The activation of redox-sensitive transcription factors triggers the production of proinflammatory cytokines, which regulate inflammatory responses such as macrophage activation, nitric oxide production, and smooth muscle cell proliferation. The most studied cytokines are tumor necrosis factor (TNF), IL-6, and interleukin-8 (IL-8), which are regulated by the activation of NF-κB and AP-1 (Lavie and Lavie 2006; Panes and Granger 1998; Haddad and Harb 2005). Elevated levels of proinflammatory cytokines, adipokines, and adhesion molecules also show activation and acquired prothrombotic phenotype in blood cells and endothelial cells of patients with OSA (Lavie 2009).

Studies have shown that sleep apnea increases atherogenic events. This process seems to start at the onset of sleep apnea syndrome. Although the patients referred to clinics after developing the major symptoms of OSAS tend to be in the fifth decade of life, Wisconsin studies revealed that of men in the third decade of life, 17 % have mild and 6.2 % have moderate sleep apnea (Young et al. 1993). People with disordered breathing are likely to develop hypertension within 4 years (Lavie and Lavie 2006). These findings show that the cardiovascular damage in OSAS is progressive and accumulates over time. When the diagnosis is late, the risks of mortality and morbidity are higher (Lavie and Lavie 2006).

CPAP therapy is the preferred treatment option for patients with OSAS. CPAP treatment is usually delivered via a nasal mask and helps to maintain upper airway patency, so it is a treatment, not a cure for the disease, and CPAP treatment has many benefits, such as decreasing daytime sleepiness, improving neurocognitive function, and reducing cardiovascular disease (Friedman et al. 2012). Barcelo et al. (2006) studied the effects of CPAP treatment on oxidative stress in patients with OSAS and found that continuous CPAP treatment improves the antioxidant defense. As oxidative stress and endothelial dysfunction are important predictors of an increased risk of cardiovascular disease, this might explain the decrease in cardiovascular disorders after CPAP treatment (Barcelo et al. 2006). Tothova et al. demonstrated that evening concentrations of the salivary thiobarbituric acid-reacting substances (p < 0.001), advanced glycation end products (p < 0.001), and advanced oxidation protein products (p < 0.01) were significantly lower than morning values during the diagnostic night. However, they found that salivary concentrations of none of the oxidative stress markers were significantly influenced by the CPAP treatment. No changes in salivary antioxidant status after CPAP therapy were found (Tothova et al. 2013).

Sadasivam et al. (2011) suggested that oral intake of the antioxidant N-acetylcysteine improves sleep parameters and produces beneficial effects on oxygen saturation.

Skelly et al. (2013) studied the oxidative stress in upper airway muscles; they found that intermittent hypoxia and hypoxia reoxygenation have an equivalent negative inotropic effect on isolated rat sternohyoid muscle force. A superoxide scavenger TEMPOL increases sternohyoid muscle sensitivity to electrical stimulation and was modestly effective in preventing muscle weakness, but, however, failed to recover decreased upper airway muscle performance during sustained hypoxia. Akpinar et al. (2012) studied on the salivary myeloperoxidase levels in the saliva of the OSAS patients and normal controls; they found that salivary myeloperoxidase was higher in OSAS patients which may show the local inflammation. According to these studies, it can be supposed that OSAS is both a systemic and local oxidative stress disorder.

Lee et al. (2009) studied on the effects of uvulopalatopharyngoplasty (UPPP) on serum levels of nitric oxide derivatives (NOx) and endothelial function by endothelium-dependent flow-mediated dilation (FMD) in OSAS. They found that success of the procedure was correlated with renormalization of NOx levels and FMD. These results are consistent with the measurement of NOx levels in patients whose OSAS was successfully treated with CPAP.

Gozal et al. (2007c) have shown that nonobese children with OSA are at risk for endothelial dysfunction which has a correlation with circulating levels of sCD40L in these children. The marker for endothelium-related activation and dysfunction is soluble CD40 ligand (sCD40L), which binds CD40 on the surface of various cell types; such as endothelial cells, and triggers the increment in the expression of inflammatory mediators, growth factors, and the procoagulant tissue factor. They concluded that the effective treatment of OSA by adenotonsillectomy may not be associated with reversibility of the functional endothelial deficits.