI - 2.96, [- 3.91, - 2.00]). Compared with multiple sclerosis with ON, AQP4-ON had thinner pRNFL (- 13.56, 95%CI [- 16.51, - 10.60]) and GCIPL (- 9.12, 95% CI [- 11.88, - 6.36]). AQP4-ON and myelin oligodendrocyte glycoprotein antibody-associated demyelination with ON (MOG-ON) had similar pRNFL (0.59, 95% CI [- 6.61, 7.79]) and GCIPL thickness (- 0.55, 95% CI [- 2.92, 1.82]). AQP4-NON had similar pRNFL and GCIPL thickness to MOG-NON and multiple sclerosis without ON.
CONCLUSIONS
The average thickness of pRNFL and GICPL decreased both in AQP4-ON and AQP4-NON eyes. AQP4-ON eyes had a similar level of pRNFL and GICPL thinning to MOG-ON eyes, so did AQP4-NON to MOG-NON eyes.
Topics: Humans; Neuromyelitis Optica; Immunoglobulin G; Aquaporin 4; Tomography, Optical Coherence; Retina; Optic Neuritis; Multiple Sclerosis; Autoantibodies; Myelin-Oligodendrocyte Glycoprotein
PubMed: 36355186
DOI: 10.1007/s00415-022-11482-4 -
Developmental Cognitive Neuroscience Dec 2022Structural and functional brain alterations are found in adults with depression. It is not known whether these changes are a result of illness or exist prior to disorder... (Review)
Review
Structural and functional brain alterations are found in adults with depression. It is not known whether these changes are a result of illness or exist prior to disorder onset. Asymptomatic offspring of parents with depression offer a unique opportunity to research neural markers of familial risk to depression and clarify the temporal sequence between brain changes and disorder onset. We conducted a systematic review to investigate whether asymptomatic offspring at high familial risk have structural and functional brain changes like those reported in adults with depression. Our literature search resulted in 44 studies on 18,645 offspring ranging from 4 weeks to 25 years old. Reduced cortical thickness and white matter integrity, and altered striatal reward processing were the most consistent findings in high-risk offspring across ages. These alterations are also present in adults with depression, suggesting the existence of neural markers of familial risk for depression. Additional studies reproducing current results, streamlining fMRI data analyses, and investigating underexplored topics (i.e intracortical myelin, gyrification, subcortical shape) may be among the next steps required to improve our understanding of neural markers indexing the vulnerability to depression.
Topics: Adult; Humans; Depression; Genetic Predisposition to Disease; Reward; Magnetic Resonance Imaging; Brain
PubMed: 36242901
DOI: 10.1016/j.dcn.2022.101161 -
Frontiers in Neurology 2017Multiple system atrophy (MSA) is a rare, adult-onset, rapidly progressive fatal synucleinopathy that primarily affects oligodendroglial cells in the brain. Patients with... (Review)
Review
BACKGROUND
Multiple system atrophy (MSA) is a rare, adult-onset, rapidly progressive fatal synucleinopathy that primarily affects oligodendroglial cells in the brain. Patients with MSA only rarely have visual complaints, but recent studies of the retina using optical coherence tomography (OCT) showed atrophy of the peripapillary retinal nerve fiber layer (RNFL) and to a lesser extent the macular ganglion cell layer (GCL) complex.
METHODS
We performed a literature review and meta-analysis according to the preferred reporting items for systematic reviews and meta-analyses guidelines for studies published before January 2017, identified through PubMed and databases, which reported OCT-related outcomes in patients with MSA and controls. A random-effects model was constructed.
RESULTS
The meta-analysis search strategy yielded 15 articles of which 7 met the inclusion criteria. The pooled difference in the average thickness of the RNFL was -5.48 μm (95% CI, -6.23 to -4.73; < 0.0001), indicating significant thinning in patients with MSA. The pooled results showed significant thinning in all the specific RNFL quadrants, except in the temporal RNFL quadrant, where the thickness in MSA and controls was similar [pooled difference of 1.11 µm (95% CI, -4.03 to 6.26; = 0.67)]. This pattern of retinal damage suggests that MSA patients have preferential loss of retinal ganglion cells projecting to the magnocellular pathway (M-cells), which are mainly located in the peripheral retina and are not essential for visual acuity. Visual acuity, on the other hand, relies mostly on macular ganglion cells projecting to the parvocellular pathway (P-cells) through the temporal portion of the RNFL, which are relatively spared in MSA patients.
CONCLUSION
The retinal damage in patients with MSA differs from that observed in patients with Parkinson disease (PD). Patients with MSA have more relative preservation of temporal sector of the RNFL and less severe atrophy of the macular GCL complex. We hypothesize that in patients with MSA there is predominant damage of large myelinated optic nerve axons like those originating from the M-cells. These large axons may require higher support from oligodendrocytes. Conversely, in patients with PD, P-cells might be more affected.
PubMed: 28596752
DOI: 10.3389/fneur.2017.00206 -
Frontiers in Neurology 2021Coexisting anti-NMDAR and MOG antibody (anti-NMDAR-IgG/MOG-IgG)-associated encephalitis have garnered great attention. This study aimed to perform a secondary analysis...
Coexisting anti-NMDAR and MOG antibody (anti-NMDAR-IgG/MOG-IgG)-associated encephalitis have garnered great attention. This study aimed to perform a secondary analysis to determine the clinical features of this disease. We searched several databases for related publications published prior to April 2021. A pooled analysis was conducted with the fixed-effects model using the Mante-Haenszel method ( ≤ 50%), or the random-effects model computed by the DerSimonian-Laird method ( > 50%). Stata software (version 15.0 SE) was used for the analyses. Nine observational studies and 16 case reports (58 cases with anti-NMDAR-IgG/MOG-IgG, 21.0 [8.5, 29.0] years, male 58.6%) were included. The incidences (95%CI) of anti-NMDAR-IgG/MOG-IgG in the patients with serum MOG-IgG and CSF anti-NMDAR-IgG were 0.09 (0.02-0.19) and 0.07 (0.01-0.19), respectively. The median [IQR] of CSF anti-NMDAR antibody titer was 32 [10, 100], and the serum anti-MOG antibody titer was 100 [32, 320]. The prominent clinical symptoms were encephalitic manifestations, including seizures (56.9%) and abnormal behavior (51.7%), rather than demyelinating manifestations, such as speech disorder (34.5%) and optic neuritis (27.6%). Relapse occurred in 63.4% of anti-NMDAR-IgG/MOG-IgG patients, in whom 50.0% of cases relapsed with encephalitic manifestations, and 53.8% relapsed with demyelinating manifestations. The common MRI changes were in the cortex or subcortex (70.7%) and brainstem (31.0%). 31.3% of patients presented with unilateral cerebral cortical encephalitis with epilepsy and 12.5% displayed bilateral frontal cerebral cortex encephalitis. Anti-NMDAR-IgG/MOG-IgG patients showed more frequent mental behavior (OR, 95%CI, 68.38, 1.36-3,434.37), involuntary movement (57.86, 2.53-1,325.11), sleep disorders (195.00, 7.07-5,380.15), and leptomeninge lesions (7.32, 1.81-29.58), and less frequent optic neuritis (0.27, 0.09-0.83) compared to anti-NMDAR-IgG/MOG-IgG patients and presented more common relapse (5.63, 1.75-18.09), preceding infection (2.69, 1.03-7.02), subcortical lesions (116.60, 4.89-2,782.09), basal ganglia lesions (68.14, 2.99-1,554.27), brainstem lesions (24.09, 1.01-574.81), and spinal cord lesions (24.09, 1.01-574.81) compared to anti-NMDAR-IgG/MOG-IgG. In conclusion, anti-NMDAR-IgG/MOG-IgG was rarely observed, but the incidence rate of relapse was very high. The overall symptoms seemed to be similar to those of NMDAR encephalitis.
PubMed: 34512521
DOI: 10.3389/fneur.2021.711376