A mandibular advancement device attenuates the abnormal morphology and function of mitochondria from the genioglossus in obstructive sleep apnea–hypopnea syndrome rabbits

Abstract Background Obstructive sleep apnea hypopnea syndrome (OSAHS) is a serious and potentially life‐threatening disease. Mandibular advancement device (MAD) has the characteristics of non‐invasive, comfortable, portable and low‐cost, making it the preferred treatment for mild‐to‐moderate OSAHS. Our previous studies found that abnormal contractility and fibre type distribution of the genioglossus could be caused by OSAHS. However, whether the mitochondria participate in these tissue changes is unclear. The effect of MAD treatment on the mitochondria of the genioglossus in OSAHS is also uncertain. Objective To examine the morphology and function of mitochondria from the genioglossus in a rabbit model of obstructive sleep apnea–hypopnea syndrome (OSAHS), as well as these factors after insertion of a mandibular advancement device (MAD). Methods Thirty male New Zealand white rabbits were randomised into three groups: control, OSAHS and MAD, with 10 rabbits in each group. Animals in Group OSAHS and Group MAD were induced to develop OSAHS by injection of gel into the submucosal muscular layer of the soft palate. The rabbits in Group MAD were fitted with a MAD. The animals in the control group were not treated. Further, polysomnography (PSG) and cone‐beam computed tomography (CBCT) scan were used to measure MAD effectiveness. CBCT of the upper airway and PSG suggested that MAD was effective. Rabbits in the three groups were induced to sleep for 4–6 h per day for eight consecutive weeks. The genioglossus was harvested and detected by optical microscopy and transmission electron microscopy. The mitochondrial membrane potential was determined by laser confocal microscopy and flow cytometry. Mitochondrial complex I and IV activities were detected by mitochondrial complex assay kits. Results OSAHS‐like symptoms were induced successfully in Group OSAHS and rescued by MAD treatment. The relative values of the mitochondrial membrane potential, mitochondrial complex I activity and complex IV activity were significantly lower in Group OSAHS than in the control group; however, there was no significant difference between Group MAD and the control group. The OSAHS‐induced injury and the dysfunctional mitochondria of the genioglossus muscle were reduced by MAD treatment. Conclusion Damaged mitochondrial structure and function were induced by OSAHS and could be attenuated by MAD treatment.