Accéder au contenu
Merck

Sleep deprivation worsened oral ulcers and delayed healing process in an experimental rat model.

Life sciences (2019-06-25)
Pan Chen, Hongliang Yao, Weiwei Su, Yudong He, Keling Cheng, Yonggang Wang, Wei Peng, Peibo Li
RÉSUMÉ

Sleep deficiency has been reported to be associated with some oral health problems. Oral ulcers are very common lesions of the oral mucosa, which severely impact patients' quality of life. However, the association between sleep deficiency and the oral ulcer remains unknown. The present study aims to explore the effects of sleep deficiency on oral ulcers. Rats were divided into normal control group (n = 30) and oral ulcer group (OU group, n = 50). Model rats with phenol-induced oral ulcers were deprived of sleep for 72 h by using the modified multiple platform technique. Sleep deprivation worsened oral ulcers and delayed healing process in rats. In addition, sleep deprivation increased the γ-aminobutyric acid (GABA, P < 0.01) and 5-hydroxytryptamine (5-HT, P < 0.05) levels in serum and brain, the corticotrophin (ACTH, P < 0.05), corticosterone (CORT, P < 0.01), immunoglobulin (Ig)M (P < 0.01), tumor necrosis factor-alpha (TNF-α) (P < 0.01), interleukin (IL)-1β (P < 0.01), IL-6 (P < 0.01), IL-8 (P < 0.01), monocyte chemoattractant protein-1 (MCP-1) (P < 0.01), and 8-hydroxy-deoxyguanosine (8-OHdG, P < 0.01) levels in serum. Sleep deprivation also up-regulated malonaldehyde (MDA) (P < 0.05), TNF-α (P < 0.05), and IL-1β (P < 0.01) levels in oral mucosa tissue and delayed superoxide dismutase (SOD, P < 0.05) activity recovery. These data suggest that sleep deprivation impaired the oral ulcer healing in rat oral mucosa, and the mechanisms of this effect are probably related to neuro-immuno-endocrine system and oxidative stress.