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Syftet med studien var att undersöka patientupplevelsen vid behandling med sömnapnéskena hos patienter med diagnosen obstruktiv sömnapné utförda i allmän tandvårdspraxis. Studien genomfördes som en tvärsnittsundersökning i en av de större regionerna i Sverige, region Skåne. Undersökningen var retrospektiv i sin design och bestod av en enkät sänd till de patienter med en verifierad obstruktiv sömnapné som fått sin odontologiska behandling som ett led i sjukdomsbehandling. Behandlingen skulle ha pågått minst 6 månader. Enkäten skickades ut till 1148 patienter, varav 738 svarade (64 %). Enkäten bestod av 70 frågor och påståenden inom olika domäner som: allmänhälsa/livsstil, användning av sömnapnéskena, symtomförändringar, sömnrelaterade upplevelseförändringar, vårdbemötande, utvärdering av behandling, värde av behandling, förändringar i livssituation och dagsömnighet.Behandling med sömnapnéskena gav symtomlindring vid obstruktiv sömnapné för majoriteten av patienterna. Livskvalitet, somatiska och kognitiva symtom förändrades signifikant positivt för patienterna som använde sin behandling frekvent. Dagtröttheten reducerades för majoriteten av de behandlade patienterna. Nöjdhet med behandlingen och att rekommendera liknande behandling för en vän var hög.Behandling av obstruktiv sömnapné med intra-oral apparatur utförd i allmän praxis lindrade tillståndet och dess konsekvenser enligt patientens egenbedömning. / The purpose of this study was to investigate the patient’s experiences in treatment of obstructive sleep apnoea with a mandibular advancement oral appliance conducted in general dental practice. The study was conducted to study a cross-section of patients in one of the major regions of Sweden, region Scania. The study was retrospective in its design and consisted of a postal questionnaire to 1148 patients with a treatment period of more than 6 months. The questionnaire comprised 70 questions and assertions in various domains: general health/ lifestyle, use of oral appliance, changes in symptoms, sleep-related experience changes, evaluation of treatment, value of treatment, changes in life situation and daytime sleepiness. The responder rate was 64%. Treatment with oral appliance gave relief of symptoms in the majority of patients with obstructive sleep apnoea. Quality of life, somatic and cognitive symptoms changed significant positively in patients who used the treatment frequent. The daytime sleepiness was reduced for the majority of the treated patients. The satisfaction with the treatment and the will to recommend a similar treatment for a friend was high. Treatment of obstructive sleep apnoea with an oral appliance performed in general dental practice relieved the condition and its consequences according to the patient's own judgement.

Objective: Obstructive sleep apnea (OSA) is defined by recurrent breathing cessations accompanied by a collapse of the pharyngeal airway. Co-morbid conditions include obesity, cardiovascular disease, diabetes, and in some cases, retrognathia and muscle dysfunction. The latter two conditions may prompt orthognathic correction. Past investigations have shown a genetic association with OSA. Given that masseter muscle influences skeletal malocclusion and is active during OSA, we investigated whether the expression of OSA-associated genes is altered in a Class II open bite OSA subject. Methods: Eleven mandibular advancement surgery patients were classified as skeletal Class II or III and open or deep bite malocclusion, including a Class II open bite patient with OSA. Masseter muscle samples were collected at surgery and frozen. Tissue was used for gene expression analysis on Affymetrix HT2.0 microarray chips and quantitative RT-PCR. Data for ten genes associated with OSA were individually evaluated in the microarray and compared between the OSA patient and eight symmetrical malocclusion subjects. In order to corroborate these expression data, one gene of interest, tumor necrosis factor (TNF), was quantified in the ten malocclusion subjects from the microarray, an OSA subject from the microarray and one additional OSA subject by RT-PCR. Results: Among OSA-associated genes on the microarray, interleukin genes IL1B, IL1R2, IL6 and IL8 were +2.5 to +9.2 fold greater (p < 0.02) and chemokine genes CCL2, CCL3, CCL3L3, CCL4 and CXCR1 were +2.0 to +12.1 fold greater (p < 0.05). Likewise, TNF expression differed significantly in the muscle of the OSA subject (+2.2 fold greater; p < 0.001). By quantitative RT-PCR, TNF expression was significantly greater in malocclusion subjects with OSA compared to those without OSA (p = 0.0004). Conclusions: Our findings support evidence that OSA is an inflammatory disorder, which may elicit hypoxia-induced inflammatory responses believed to promote skeletal muscle dysfunction. Specifically, we report that inflammatory gene expression is significantly increased in masseter muscle in Class II open bite subjects with OSA. In turn, malocclusion may contribute to OSA, which negatively affects masseter function, resulting in exacerbation of both disorders. Because OSA is reported to associate with a polymorphism in the TNF-alpha; gene in children, future studies are needed to test for similar genetic associations in malocclusion subjects with OSA. / Oral Biology

Introduction: Untreated obstructive sleep apnea (OSA) has deleterious effects on one's overall health. Recent literature suggests that craniofacial abnormalities, as noted on a lateral cephalometric radiograph (ceph) or clinically by the presence of a posterior crossbite, may be associated with OSA. Literature also suggests that if abnormal ceph measurements are noted or if a patient presents with a posterior crossbite, then further questioning about that patients sleep habits and snoring should be addressed. The primary purpose of this study is to explore any possible associations between ceph measurements, and/or presence of a posterior crossbite with OSA, as determined by the Berlin sleep questionnaire, in the orthodontic population. The second purpose of this research is to outline a part 2 follow-up study through administration of an at home sleep test, the Nox-T3 sleep monitor, to further validate presence of OSA. The overall goal is to see if the combined data from the Berlin score, the clinical presence or absence of a posterior crossbite, and standard orthodontic ceph measurements can increase the predictive value of patients in the orthodontic office who might be suffering from obstructive sleep apnea. Methods: A total of 85 consecutive subjects who were already undergoing records in 5 private practice orthodontic offices around the greater Philadelphia area were recruited for voluntary participation in the study. A Berlin questionnaire, lateral ceph, and any noted presence of a posterior crossbite were collected on all subjects. 12 ceph measurements (SNA, SNB, ANB, Co-A, Co-Gn, A-Na perp, Pg-Na perp, SN-MP, FH-MP, Ba-SN, Wits, and MP-Hyoid) were traced by a second year orthodontic resident. 5 subjects were then selected using a random numbers table and given the Nox-T3 sleep monitor for self-administration to record their sleep for one night. Statistical analyses were run using SAS version 9.2 to evaluate any associations. Results: A total of 76 subjects completed data collection, whereas 9 subjects either failed to report their height, and/or weight, and/or failed to complete the Berlin questionnaire in its entirety thus excluding them from the study. A total of 11, or 14% of subjects scored high on the Berlin, meaning a high risk of suffering from OSA. Of all ceph measurements, the only one that showed a statistically significant association with the high Berlin score was MP-Hyoid (p=0.0033). BMI alone was not found to be associated with the Berlin score (p=0.3712). Presence of a posterior crossbite also did not show any correlation with the Berlin score (p= 0.1000). Conclusions: 1) BMI was not found to be associated with the Berlin score among the orthodontic subject population. 2) MP-hyoid was found to be associated with the Berlin score, at a high level of statistical significance. 3) All other cephalometric measurements, including SNA, SNB, ANB, Co-A, Co-Gn, A-Na perp, Pg-Na perp, SN-MP, FH-MP, Ba-SN, and Wits, failed to show any statistically significant correlation to the Berlin score. 4) Posterior crossbite was not found to be associated with the Berlin Score among the orthodontic subject population. Key words: Obstructive sleep apnea, Berlin sleep questionnaire, cephalometric, posterior crossbite, Nox-T3 sleep monitor, orthodontic population / Oral Biology

No description available.

Bakgrund: Obstruktivt sömnapnésyndrom (OSA) kan påverkas positivt av fysioterapeutiska interventioner. Det är därför intressant att veta hur initial motivation och self-efficacy påverkar livsstilsförändring i form av fysisk aktivitetsnivå och fysisk kapacitet. Syfte: Undersöka hur initial motivation och self-efficacy förändrar fysisk aktivitetsnivå, och hur initial self-efficacy förändrar fysisk kapacitet, hos personer med OSA. Metod: Kvantitativ dataanalys med data från en tidigare RCT där personer med OSA fick Behavioral Sleep Medicine. Motivation (vid baslinje) och self-efficacy (vid baslinje) korrelerades med förändringen av fysisk aktivitetsnivå (från baslinje till 6 månader), och motivation (vid baslinje) korrelerades med förändringen av fysisk kapacitet (från baslinje till 6 månader). Kontroll- och interventionsgruppen jämfördes även i skillnad på aktivitetsnivå mellan baslinje och 6 månader. Resultat: Inga statistiskt signifikanta samband kunde påvisas mellan motivation och förändring av fysisk aktivitetsnivå (p = 0.439 och 0.615 för kontroll- respektive interventionsgruppen), motivation och förändring av fysisk kapacitet (p = 0.538 och 0.375 för kontroll- respektive interventionsgruppen), self-efficacy och förändring av fysisk aktivitetsnivå (p = 0.392 och 0.925 för kontroll- respektive interventionsgruppen), eller skillnad i förändring av aktivitetsnivå mellan kontroll- respektive interventionsgrupp (p = 0.545). Konklusion: Ingen tydlig koppling mellan initial motivation och self-efficacy till förändring av fysisk aktivitetsnivå och fysisk kapacitet kunde påvisas hos personer med OSA. / Background: Obstructive sleep apnea (OSA) can be positively affected by physiotherapeutic interventions. It is therefore interesting to know how motivation and self-efficacy affects lifestyle changes in the form of physical activity level and physical capacity. Purpose: To analyze how initial motivation and self-efficacy changes physical activity levels, and how initial motivation changes physical capacity, in people with OSA. Method: Quantitative data analysis using data from a previous RCT in which people with OSA were treated with Behavioral Sleep Medicine. Motivation (at baseline) and self-efficacy (at baseline) was correlated with the change in physical activity levels (from baseline to 6 months), and motivation (at baseline) was correlated with the change in physical capacity (from baseline to 6 months). The difference in the change in activity levels from baseline to 6 months was also compared between the control and intervention groups. Results: No statistically significant correlations were found between motivation and physical activity level (p = 0.439 and 0.615 for the control and intervention group respectively), motivation and physical capacity (p = 0.538 and 0.375 for the control and intervention group respectively), self-efficacy and change of physical activity level (p = 0.392 and 0.925 for the control and intervention group respectively), or difference in the control versus intervention group regarding change in physical activity level (p = 0.545). Conclusion: No clear connection between initial motivation and self-efficacy to change in physical activity levels and physical capacity could be found in people with OSA.

The purpose of the current study was to test the hypothesis that chronic hypoxia associated with sleep-disordered breathing relates to abnormal Nitric Oxide (NO) production and vascular endothelial growth factor (VEGF) expression patterns that contribute to aberrancy of specific determinates of cardiovascular and cardiopulmonary function before, during, and after graded exercise. These patterns may further reflect pathologic alteration of signaling within the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt-1) transduction network. To this end, 7 medically diagnosed OSA patients (3 male, 4 female), mean age 48 years and 7 apparently healthy control subjects (3 male, 4 female), mean age 42 years, underwent baseline venous blood draws and maximal bicycle ergometry. Mononuclear cells isolated from peripheral blood were utilized as reporter cells for measurement of VEGF, Akt-1, hypoxia inducible factor-1 alpha (HIF-1 alpha), and vascular endothelial growth factor receptor-2 (VEGFR2) gene expression by redundant oligonucleotide DNA microarray and real-time PCR technologies. Circulating angiogenic progenitor cells expressing VEGFR2 were profiled by flow cytometry. Plasma and serum concentrations of VEGF, nitrates/nitrites, catecholamines, and dopamine were measured by enzyme-linked immunosorbent assay (ELISA) and high performance liquid chromatography (HPLC). Arterial blood pressure, cardiac output, oxygen consumption and total peripheral resistance were determined at Baseline, 100W, and peak ergometric stress by standard techniques. There were no apparent differences (p < .05) observed in biochemical markers relating to vascular function and adaptation including, serum nitrates/nitrites, norepinephrine, dopamine, and plasma VEGF. No differences were found relative to cardiac output, stroke volume, cardiopulmonary or myocardial oxygen consumption, expired ventilation, heart rate, arteriovenous oxygen difference, total peripheral resistance, and mean arterial pressure. Due to methodological issues related to the redundant oligonucleotide DNA microarray and real-time PCR gene expression analyses, results of these experiments were uninterpretable. Thus, the research hypothesis was rejected. Conversely, significant (p < .05) differences were observed in waist: hip ratios, recovery: peak systolic blood pressure ratio at 1 minute post-exercise and %VEGFR2 expression. OSA was associated with elevations in both waist: hip ratios and recovery: peak systolic blood pressure ratio at 1 minute post-exercise as well as significant depression of %VEGFR2 profiles. Moreover, significant negative correlations were found regarding waist: hip ratios and %VEGFR2 expression (r = -.69;p =.005) and recovery: peak systolic blood pressure ratio at 1 minute post-exercise and %VEGFR2 expression (r = -.65;p =.01). These findings did not provide evidence that NO-dependent vasoactive mechanisms are suppressed nor did they support the supposition that angiogenic mechanisms are pathologically activated in sleep-disordered breathing. / Ph. D.

Obstructive sleep apnea syndrome (OSAS), a chronic respiratory disorder affecting as many as 1 in 5 adults, is associated with repetitive collapse of the upper airway during sleep and results in fragmented sleep and intermittent periods of hypoxia and hypercapnia. If left untreated, OSAS increases the risk for hypertension, insulin resistance, metabolic syndrome (MetS) in a manner that is independent of obesity in mid-adulthood. However, it is still unknown if evidence of these relationships is apparent in young adults with OSAS who are otherwise healthy and free of other chronic comorbidities. Objectives: To determine if functional and biochemical evidence of insulin resistance, MetS, and vascular endothelial dysfunction (VED) exists in young, overweight men with OSAS and if the combined effects of obesity and OSAS augments the evidence of chronic disease pathogenesis beyond the effects of obesity alone. Subjects: Subjects were 12 overweight men with OSAS (age = 22.8 ± 0.8; BMI = 32.4 ± 1.0; apnea-hypopnea index (AHI) = 25.4 ± 5.4), 17 overweight men without OSAS (age = 22.5 ± 0.7; BMI = 31.6 ± 1.1; AHI = 2.2 ± 0.3), and 18 normal weight men without OSAS (age = 21.1 ± 0.5; BMI = 22.4 ± 0.4; AHI = 1.9 ± 0.3). Methods: Subjects were evaluated for OSAS using an unsupervised, portable polysomnography test. Total fat and central abdominal fat (CAF) were assessed using dual energy x-ray absorptiometry (DEXA). Fasting blood samples were used to quantify biochemical markers for insulin resistance (glucose, insulin, adiponectin, IL-6, and TNF-á) and endothelial dysfunction (CRP, VEGF, and VEGFR2) using ELISA, RIA, and flow cytometry. MetS was defined according to Adult Treatment Panel III (ATP III) clinical standards. Triglycerides, HDL cholesterol, and glucose were measured using a commercial lipid panel. Resting blood pressure was obtained manually via auscultation. VED was measured via strain gauge plethysmography, with endothelium-dependent vasodilatation being assessed from forearm reactive hyperemia after a 5-minute period of upper arm occlusion. Statistics: One-way ANOVA was used to determine group differences in variables. Two-way ANOVA was used to evaluate group x time interactions during the 2-minute recovery period following upper arm occlusion. Pearson partial correlation was used to assess relationships between continuous variables, with analyses being controlled for CAF or OSAS severity. Spearman correlation was used to assess relationships between number of MetS components present and both indices of adiposity and OSAS severity. Stepwise multiple linear regression analysis was used to determine significant predictors of OSAS severity, insulin resistance, components of the MetS, and endothelial dysfunction. Results: Overweight subjects with OSAS had more CAF, higher fasting triglycerides, and lower serum adiponectin concentrations than both overweight and normal weight non-apneic controls. Furthermore, fasting triglycerides were directly correlated to OSAS severity, even after the influence of central abdominal fat was removed. OSAS severity was an independent predictor of triglyceride levels, and vice versa. Insulin resistance, leptin, insulin, and CRP were all higher in overweight subjects than controls, but no further differences were attributable to severity of OSAS. No differences in IL-6, TNF-á, ADMA, and expression of VEGFR2 were noted between any groups. No group or group x time interaction differences existed in regards to postocclusive reactive hyperemia responses. Conclusions: Young men with OSAS exhibit several unique anthropometric and biochemical abnormalities that may indicate early pathogenesis of or increased risk for future development for cardiovascular and metabolic disorders. Identification and treatment of OSAS at this age may be critical to prevent the onset and progression of these chronic disorders. / Ph. D.