Abstract
There is low evidence for the possible association between obstructive sleep apnea-hypopnea syndrome (OSAHS) and periodontitis, necessitating further research. This study was aimed at investigating this association. For the in vitro study, 8-day-old Wistar rats were divided into the unilateral nasal obstruction group (UNO) and the sham surgery group (SHAM). Rats in the former group were subjected to UNO by cauterization of the external nostril at the age of 8 days. Immunofluorescence analysis, quantitative real-time polymerase chain reaction, and western blot were performed to assess the expression of thioredoxin-interacting protein (TXNIP), NLR family pyrin domain-containing 3 (NLRP3) inflammasome-associated factors, and interleukin-1β (IL-1β). Throughout the experimental period, the weights of rats in the two groups were similar. The mRNA and protein expression of TXNIP and IL-1β was significantly higher in the UNO than in the SHAM groups. Compared with SHAM, NLRP3 inflammasome-associated factors were activated in the UNO group. For the in vitro study, a cellular hypoxia model was established by treating human periodontal ligament cells (HPDLCs) with cobalt chloride. The studies showed that hypoxia can induce an excessive production and accumulation of reactive oxygen species (ROS) in HPDLCs and induce abnormal expression of TNXIP, NLRP3 inflammasome-related factors, and IL-1β. More importantly, N-acetylcysteine induced reduction of ROS in HPDLCs, downregulated TXNIP expression, inhibited the expression and aggregation of NLRP3 inflammasome-related factors, and abrogated the inflammatory response to hypoxia. In conclusion, hypoxia-induced ROS can activate the TXNIP/NLRP3 inflammasome signaling pathway in response to oxidative stress, resulting in the increased expression of inflammatory factors in HPDLCs. Our findings provide evidence for the mechanism underlying the possible association between OSAHS and periodontal disease.
Highlights
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a condition characterized by obstructive sleep apnea and insufficient ventilation caused by a collapse or blockage of the upper airway during sleep
Body weight was used as an indicator of the influence of hypoxia on rats, and the statistical results showed that there was no significant difference in body weight between the SHAM and unilateral nasal obstruction group (UNO) groups (Figures 1(a) and 1(b))
The results show that apoptosis is a response to oxidative stress and is a product of the inflammatory response
Summary
Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a condition characterized by obstructive sleep apnea and insufficient ventilation caused by a collapse or blockage of the upper airway during sleep. The incidence of periodontal disease in patients with OSAHS is higher than that in healthy people [5,6,7]. Periodontal disease is initiated and sustained by the imbalance between the oral microbial community in microbial biofilms and the host inflammatory response [8, 9]. It is characterized by its occurrence in the supporting tissues of the teeth, including gingival disease involving only gingival tissues and periodontitis affecting deep periodontal tissues, thereby causing alveolar bone resorption and leading to tooth loss [10]. Periodontal disease is associated with a variety of systemic diseases, such as cardiovascular diseases, diabetes, and inflammatory bowel disease [11, 12]
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