Injury and Apoptosis in the Palatopharyngeal Muscle in Patients with Obstructive Sleep Apnea-Hypopnea Syndrome.

Abstract

BackgroundThis study aimed to elucidate the possible activity of the mitochondrial-mediated apoptotic pathway (MMAP) in obstructive sleep apnea-hypopnea syndrome (OSAHS).Material/MethodsA control group, a mild OSAHS group, a moderate OSAHS group, and a severe OSAHS group were included. Masson staining, hematoxylin and eosin staining, and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay were performed to assess collagen fiber hyperplasia, pathological morphology, and cell apoptosis, respectively, in muscle samples.ResultsIn the OSAHS groups, the palatopharyngeal muscle fibers were larger, with apparent hypertrophy and increased elastic fiber content. The proportions of type I fibers were markedly higher in the control group than in the moderate and severe OSAHS groups (P<0.05). Moreover, apoptosis was significantly enhanced in the muscle cells of the OSAHS groups. The Bax expression levels gradually increased across the 4 groups (lowest in the control group and highest in the severe OSAHS group) (P<0.05); conversely, the p38 and p62 expression levels did not significantly differ among groups (P>0.05).ConclusionsA decrease in the proportion of the different fiber types can result in collapse of the upper airway. The pathogenesis of OSAHS appears to involve muscle cell apoptosis via MMAP.