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It is a sleep-related respiratory condition, characterized by the complete or partial collapse of breathing because of a narrowing or closure of the upper airway during sleep, resulting in intermittent cessations of breathing apneas or reductions in airflow hypopneas despite ongoing respiratory effort [ 2 ]. The symptoms include excessive daytime sleepiness, Mood changes, Fragmented sleep, as well as the decreased health-related quality of life.

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Patients often complain of snoring, Gasping or choking, frequent nocturnal awakenings, early morning headaches, poor concentration and coordination, anxiety, irritability, and insomnia, yet many patients are unaware of these symptoms and disease onset is insidious [ 3 , 4 ].

The underlying mechanism of OSA is still under investigation, but it is precisely multifaceted. Moreover, mounting evidence suggests that OSA can increase the risk of cardiovascular diseases hypertension, coronary heart failure, stroke etc. It is higher in patients with obesity; diabetes mellitus type II and other cardiovascular disorders which includes ischemic heart disease, heart failure, cardiac arrhythmias, stroke, atherosclerosis and myocardial infarction [ 8 , 10 ]. Among the pediatric population, the rate affects between 1.

The pathogenesis of OSA can be multifactorial, complex and incompletely understood [ 13 , 14 ]. Certain factors that may contribute to OSA include obesity, thickened lateral pharyngeal walls, nasal congestion, enlarged uvula, facial malformations, and tonsillar hypertrophy. As the patient falls asleep, the muscle tone of the nasopharynx is reduced during sleep and airways become contracted. These episodes are typically accompanied by repeated oxyhemoglobin desaturation, oxygen levels in the body start to drop and carbon dioxide levels rise by short micro-arousals by the patient when the airway patency is restored.

This causes activation in sympathetic nervous system and contraction of nasopharyngeal tissue, which results in obstruction of the airway. Several studies have confirmed that the airway dilating muscles in OSA patients can no longer resist the negative pressure in airways during inspiration.

The frequency of apneas and hypopneas per hour of sleep.

The respiratory effort related arousal RERA can also be used. RERA is defined as an episode characterized by an increased respiratory effort caused by upper airway airflow reduction resolved with arousal and accompanied in most cases with hypoxemia. The diagnosis of Obstructive sleep apnea starts with thorough history and physical examination to elucidate the signs and symptoms of the syndrome. Common symptoms patients complain of snoring, disturbed sleep, daytime somnolence, decreased libido as well as a history of hypertension, cardiovascular disease, and diabetes.

Advances in sleep medicine and the availability of improved diagnostic tools have led to a better recognition and treatment of the disease. The outpatient examination should be repeated and the patients should be then referred, depending on the result of the follow-up examination, to a sleep laboratory [ 8 ].

The diagnostic PSG was performed using the computerized polysomnographic system including the monitoring of electroencephalogram EEG , submental and anterior tibial electromyogram EMG , oxygen saturation SaO 2 , electrocardiogram ECG , inductance plethysmography of chest walls and abdomen, nasal pressure sensor, and oronasal thermistor.

The polysomnographic recording was scored manually by the sleep specialist. Additional diagnostic models for OSA include portable sleep monitors, radiographic studies for anatomic analysis. It is necessary to remember that OSA can occur and progress over short periods of time, and its association with significant morbidity, coupled with the relatively low risk and high reward of therapy, that requires a thorough workup and treatment plan [ 13 ]. Several risk factors have been identified in the development of OSA namely male gender up to age 65 , increasing age, menopause, overweight, truncal obesity reflected by several markers including BMI, neck circumference, and waist-to-hip ratio, craniofacial abnormalities, upper airway anatomy, smoking, alcohol, and genetic predisposition [ 21 ].

Obesity is considered as the most important clinical risk factor for the development of OSA. Several studies have shown that more than half of the prevalence of OSA is attributable to excess body weight as opposed to substantial improvement with weight reduction [ 19 ]. Fat Deposition around the pharyngeal airway and abdomen may likely to reduce residual capacity function, which would be predicted to reduce lung volume tethering effects on the upper airway [ 22 ]. This latter mechanism emphasizes the great importance of central obesity as compared with peripheral obesity since it is the abdomen much more than the thighs that affect upper-airway size.

Therefore, obesity has been associated with functional impairment in upper airway muscles [ 23 ]. The prevalence of OSA increases with age and the gender differences diminish significantly after menopause [ 21 ]. Although several potential mechanisms have been proposed, the explanation for this aging increase in the prevalence of OSA remains unknown.

The exact mechanism of OSA was not fully known but, it begins as just loud snoring, then gradually over a period of time cessations of breathing and symptoms of excessive sleepiness develop, and thereafter may remain stable or worsen with weight gain. Numerous studies have attempted to know the cause of the age-related impact on OSA, no definitive conclusions have been reached [ 22 ].

Anatomical and pathophysiological susceptibility to OSA appears to increase with age in older people, who had a poorer responsiveness of pharyngeal dilator muscles, the genioglossus negative pressure stimuli appear to deteriorate with aging [ 23 ]. Craniofacial anatomy is probably one of the important factors in non-obese cases with OSA. Several soft and hard tissue factors may alter the mechanical properties of the upper airway muscles and increase its propensity to collapse during sleep. Features such as retrognathia, tonsillar hypertrophy, soft palate, inferiorly positioned hyoid bone, maxillary and mandibular retroposition, can narrow upper airway dimensions and promote the occurrence of apneas and hypopneas during sleep.

Differences in craniofacial structures may alter the risk for obstructive sleep apnea across different racial groups. Therefore, different racial groups are prone to develop obstructive sleep apnea at varying degrees of obesity, clinicians should consider the possibility of this disorder particularly in the presence of clinically detectable craniofacial abnormalities [ 4 ].

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According to clinic-based studies, the significant gender gap in the prevalence of OSA was reported. Recent population-based studies have confirmed that the prevalence of OSA is higher in men than women. This difference between clinic and epidemiological prevalence suggests several explanations for the gender gap. Firstly, women may not present with a similar symptomatic profile as men loud snoring, nocturnal snorting or gasping, and witnessed apneas.

Women were more likely to present with atypical complaints namely insomnia, depression, fatigue, and lack of energy, less likely to have apnea.

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The other reasons for this gender disparity are differences in body fat distribution or other gender-related upper airway anatomy differences , control of ventilation, physiology of the pharyngeal airway dilator muscles activation, and hormonal differences. Therefore, the evidence suggests that women are underdiagnosed and untreated for OSA compared to men [ 21 ].

Social factors such as smoking and alcohol consumption are considered as possible risk factors for progression of obstructive symptoms [ 13 ]. Epidemiological studies show that current smoking is associated with high prevalence of snoring and obstructive sleep apnea. Smoking can alter the upper airway properties and increase its collapsibility during sleep [ 4 ].

Ingestion of alcohol especially at dinner or during the evening relaxes dilator muscles, increases upper airway resistance, and decreases respiratory reflexes, and so it leads to snoring and apnea episodes in susceptible individuals [ 24 ]. Familial aggregation of obstructive sleep apnea was first recognized in the s by Strohl and co-workers in a family with several affected individuals.

The relative risk of obstructive sleep apnea can be two-four fold higher in first-degree relatives [ 23 ]. Genetic factors of obesity, soft tissue characteristics, and craniofacial abnormalities together given the wealth of evidence implicating these factors in the pathogenesis of the disorder. However, the genetic basis of obstructive sleep apnea needs a better attention, the available study reports suggest that inquires about family history can help the clinician to diagnose the disorder early for further treatment [ 4 ].

Medications such as muscle relaxants, sedative hypnotics benzodiazepines and barbiturates , narcotics, opioid analgesics and other central nervous system depressants, preferentially inhibit upper airway muscle activity while also depressing the respiratory centers of the brain [ 24 ].

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There are several other risk factors associated with OSA namely nasal congestion, pregnancy, menopause, hypothyroidism, diabetes and pregnancy. Available data suggest that OSA is three times higher in patients with insulin resistance than it is in the general population. Hypothyroidism leads to deposition of mucoproteins in the upper airway that causes enlargement of the soft palate, pharyngeal and laryngeal mucous membranes, thereby increasing the propensity for upper airway collapse during sleep.

Thus, patients with hypothyroidism may have increased susceptibility to obstructive sleep apnea. Pregnant women also experience higher rates of snoring particularly in the third trimester due to some of the physiologic changes that accompany pregnancy e. Thus, early case identification may have implications for maternal and fetal outcomes.

Knowledge of risk factors for obstructive sleep apnea is therefore crucial for proper diagnosis and treatment at those with the highest risk [ 4 , 21 ]. OSA is a common condition in which nasal and oral airway ceases in spite of continued diaphragmatic efforts and is associated with poor quality of life, increased healthcare-related costs.

Numerous efficacious treatments are available, but the patient should not shy away from therapeutic options, and medical practitioners should not hesitate to implement treatment regimens in addressing the problem of OSA. PAP devices work as pneumatic support that allows maintaining adequate airway patency above a critical value pressure value below which the airway collapses. The device is applied to the patient, through a nasal or oronasal mask during sleep in overnight at a required positive pressure.

The pressure can be varying with the severity of OSA and high pressures are required to avoid apneas during rapid eye movement sleep REM in the supine position or in severe obesity cases. Since its initial description, the device is considered as the gold standard treatment for OSA.

The clinical application of this CPAP has deeply modified the course of the disease over the last three decades, offering to thousands of patients the first non-invasive method to control their disorder. Continuous PAP CPAP , generally administered through the nose nCPAP , delivers a single pressure to the posterior pharynx throughout the night and acts as a pneumatic splint that maintains the patency of the upper airway in a dose-dependent fashion.

The best pressure for CPAP treatment is typically determined during an in-laboratory attended sleep study. CPAP therapy is indicated in all patients with an AHI greater than 15, independently from the presence of comorbidities, type of work and severity of symptoms; if the AHI is above 5 and below 15, CPAP is indicated in the presence of symptoms i. The most frequently used oral appliances are mandibular advanced splints MAS. These splints attach to both the upper and lower dental arches in order to advance and retain the mandible in a forward position, further the size of upper airway will be widened particularly in its lateral dimension, and the function of upper airway dilator muscles, particularly the genioglossus, will improve through the protrusion of the jaw during sleep [ 30 ].

As the pharyngeal collapsibility is reduced, the risk of apnoeic events will be lowered. Side effects that are more persistent include arthralgia, teeth pain and occlusal changes [ 8 ]. It has been demonstrated that the treatment success is achieved in patients with the following characteristics: young people, women, patients with small necks, and milder OSA [ 29 ].

Another group of oral appliances includes the orthodontic micro-implants that are connected to the extra-orally anchored mask.

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