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Dental sleep medicine as a discipline was first described about a quarter of a century ago. Snoring, obstructive sleep apnea, sleep bruxism, xerostomia, hypersalivation, gastroesophageal reflux disease, and orofacial pain were identified as dental sleep-related conditions. This scoping review aimed to: i) identify previously unidentified dental sleep-related conditions; and ii) identify the role of oral healthcare pro-viders in the prevention, assessment, and management of dental sleep-related conditions in adults. A systematic literature search was conducted in PubMed, Embase.com, Web of Science, and Cochrane. Studies that reported an actual or likely role of oral healthcare providers in the prevention, assessment, and/or management of sleep-related conditions were included. Of the 273 included studies, 260 were on previously listed dental sleep-related conditions; the other 13 were on burning mouth syndrome. Burning mouth syndrome was therefore added to the list of dental sleep-related conditions for the first aim and categorized into sleep-related orofacial pain. For the second aim, the role of oral healthcare providers was found to be significant in the prevention, assessment, and management of obstructive sleep apnea and sleep bruxism; in the assessment and management of snoring, sleep-related orofacial pain, and oral dryness; and in the assessment of sleep-related gastroesophageal reflux condition.(c) 2022 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Objective: This paper aims to present and describe the Standardised Tool for the Assessment of Bruxism (STAB), an instrument that was developed to provide a multidimensional evaluation of bruxism status, comorbid conditions, aetiology and consequences. Methods: The rationale for creating the tool and the road map that led to the selection of items included in the STAB has been discussed in previous publications. Results: The tool consists of two axes, specifically dedicated to the evaluation of bruxism status and consequences (Axis A) and of bruxism risk and etiological factors and comorbid conditions (Axis B). The tool includes 14 domains, accounting for a total of 66 items. Axis A includes the self-reported information on bruxism status and possible consequences (subject-based report) together with the clinical (examiner report) and instrumental (technology report) assessment. The Subject-Based Assessment (SBA) includes domains on Sleep Bruxism (A1), Awake Bruxism (A2) and Patient's Complaints (A3), with information based on patients' self-report. The Clinically Based Assessment (CBA) includes domains on Joints and Muscles (A4), Intra- and Extra-Oral Tissues (A5) and Teeth and Restorations (A6), based on information collected by an examiner. The Instrumentally Based Assessment (IBA) includes domains on Sleep Bruxism (A7), Awake Bruxism (A8) and the use of Additional Instruments (A9), based on the information gathered with the use of technological devices. Axis B includes the self-reported information (subject-based report) on factors and conditions that may have an etiological or comorbid association with bruxism. It includes domains on Psychosocial Assessment (B1), Concurrent Sleep-related Conditions Assessment (B2), Concurrent Non-Sleep Conditions Assessment (B3), Prescribed Medications and Use of Substances Assessment (B4) and Additional Factors Assessment (B5). As a rule, whenever possible, existing instruments, either in full or partial form (i.e. specific subscales), are included. A user's guide for scoring the different items is also provided to ease administration. Conclusions: The instrument is now ready for on-field testing and further refinement. It can be anticipated that it will help in collecting data on bruxism in such a comprehensive way to have an impact on several clinical and research fields.

Aims Sleep apnoea and congestive heart failure (CHF) commonly co‐exist, but their interaction is unclear. Metabolomics may clarify their interaction and relationships to outcome. Methods and results We assayed 372 circulating metabolites and lipids in 1919 and 1524 participants of the Framingham Heart Study (FHS) (mean age 54 ± 10 years, 53% women) and Women's Health Initiative (WHI) (mean age 67 ± 7 years), respectively. We used linear and Cox regression to relate plasma concentrations of metabolites and lipids to echocardiographic parameters; CHF and its subtypes heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF); and sleep indices. Adenine dinucleotide phosphate (ADP) associated with left ventricular (LV) fractional shortening; phosphocreatine with LV wall thickness; lysosomal storage molecule sphingomyelin 18:2 with LV mass; and nicotine metabolite cotinine with time spent with an oxygen saturation less than 90% (β = 2.3 min, P = 2.3 × 10−5). Pro‐hypertrophic metabolite hydroxyglutarate partly mediated the association between LV wall thickness and HFpEF. Central sleep apnoea was significantly associated with HFpEF (P = 0.03) but not HFrEF (P = 0.5). There were three significant metabolite canonical variates, one of which conferred protection from cardiovascular death [hazard ratio = 0.3 (0.11, 0.81), P = 0.02]. Conclusions Energetic metabolites were associated with cardiac function; energy‐ and lipid‐storage metabolites with LV wall thickness and mass; plasma levels of nicotine metabolite cotinine were associated with increased time spent with a sleep oxygen saturation less than 90%, a clinically significant marker of outcome, indicating a significant hazard for smokers who have sleep apnoea.

Naima Laharnar,1,* Sebastian Herberger,1,* Lisa-Kristin Prochnow,1 Ning-Hung Chen,2 Peter A Cistulli,3,4 Allan I Pack,5 Richard Schwab,5 Brendan T Keenan,5 Diego R Mazzotti,5,6 Ingo Fietze,1,7 Thomas Penzel1,8 1Department of Internal Medicine and Dermatology, Interdisciplinary Center of Sleep Medicine, Charité – Universitätsmedizin Berlin, Berlin, Germany; 2Department of Pulmonary and Critical Care Medicine, Sleep Center, Chang Gung Memorial Hospital, Taipei, Taiwan; 3Charles Perkins Centre, University of Sydney, Sydney, NSW, Australia; 4Department of Respiratory Medicine, Royal North Shore Hospital, Sydney, NSW, Australia; 5Department of Medicine/Division of Sleep Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA; 6Department of Internal Medicine, Division of Medical Informatics, University of Kansas Medical Center, Kansas City, KS, USA; 7The Federal State Autonomous Educational Institution of Higher Education I.M. Sechenov, First Moscow State Medical University of the Ministry of Health of the Russian Federation, Moscow, Russia; 8Department of Biology, Saratov State University, Saratov, Russia*These authors contributed equally to this workCorrespondence: Naima LaharnarDepartment of Internal Medicine and Dermatology, Interdisciplinary Center of Sleep Medicine, Charité – Universitätsmedizin Berlin, Campus Charité Mitte, Chariteplatz 1, Berlin, 10117, GermanyTel +49-30 450 513 120Email naima.laharnar@charite.dePurpose: An early prescreening in suspected obstructive sleep apnea (OSA) patients is desirable to expedite diagnosis and treatment. However, the accuracy and applicability of current prescreening tools is insufficient. We developed and tested an unbiased scoring system based solely on objective variables, which focuses on the diagnosis of severe OSA and exclusion of OSA.Patients and Methods: The OSA prediction score was developed (n = 150) and validated (n = 50) within German sleep center patients that were recruited as part of the Sleep Apnea Global Interdisciplinary Consortium (SAGIC). Six objective variables that were easy to assess and highly correlated with the apnea–hypopnea index were chosen for the score, including some known OSA risk factors: body-mass index, neck circumference, waist circumference, tongue position, male gender, and age (for women only). To test the predictive ability of the score and identify score thresholds, the receiver-operating characteristics (ROC) and curve were calculated.Results: A score ≥ 8 for predicting severe OSA resulted in an area under the ROC curve (ROC-AUC) of 90% (95% confidence interval: 84%, 95%), test accuracy of 82% (75%, 88%), sensitivity of 82% (65%, 93%), specificity of 82% (74%, 88%), and positive likelihood ratio of 4.55 (3.00, 6.90). A score ≤ 5 for predicting the absence of OSA resulted in a ROC-AUC of 89% (83%, 94%), test accuracy of 80% (73%, 86%), sensitivity of 72% (55%, 85%), specificity of 83% (75%, 89%), and positive likelihood ratio of 4.20 (2.66, 6.61). Performance characteristics were comparable in the small validation sample.Conclusion: We introduced a novel prescreening tool combining easily obtainable objective measures with predictive power and high general applicability. The proposed tool successfully predicted severe OSA (important due to its high risk of cardiovascular disease) and the exclusion of OSA (rarely a feature of previous screening instruments, but important for better differential diagnosis and treatment).Keywords: obstructive sleep apnea, diagnostic, sensitivity, specificity, screening

For obstructive sleep apnoea (OSA), few mechanical treatment options are available and no pharmacotherapy is approved [1–3]. However, safe and efficacious pharmacotherapy would have substantial appeal for many people with OSA., BAY 2253651 is a nasally applied genioglossus muscle activator via pharyngeal mucosal receptor stimulation (potassium channel blocker) aimed to treat obstructive sleep apnoea. Although well-tolerated and safe, there was no significant therapeutic effect. https://bit.ly/3zDbyia

BACKGROUND: Prediction tools without patient-reported symptoms could facilitate widespread identification of OSA. RESEARCH QUESTION: What is the diagnostic performance of OSA prediction tools derived from machine learning using readily available data without patient responses to questionnaires? Also, how do they compare with STOP-BANG, an OSA prediction tool, in clinical and community-based samples? STUDY DESIGN AND METHODS: Logistic regression and machine learning techniques, including artificial neural network (ANN), random forests (RF), and kernel support vector machine, were used to determine the ability of age, sex, BMI, and race to predict OSA status. A retrospective cohort of 17,448 subjects from sleep clinics within the international Sleep Apnea Global Interdisciplinary Consortium (SAGIC) were randomly split into training (n = 10,469) and validation (n = 6,979) sets. Model comparisons were performed by using the area under the receiver-operating curve (AUC). Trained models were compared with the STOP-BANG questionnaire in two prospective testing datasets: an independent clinic-based sample from SAGIC (n = 1,613) and a community-based sample from the Sleep Heart Health Study (n = 5,599). RESULTS: The AUCs (95% CI) of the machine learning models were significantly higher than logistic regression (0.61 [0.60-0.62]) in both the training and validation datasets (ANN, 0.68 [0.66-0.69]; RF, 0.68 [0.67-0.70]; and kernel support vector machine, 0.66 [0.65-0.67]). In the SAGIC testing sample, the ANN (0.70 [0.68-0.72]) and RF (0.70 [0.68-0.73]) models had AUCs similar to those of the STOP-BANG (0.71 [0.68-0.72]). In the Sleep Heart Health Study testing sample, the ANN (0.72 [0.71-0.74]) had AUCs similar to those of STOP-BANG (0.72 [0.70-0.73]). INTERPRETATION: OSA prediction tools using machine learning without patient-reported symptoms provide better diagnostic performance than logistic regression. In clinical and community-based samples, the symptomless ANN tool has diagnostic performance similar to that of a widely used prediction tool that includes patient symptoms. Machine learning-derived algorithms may have utility for widespread identification of OSA.

Study Objectives The impact of therapy with continuous positive airway pressure (CPAP) and mandibular advancement device (MAD) has not been directly compared in patients with severe obstructive sleep apnea (OSA). The purpose of this individual participant data meta-analysis was to compare the treatment effects of CPAP and titratable MAD on sleepiness, quality of life, sleep-disordered breathing severity, and sleep structure in patients with severe OSA. Methods Randomized controlled trials (RCTs) that included severe OSA patients were identified in order to compare the impact of the two treatments. Individual data from severe OSA patients were extracted from the databases and pooled for analysis. Results Of the seven studies identified, three crossover RCT and one parallel-group RCT corresponding to 151 patients and 249 observations (125 in the CPAP treatment arm and 124 in the MAD treatment arm) were included in the analysis. Titratable MAD had a similar impact to CPAP on major patient-centered outcomes (sleepiness and quality of life). CPAP was more effective in reducing AHI and ODI. However, the two treatments had a similar impact on sleep structure with an increase of N3 and REM sleep. Finally, treatment adherence and preference were largely in favor of MAD. Conclusion This meta-analysis suggests that MAD represents an effective alternative treatment in severe OSA patients intolerant to CPAP or who prefer alternate therapy.

Galileo Galilei’s quote “measure what is measurable, and make measurable what is not so”\ud has particular relevance to health behaviours, such as physical activity (PA), sitting and\ud sleep, whose measurement during free living is notoriously difficult. To date, much of what\ud we know about how these behaviours affect our health is based on self-report by\ud questionnaires which have limited validity, are prone to bias, and inquire about selective\ud aspects of these behaviours. Although self-reported evidence has made great contributions\ud to shaping public health and exercise medicine policy and guidelines until now1, the ongoing\ud advancements of accelerometry-based measurement and evidence synthesis methods are\ud set to change the landscape. The aim of this editorial is to outline new directions in PA and\ud sleep related epidemiology that open new horizons for guideline development and\ud improvement; and to describe a new research collaboration platform: the Prospective\ud Physical Activity, Sitting, and Sleep consortium (ProPASS).

Avoiding food before bedtime is a widely accepted sleep hygiene practice, yet few studies have assessed meal timing as a risk factor for disrupted sleep. This study examined the relationship between evening meal timing and sleep quality in young adults. A total of N = 793 participants (26% male) aged between 18 and 29 years responded to an online survey, which captured sociodemographic information, lifestyle variables, and sleep characteristics. Meal timing was defined as meals more than 3 h before or within 3 h of bedtime. The outcomes were as follows: one or more nocturnal awakenings, sleep onset latency of &gt, 30 min, and sleep duration of &le, 6 h. Logistic regression analyses showed that eating within 3 h of bedtime was positively associated with nocturnal awakening (OR = 1.61, 95% CI = 1.15&ndash, 2.27) but not long sleep onset latency (1.24, 0.89&ndash, 1.73) or short sleep duration (0.79, 0.49&ndash, 1.26). The relationship remained significant after adjusting for potential confounders of ethnicity and body mass index (OR = 1.43, 95% CI = 1.00&ndash, 2.04). Meal timing appears to be a modifiable risk factor for nocturnal awakenings and disrupted sleep. However, this is a preliminary cross-sectional study and highlights the need for additional research on the influence of the timing of food intake on sleep.

Humans have internal circadian clocks that ensure that important physiological functions occur at specific times of the day. These molecular clocks are regulated at the genomic level and exist in most cells of the body. Multiple circadian resetting cues have been identified, including light, temperature, and food. Recently, oxygen has been identified as a resetting cue, and emerging science indicates that this occurs through interactions at the cellular level between the circadian transcription-translation feedback loop and the hypoxia-inducible pathway (hypoxia-inducible factor; subject of the 2019 Nobel Prize in Physiology or Medicine). This review will cover recently identified relationships between HIF and proteins of the circadian clock. Interactions between the circadian clock and hypoxia could have wide-reaching implications for human diseases, and understanding the molecular mechanisms regulating these overlapping pathways may open up new strategies for drug discovery.

Rationale: Oral appliance therapy is efficacious in many patients with obstructive sleep apnea (OSA), but prediction of treatment outcome is challenging. Small, detailed physiological studies have identified key OSA endotypic traits (pharyngeal collapsibility and loop gain) as determinants of greater oral appliance efficacy. Objectives: We used a clinically applicable method to estimate OSA traits from routine polysomnography and identify an endotype-based subgroup of patients expected to show superior efficacy. Methods: In 93 patients (baseline apnea–hypopnea index [AHI], ≥20 events/h), we examined whether polysomnography-estimated OSA traits (pharyngeal: collapsibility and muscle compensation; nonpharyngeal: loop gain, arousal threshold, and ventilatory response to arousal) were associated with oral appliance efficacy (percentage reduction in AHI from baseline) and could predict responses to treatment. Multivariable regression (with interactions) defined endotype-based subgroups of “predicted” responders and nonresponders (based on 50% reduction in AHI). Treatment efficacy was compared between the predicted subgroups (with cross-validation). Results: Greater oral appliance efficacy was associated with favorable nonpharyngeal traits (lower loop gain, higher arousal threshold, and lower response to arousal), moderate (nonmild, nonsevere) pharyngeal collapsibility, and weaker muscle compensation (overall R(2) = 0.30; adjusted R(2) = 0.19; P = 0.003). Predicted responders (n = 54), compared with predicted nonresponders (n = 39), exhibited a greater reduction in AHI from baseline (mean [95% confidence interval], 73% [66–79] vs. 51% [38–61]; P

Study Objectives Obstructive sleep apnea (OSA) is a serious and costly public health problem. The main medical treatment, continuous positive airway pressure, is efficacious when used, but poorly tolerated in up to 50% of patients. Upper airway reconstructive surgery is available when medical treatments fail but randomized trial evidence supporting its use is limited. This protocol details a randomized controlled trial designed to assess the clinical effectiveness, safety, and cost-effectiveness of a multilevel upper airway surgical procedure for OSA. Methods A prospective, parallel-group, open label, randomized, controlled, multicenter clinical trial in adults with moderate or severe OSA who have failed or refused medical therapies. Six clinical sites in Australia randomly allocated participants in a 1:1 ratio to receive either an upper airway surgical procedure consisting of a modified uvulopalatopharyngoplasty and minimally invasive tongue volume reduction, or to continue with ongoing medical management, and followed them for 6 months. Results Primary outcomes: difference between groups in baseline-adjusted 6 month OSA severity (apnea–hypopnea index) and subjective sleepiness (Epworth Sleepiness Scale). Secondary outcomes: other OSA symptoms (e.g. snoring and objective sleepiness), other polysomnography parameters (e.g. arousal index and 4% oxygen desaturation index), quality of life, 24 hr ambulatory blood pressure, adverse events, and adherence to ongoing medical therapies (medical group). Conclusions The Sleep Apnea Multilevel Surgery (SAMS) trial is of global public health importance for testing the effectiveness and safety of a multilevel surgical procedure for patients with OSA who have failed medical treatment. Clinical Trial Registration Multilevel airway surgery in patients with moderate-severe Obstructive Sleep Apnea (OSA) who have failed medical management to assess change in OSA events and daytime sleepiness. https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366019&isReview=true Australian New Zealand Clinical Trials Registry ACTRN12614000338662, prospectively registered on 31 March 2014.

Aim: The primary aim of this study was to assess the differences in the upper airway morphology between responders and non-responders to mandibular advancement splint (MAS) treatment in obstructive sleep apnoea (OSA) management. The secondary aim was to assess the correlation between the minimum cross-sectional area of the upper airway and the anatomical structures (i.e. mandibular external length, maxillary length, soft palate length, area of the tongue, maxillomandibular enclosure size, and anatomical balance ratio) surrounding the upper airway. The third aim was to assess the differences in the overall skeletal configuration between responders and non-responders to MAS treatment.Methods: Data from 64 patients (23 females and 41 males) diagnosed with OSA by polysomnography (PSG) at baseline and provided with an adjustable MAS were analysed. All patients had NewTom3G cone beam computed tomography (CBCT) scans, performed in the supine position, at baseline. After acclimatization to MAS, follow-up PSG tests were performed to assess the apnoea–hypopnea index (AHI) with the MAS in situ. Responders were defined by a post-treatment AHI less than 10/hour and at least 50 per cent reduction in AHI, and non-responders by a post-treatment AHI at least 10/hour or less than 50 per cent reduction in AHI. Several upper airway and anatomical variables surrounding the upper airway based on CBCT images were measured to determine the differences between responders and non-responders to MAS.Results: There were 36 responders (AHI = 24.8 ± 11.9 at baseline) and 28 non-responders (AHI = 31.2 ± 20.3 at baseline) to MAS. There were no significant differences in the upper airway morphology between responders and non-responders (P = 0.17–0.93) or in the anatomical structure surrounding the upper airway (P = 0.24–0.58).Conclusion: Within the limitations of this study, it can be concluded that there are no significant differences in upper airway morphology and in anatomical structures surrounding the upper airway between responders and non-responders to MAS treatment. These findings suggest that the craniofacial anatomical structures analyzed in this study cannot explain the response to MAS treatment.

Background and objective: Obstructive sleep apnoea (OSA) is a prevalent sleep disorder associated with increased cardiovascular morbidity and mortality. Whether treatment of OSA improves cardiovascular risk remains controversial. Our aim was to determine a consensus opinion of key sleep medicine stakeholder groups as to the cardiovascular benefits of treating moderate–severe OSA. Methods: A multidisciplinary panel was assembled from representatives from the Australasian Sleep Association, Sleep Health Foundation, Australasian Sleep Technologists Association, the Sleep Health Foundation Business Council and the Sleep Disorders Australia patient support group. Three statements reflecting areas of controversy related to cardiovascular benefits of OSA treatment were created. A modified RAND/UCLA appropriateness methodology was applied determining the panel's level of consensus and agreement with each statement. Results: Voting results indicated the panel: (1) remained unsure whether moderate–severe OSA treatment improves rates of cardiovascular events/death, (2) agreed that moderate–severe OSA treatment improves blood pressure in patients with hypertension and (3) mostly agreed that moderate–severe OSA treatment improves left ventricular function in patients with heart failure. Consensus of opinion was achieved for statements (1) and (2), but was narrowly missed for statement (3). Conclusion: The panel believed that findings from large-scale randomized trials indicate that treatment of moderate–severe OSA has not been established to improve cardiovascular event or morbidity/mortality rates. Strong evidence supports the ability of treatment to reduce blood pressure. Whilst many panel members believed that treatment improves left ventricular function, some were uncertain of the clinical significance of this secondary endpoint measure derived from lesser quality evidence. Refereed/Peer-reviewed

PURPOSE: To determine the agreement between the manual scoring of home sleep apnea tests (HSATs) by international sleep technologists and automated scoring systems. METHODS: Fifteen HSATs, previously recorded using a type 3 monitor, were saved in European Data Format. The studies were scored by nine experienced technologists from the sleep centers of the Sleep Apnea Global Interdisciplinary Consortium (SAGIC) using the locally available software. Each study was scored separately by human scorers using the nasal pressure (NP), flow derived from the NP signal (transformed NP), or respiratory inductive plethysmography (RIP) flow. The same procedure was followed using two automated scoring systems: Remlogic (RLG) and Noxturnal (NOX). RESULTS: The intra-class correlation coefficients (ICCs) of the apnea-hypopnea index (AHI) scoring using the NP, transformed NP, and RIP flow were 0.96 [95% CI 0.93–0.99], 0.98 [0.96–0.99], and 0.97 [0.95–0.99], respectively. Using the NP signal, the mean differences in AHI between the average of the manual scoring and the automated systems were – 0.9 ± 3.1/h (AHI(RLG) vs AHI(MANUAL)) and – 1.3 ± 2.6/h (AHI(NOX) vs AHI(MANUAL)). Using the transformed NP, the mean differences in AHI were – 1.9 ± 3.3/h (AHI(RLG) vs AHI(MANUAL)) and 1.6 ± 3.0/h (AHI(NOX) vs AHI(MANUAL)). Using the RIP flow, the mean differences in AHI were – 2.7 ± 4.5/h (AHI(RLG) vs AHI(MANUAL)) and 2.3 ± 3.4/h (AHI(NOX) VS AHI(MANUAL)). CONCLUSIONS: There is very strong agreement in the scoring of the AHI for HSATs between the automated systems and experienced international technologists. Automated scoring of HSATs using commercially available software may be useful to standardize scoring in future endeavors involving international sleep centers.

Study objectives A recent study of patients with moderate-severe obstructive sleep apnea (OSA) in Iceland identified three clinical clusters based on symptoms and comorbidities. We sought to verify this finding in a new cohort in Iceland and examine the generalizability of OSA clusters in an international ethnically diverse cohort. Methods Using data on 972 patients with moderate-severe OSA (apnea-hypopnea index [AHI] ≥ 15 events per hour) recruited from the Sleep Apnea Global Interdisciplinary Consortium (SAGIC), we performed a latent class analysis of 18 self-reported symptom variables, hypertension, cardiovascular disease, and diabetes. Results The original OSA clusters of disturbed sleep, minimally symptomatic, and excessively sleepy replicated among 215 SAGIC patients from Iceland. These clusters also generalized to 757 patients from five other countries. The three clusters had similar average AHI values in both Iceland and the international samples, suggesting clusters are not driven by OSA severity; differences in age, gender, and body mass index were also generally small. Within the international sample, the three original clusters were expanded to five optimal clusters: three were similar to those in Iceland (labeled disturbed sleep, minimal symptoms, and upper airway symptoms with sleepiness) and two were new, less symptomatic clusters (labeled upper airway symptoms dominant and sleepiness dominant). The five clusters showed differences in demographics and AHI, although all were middle-aged (44.6-54.5 years), obese (30.6-35.9 kg/m2), and had severe OSA (42.0-51.4 events per hour) on average. Conclusions Results confirm and extend previously identified clinical clusters in OSA. These clusters provide an opportunity for a more personalized approach to the management of OSA.

Objective To examine whether a social cognitive therapy (SCT) intervention increases continuous positive airway pressure (CPAP) use compared to equivalent social interaction (SI) time. Participants Individuals with obstructive sleep apnea (OSA) referred for CPAP therapy. Intervention Participants received a 30-min group education session regarding OSA and CPAP. Groups of three to four participants were then randomly assigned to an SCT session or social interaction. Measurements CPAP usage was assessed at 7 nights, then 1, 3, and 6 months. The two primary outcomes were adherence, usage ≥ 4 h per night at 6 months, and uptake of CPAP. Questionnaires were given pretreatment and posttreatment. Results Two hundred six individuals were randomized to SI (n = 97) or SCT (n = 109). CPAP uptake was not different between groups (82% in SI, 88% in SCT groups, P = 0.35). There were no differences between groups in adherence: 63-66% at 1 week, and at 6 months 55-47% (P = 0.36). Higher pretreatment apnea-hypopnea index, higher baseline self-efficacy, and use of CPAP (≥ 4 h) at 1 week were independent predictors of CPAP adherence at 6 months. CPAP adherence increased by a factor of 1.8 (odds ratio = 1.8, 95% confidence interval 1.1-3.0) for every one-unit increase in self-efficacy. There was no difference between groups postintervention in self-efficacy scores, sleepiness, mood, or sleep quality. Conclusions In this randomized trial, a single SCT application did not increase adherence when compared with SI time. Although self-efficacy scores prior to CPAP predicted adherence, self-efficacy was not increased by the interventions. Increasing intensity and understanding of SCT interventions may be needed to improve CPAP adherence. Clinical trials registration Australian New Zealand Clinical Trials Registry, ACTRN12607000424404.

We hypothesized that the facial phenotype is closely linked to upper airway anatomy. The aim of this study was to investigate the relationship between surface facial dimensions and upper airway structures using magnetic resonance imaging (MRI) in subjects with obstructive sleep apnea (OSA).Cohort study.Sleep investigation unit.Sixty-nine patients (apnea-hypopnea indexor = 10/h) underwent MRI as part of a study of upper airway anatomy in oral appliance therapy.Measurements of a range of surface facial dimensions and upper airway soft tissue volumes were performed on the MR images using image-analysis software. Pearson correlation analyses were performed.Significant correlations were identified between a number of surface facial dimensions and neck circumference. Significant positive correlations were demonstrated between surface facial dimensions (including facial widths, facial heights, nose width, interocular and intercanthal widths) and upper airway structures. The strongest associations were between the tongue volume and the midface width (r = 0.70, P0.001), and lower-face width (r = 0.60, P0.001). Surface facial dimensions in combination were also strong determinants for tongue volume (r2 = 0.69). Correlations between surface soft tissue thickness and upper airway soft tissue volumes occurred at the level of the midface but not at the level of the lower face.This study demonstrates that there is a relationship between surface facial dimensions and upper airway structures in subjects with OSA. These findings support the potential role of surface facial measurements in anatomic phenotyping for OSA.

THE CLINICAL SPECTRUM OF OBSTRUCTIVE SLEEP APNEA HAS EXPANDED WIDELY SINCE THE EARLIEST REPORTS OF THE CONDITION. TODAY, OSA IS KNOWN to be a multisystem disorder, with evidence of wide-ranging consequences, including neurocognitive, cardiovascular, endocrine, and metabolic sequelae. In this issue of SLEEP, Epstein and colleagues provide new evidence implicating OSA as an independent risk factor for pulmonary embolism (PE), potentially further expanding the clinical spectrum of OSA. PE is a common and potentially fatal disease with a highly variable clinical presentation. It can occur in acute or chronic forms. Most pulmonary emboli arise from thrombi in the deep veins of the lower limbs (deep vein thrombosis – DVT). The process by which thrombi occur and propagate through the veins is known as venous thromboembolism (VTE), the collective term for DVT and PE. The incidence of VTE is approximately 100 per 100,000, rises exponentially with age, and varies according to risk factors. Clinical risk factors include immobility, hospitalization, surgery, major trauma, malignancy, pregnancy, and drugs (e.g., oral contraceptives, hormone replacement therapy). In addition, there are factors that overlap with those for coronary artery disease including diabetes, smoking, obesity, hypertension, and dyslipidemia. Overall, 25% to 50% of patients with first-time VTE do not have a readily identifiable risk factor.2 Epstein and colleagues1 raise the question of whether OSA should be added to the list of VTE risk factors. While a potential association between OSA and PE has been previously reported in the literature, the study by Epstein et al.,1 is a big step forward because it is the first controlled study to examine this potentially important association. They performed a prospective, cross-sectional study aimed at determining the prevalence of snoring and OSA risk in patients undergoing computed tomographic (CT) pulmonary angiography for suspected acute PE in a tertiary care teaching hospital setting. Snoring and OSA risk (assessed by the Berlin questionnaire) were compared between patients proven to have PE and a control group of patients with negative CT pulmonary angiograms. The key findings were that PE patients had a higher prevalence of snoring (OR 2.91; 95% CI: 1.60, 5.33, P = 0.001), and a higher OSA risk (OR 3.25; 95% CI: 1.84, 5.72, P < 0.001). Multivariate analyses, incorporating age, gender, hereditary risk factors and OSA risk, showed significant associations of PE with male gender (OR 2.37), presence of hereditary risk factors (OR 4.37), and OSA risk (OR 2.78), the latter suggesting a possible independent association between PE and OSA. These findings1 are novel and potentially important but need to be interpreted with caution, particularly given that OSA risk was assessed by questionnaire rather than objective measures. Beyond this important limitation, the cross-sectional study design does not provide direct evidence of a cause-effect relationship. It certainly remains possible that the association is simply attributable to shared risk factors. Nevertheless, there is some attraction to the possibility of a cause-effect relationship, given the recent advances in our understanding of vascular biology in OSA. It has been theorized that VTE results from alterations in blood flow, vascular endothelial injury and alterations in coagulability (inherited or acquired), or a combination thereof (Virchow's triad). OSA could potentially influence all three mechanistic pathways. Part of the answer for the association may lie in the common pathways that promote both VTE and arterial thrombosis and that are also causally related to OSA. The evidence implicating diabetes, smoking, obesity, hypertension, and dyslipidemia not only in arterial thrombosis but also in venous thromboembolic events comes from several large scale cross-sectional and cohort studies.3–4 VTE and atherothrombosis may both be caused by similar pathogenic processes (including increases in oxidative stress and vascular inflammation) that promote endothelial dysfunction in both vascular beds. Several inflammatory markers including CRP, IL-6, and TNF-alpha have been associated with increased venous thrombosis.5 Ultimately, the resulting endothelial dysfunction may lead to increased expression of von Willebrand factor, tissue factor, plasminogen activator inhibitor (PAI-1), and Factor V, which may all promote the development of a thrombus.6 These same cardiovascular risk factors and pathogenic processes are also commonly associated with OSA. Some of them are well known risk factors for OSA (obesity and smoking), while the remainder may be a consequence of OSA. Apart from hypertension, which was not a contributing factor in the study by Epstein et al.,1 and dyslipidemia, which was not documented, there are several mechanisms that are causally related to OSA that may play a role in VTE genesis. Although studies have linked OSA to arterial disease, it is noteworthy that a majority have actually derived measurements from the venous circulation. They include oxidative stress7 and inflammation8 as well as endothelial dysfunction in both the arterial 9and venous10 beds. It is also noteworthy that the increase in endothelial progenitor cells and other factors linked to endothelial function and dysfunction were also measured from venous circulation.11 The end result of endothelial dysfunction is the development of a pro-thrombotic tendency, which is supported by studies cited by Epstein et al.1 and more recently by both OSA clinic12 and community13 studies. It is also feasible that OSA-related hemodynamic alterations may affect venous flow and therefore predispose to thrombosis. Immobility is known to predispose to DVT, raising the possibility that inactivity associated with OSA could be an additional factor. However, there is conflicting evidence of inactivity in OSA.14 The work of Epstein et al.1 challenges the sleep field to undertake further studies to verify the presence and nature of the association between OSA and VTE since both disorders are associated with significant morbidity and mortality. This will likely require longitudinal studies of large numbers of well-characterized patient groups to help tease out cause and effect, in addition to mechanistic studies to help narrow down the pathways involved. It is hoped that the lessons learned from cardiovascular research in the OSA field over the last decade will pave the way forward.

OBSTRUCTIVE SLEEP APNEA (OSA) IS A COMMON DISORDER IN WHICH RECURRENT SLEEP RELATED UPPER AIRWAY OBSTRUCTION CAUSES SLEEP fragmentation and intermittent hypoxemia. Ethnicity has been suggested as an important risk factor for OSA. However, defining the role of ethnicity is complex, as it incorporates genetic, environmental, and cultural factors that can, individually or in combination, influence the other recognized risk factors for OSA. Whilst earlier prevalence studies suggest that OSA may be more common in certain ethnic groups,1,2 recent data in Hong Kong Chinese,3 Indians4 and Koreans5 suggest that OSA prevalence in these ethnic groups are not dissimilar to the Caucasian populations.6 Obesity and craniofacial factors are well recognized in the pathogenesis of OSA. It is also becoming clear that the balance and interaction between these two risk factors is crucial in the development of OSA.7,8 It is likely that such interaction is strongly influenced by ethnicity. Cephalometric studies have suggested that craniofacial factors are important determinants of OSA risk in Asian cohorts.9–11 Similarly, studies evaluating the role of obesity suggest that whilst it is a consistent risk factor for OSA across ethnic groups, the risk attributable to obesity differs between racial groups.3,6 Despite suffering from a similar degree of OSA, patients from Asian groups are generally less overweight compared to their Caucasian counterparts, suggesting that ethnicity may differentially influence the attribution of these OSA risk factors. To date, studies that have explored these complex interactions remain limited, especially in a direct inter-ethnic comparison. Hence the aim of this study was to explore the differences in craniofacial structures and obesity between Caucasian and Chinese patients with OSA.

It has been recognized that nasal airway resistance (NAR) is elevated in patients with OSA. However, little is known regarding the influence of nasal resistance on mandibular advancement splint (MAS) treatment outcome in OSA patient. We hypothesized that nasal resistance differs between MAS responders and nonresponders and therefore may influence treatment outcome. Thirty-eight patients with known OSA underwent polysomnography while wearing a custom-made MAS. Treatment outcome was defined as follows: Responders (R) ≥50% reduction in AHI, and Nonresponders (NR) as

Background Quadriplegia is a severe, catastrophic injury that predominantly affects people early in life, resulting in lifelong physical disability. Obstructive sleep apnoea is a direct consequence of quadriplegia and is associated with neurocognitive deficits, sleepiness and reduced quality of life. The usual treatment for sleep apnoea is nasal continuous positive airway pressure (CPAP); however, this is poorly tolerated in quadriplegia. To encourage patients to use this therapy, we have to demonstrate that the benefits outweigh the inconvenience. We therefore propose a prospective, multinational randomized controlled trial of three months of CPAP for obstructive sleep apnoea after acute quadriplegia. Methods/design Specialist spinal cord injury centres across Australia, New Zealand, the UK and Canada will recruit medically stable individuals who have sustained a (new) traumatic quadriplegia (complete or incomplete second cervical to first thoracic level lesions). Participants will be screened for obstructive sleep apnoea using full, portable sleep studies. Those with an apnoea hypopnoea index greater than 10 per hour will proceed to an initial three-night trial of CPAP. Those who can tolerate CPAP for at least 4 hours on at least one night of the initial trial will be randomized to either usual care or a 3-month period of auto-titrating CPAP. The primary hypothesis is that nocturnal CPAP will improve neuropsychological functioning more than usual care alone. The secondary hypothesis is that the magnitude of improvement of neuropsychological function will be predicted by the severity of baseline sleepiness measures, sleep fragmentation and sleep apnoea. Neuropsychological tests and full polysomnography will be performed at baseline and 3 months with interim measures of sleepiness and symptoms of autonomic dysfunction measured weekly. Spirometry will be performed monthly. Neuropsychological tests will be administered by blinded assessors. Recruitment commenced in July 2009. Discussion The results of this trial will demonstrate the effect of nocturnal CPAP treatment of obstructive sleep apnoea in acute quadriplegia. If CPAP can improve neurocognitive function after injury, it is likely that rehabilitation and subsequent community participation will be substantially improved for this group of predominantly young and severely physically disabled people. Trial registration Australian New Zealand Clinical Trial Registry ACTRN12605000799651