Introduction: Obstructive sleep apnea (OSA) is an extensive public health problem that imposes considerable morbidity. Mandibular advancement splint (MAS) therapy is a well tolerated treatment, but success rates are difficult to predict. Our objective was to investigate the relationship of oropharyngeal airway dimensions, sleep characteristics, patient biometrics, and treatment response within an OSA patient sample.

Methods: Records of 33 adults were assessed retrospectively with the use of Dolphin 3D and Image J to measure the airway on pretreatment supine cone-beam computed tomography images and derived lateral cephalograms. The patients used Somnodent (Somnomed; Crows Nest, Australia) MAS appliances, which were titrated over 6-8 weeks. Appliance titration measurements and pre- and posttreatment polysomnograms were assessed. Respiratory disturbance index (RDI), absolute and percentage changes in RDI, non-rapid eye movement (NREM) RDI, rapid eye movement (REM) RDI, supine and nonsupine NREM and REM RDI, and minimal blood-oxygen saturation variables were evaluated. The associations of measurements from 2D and 3D minimal anterior-posterior linear distance and 3D airway variables with MAS treatment response were estimated.

Results And Conclusions: Combined effects of baseline total airway volume, body mass index, neck circumference, location of minimal cross sectional area, and OSA severity were associated with treatment response. Patients with higher initial OSA and more superiorly located airway constriction showed enhanced treatment response to MAS therapy. Airway constriction due to maxillofacial disproportions rather than soft tissue obstruction also showed better treatment response. No significant relationships were found in lateral cephalogram measurements.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.ajodo.2018.05.022DOI Listing

Publication Analysis

Top Keywords

treatment response
20
airway variables
8
obstructive sleep
8
sleep apnea
8
mandibular advancement
8
advancement splint
8
mas therapy
8
eye movement
8
rem rdi
8
airway constriction
8

Similar Publications

Drug Development.

Alzheimers Dement

December 2024

Alzheimer Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, Amsterdam, North Holland, Netherlands.

The lack of an in-vivo pathology marker for synuclein pathology has been a long standing challenge for dementia for Lewy bodies (DLB) research. This issue is critically important for phase II trials, which are often small, requiring the precise measurement of the biological effects, whether disease modifying or symptomatic. Recent advances have enabled the determination of alpha-synuclein pathology status with CSF measurements, using aggregation assays [RT-QUIC].

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Eisai Inc., Nutley, NJ, USA.

Background: Lecanemab is a humanized IgG1 monoclonal antibody that binds with high affinity to Aβ soluble protofibrils. In two clinical studies (phase 2, NCT01767311 and phase 3 ClarityAD, NCT03887455) in early Alzheimer's disease, lecanemab substantially reduced amyloid PET and significantly slowed clinical decline on multiple measures of cognition and function, including CDR-SB at 18 months. Models describing the change in amyloid PET and CDR-SB in response to lecanemab treatment were used to explore the impact of changing from the initial dosage regimen (10 mg/kg every 2 weeks [Q2W]) to a less intensive maintenance dosing regimen (10 mg/kg every 4 weeks [Q4W]) on clinical efficacy, and to explore the optimal duration of the initial dosing regimen.

View Article and Find Full Text PDF

Drug Development.

Alzheimers Dement

December 2024

Biogen, Cambridge, MA, USA.

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) composed of tau aggregates. Research in animal models has generated hypotheses on the underlying mechanisms of the interaction between Aβ and tau pathology. In support of this interaction, results from clinical trials have shown that treatment with anti-Aβ monoclonal antibodies (mAbs) affects tau pathology.

View Article and Find Full Text PDF

Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.

View Article and Find Full Text PDF

Background: Developing drugs for treating Alzheimer's disease (AD) has been extremely challenging and costly due to limited knowledge on underlying biological mechanisms and therapeutic targets. Repurposing drugs or their combination has shown potential in accelerating drug development due to the reduced drug toxicity while targeting multiple pathologies.

Method: To address the challenge in AD drug development, we developed a multi-task machine learning pipeline to integrate a comprehensive knowledge graph on biological/pharmacological interactions and multi-level evidence on drug efficacy, to identify repurposable drugs and their combination candidates RESULT: Using the drug embedding from the heterogeneous graph representation model, we ranked drug candidates based on evidence from post-treatment transcriptomic patterns, mechanistic efficacy in preclinical models, population-based treatment effect, and Phase 2/3 clinical trials.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!