Obstructive Sleep Apnea Syndrome and Upper Airway Inflammation

Inançli, Hasan Mete; Enöz, Murat

doi:10.2174/187221310789895568

Cited by 29 publications

(25 citation statements)

References 35 publications

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“…Serum sRANKL and OPG data in the OSAS patients are documented for the first time. However, previous studies demonstrated that the concentrations of IL-6 [12,41] and TNF-α [41] were higher in plasma samples of OSAS patients. The present findings did not appear to contradict the earlier study, since higher median levels of TNF-α and IL-6 were observed in our investigation but levels in OSAS groups were not statistically significantly different from the control group serum levels.…”

Section: Discussionmentioning

confidence: 82%

Is there an association between obstructive sleep apnea syndrome and periodontal inflammation?

et al. 2015

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Objectives: To assess salivary, serum biomarkers, and subgingival bacteria as putative candidates in the potential association between obstructive sleep apnea syndrome (OSAS) and periodontal disease. Materials and methods:Fifty-two patients were grouped according to the severity of OSAS: 13 participants served as controls, 17 patients had mild-to-moderate OSAS, and 22 severe OSAS. Serum, saliva, and subgingival plaque samples were collected, clinical periodontal parameters recorded. Salivary, serum concentrations of interleukin-6 (IL-6), tumour necrosis factor (TNF-α), osteoprotegerin, sRANKL, and apelin were analysed by enzyme-linked immunosorbent assay. Bacterial counts were determined by real-time QPCR on plaque microbial DNA preparations.Results: There was a significant change in the composition of microbes in plaque particularly in severe OSAS samples (p<0.01). Statistical analyses indicated significantly higher salivary IL-6 levels in both OSAS groups compared to controls (p<0.05). Salivary apelin levels were significantly higher in Serum levels of these biomarkers and salivary osteoprotegerin, sRANKL levels were similar in the study groups. The incidence and duration of apnea positively correlated with clinical periodontal parameters (p<0.05). Conclusion:OSAS appeared to alter the tested bacteria in plaque, correlate with increasing periodontal disease severity, have additive effect on salivary IL-6.Clinical relevance: OSAS is likely to interact with periodontal disease.

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Section: Discussionmentioning

confidence: 82%

Is there an association between obstructive sleep apnea syndrome and periodontal inflammation?

et al. 2015

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“…Sleep apnea and the attendant chronic intermittent hypoxia induce CNS inflammation and impair cognitive function (Gozal, 2009, McNicholas, 2009, Ryan et al, 2009, Inancli and Enoz, 2010, Kimoff et al, 2010). If chronic intermittent hypoxia-induced inflammation alters respiratory chemoreflexes and plasticity, then disease/ventilatory control interactions may contribute to the underlying pathophysiology.…”

Section: Significance Implications and Future Directionsmentioning

confidence: 99%

Systemic inflammation impairs respiratory chemoreflexes and plasticity

Huxtable¹,

Vinit²,

Windelborn³

et al. 2011

Respiratory Physiology & Neurobiology

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Many lung and central nervous system disorders require robust and appropriate physiological responses to assure adequate breathing. Factors undermining the efficacy of ventilatory control will diminish the ability to compensate for pathology, threatening life itself. Although most of these same disorders are associated with systemic and/or neuroinflammation, and inflammation affects neural function, we are only beginning to understand interactions between inflammation and any aspect of ventilatory control (e.g. sensory receptors, rhythm generation, chemoreflexes, plasticity). Here we review available evidence, and present limited new data suggesting that systemic (or neural) inflammation impairs two key elements of ventilatory control: chemoreflexes and respiratory motor (vs. sensory) plasticity. Achieving an understanding of mechanisms whereby inflammation undermines ventilatory control is fundamental since inflammation may diminish the capacity for natural, compensatory responses during pathological states, and the ability to harness respiratory plasticity as a therapeutic strategy in the treatment of devastating breathing disorders, such as during cervical spinal injury or motor neuron disease.

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“…[2] Because an altered upper airway structure and function is 1 etiology of OSA, [3,4] local pathophysiological processes such as upper airway inflammation could amplify these abnormalities and may further compromise upper airway patency during sleep. A large body of experimental evidence indicates that patients with OSA present with airway inflammation [5,6] mainly because of the mechanical trauma of recurrent snoring and oxidative stress. Furthermore, it has been reported that the repetitive hypoxia/reoxygenation phenomenon increases the levels of reactive oxygen species, which aggravate vascular endothelium injury in patients with OSA.…”

Section: Introductionmentioning

confidence: 99%