Search

Mandibular advancement devices (MADs) have emerged as a popular alternative for the treatment of sleep-disordered breathing. These devices bring the mandibula forward in order to increase upper airway (UA) volume and prevent total UA collapse during sleep. However, the precise mechanism of action appears to be quite complex and is not yet completely understood; this might explain interindividual variation in treatment success. We examined whether an UA model, that combines imaging techniques and computational fluid dynamics (CFD), allows for a prediction of the treatment outcome with MADs. Ten patients that were treated with a custom-made mandibular advancement device (MAD), underwent split-night polysomnography. The morning after the sleep study, a low radiation dose CT scan was scheduled with and without the MAD. The CT examinations allowed for a comparison between the change in UA volume and the anatomical characteristics through the conversion to three-dimensional computer models. Furthermore, the change in UA resistance could be calculated through flow simulations with CFD. Boundary conditions for the model such as mass flow rate and pressure distributions were obtained during the split-night polysomnography. Therefore, the flow modeling was based on a patient specific geometry and patient specific boundary conditions. The results indicated that a decrease in UA resistance and an increase in UA volume correlate with both a clinical and an objective improvement. The results of this pilot study suggest that the outcome of MAD treatment can be predicted using the described UA model.

Neutrophil infiltration to the airway lumen is a common feature of respiratory inflammatory processes. The aim of this study was to evaluate whether different corticosteroids exert any selective effect on the migration of isolated neutrophils. A bilayer of cultured human endothelial and bronchial epithelial cells was used as a model for neutrophil migration through the blood-air barrier. Low spontaneous migration of neutrophils (2.8+/-0.9%, n=8; mean+/-S.E.M.) occurred, while in the absence of any steroid, a migration of 28.5+/-7.6% could be induced by lipopolysaccharide. Pre-incubation during 1 h of epithelial cells with dexamethasone, budesonide, or prednisolone (10(-10)-10(-4) M) showed in all instances a concentration-dependent inhibition following a bell-shaped curve. At 10(-7) M, both dexamethasone and budesonide were on the minimum effect peak of the bell-shaped curve. The peak for prednisolone was found at 10(-8) M. However, when steroid pre-incubation was extended to 4 h, a sigmoid curve was observed, with significant inhibition of migration at concentrations >10(-7) M. Steroids can inhibit neutrophil recruitment through two different pathways with distinct result, depending on the length of incubation time.

Objective: To investigate the pre-and postoperative pattern of upper airway obstruction in obstructive sleep apnea (OSA) patients treated by uvulopalatopharyngoplasty (UPPP).Background: The response rate to UPPP in unselected OSA patients is generally about 50%.Methods: Intraluminal pressure measurements during sleep were employed to analyze the pattern of upper airway obstruction before and after surgery.Results: Ten patients with mild to moderate OSA (respiratory disturbance index 19.7 (16.9-27.5) events/hr underwent a full night polysomnography before and 114 (6 1-138) days after UPPP. UPPP resulted in a significant improvement in subjective snoring and daytime sleepiness, but did not significantly alter the severity of sleep-disordered breathing. Preoperatively, the major site of obstruction was located at the oropharynx in nine patients, seven of them had additional minor obstruction sites outside the oropharynx. Complete relief of upper airway obstruction was only observed in those two patients with collapse confined to the oropharynx.Conclusions: In unselected OSA patients, UPPP improved subjective snoring and daytime sleepiness but did not result in a significant improvement in RDI or sleep architecture. Our results emphasize the need for a pre-operative investigation of the upper airway during sleep to select patients with collapse confined to the oropharynx.

Human alveolar type II cells are thought to play a role in the pathogenesis of lung injury. Patterns of mediator release of arachidonic acid metabolism by type II cells were therefore studied after challenge with calcium ionophore A23187, opsonized zymosan and hydrogen peroxide. A time- and concentration dependent release of cyclooxygenase products was observed, with release of PGE2 greater than 6-keto-PGF1 alpha greater than TxB2. Addition of glutathione or bicarbonate further increased the production of PGE2. N-ethylmaleimide, a sulfhydryl (SH) reactant, induced a dose-dependent increase in the release of TxB2 and 6-keto-PGF1 alpha, but not of PGE2. This relates most likely to the SH-dependency and glutathione requirement of the PGE2 isomerase and SH-independence of thromboxane and prostacyclin isomerase.