Rapid Eye Movement (REM) sleep, which accounts for 20 to 25% of total sleep time, is connected with physiological changes that affect upper airway function. The pharyngeal dilator muscles' adrenergic and serotonergic regulation is reduced during REM sleep, with cholinergic-mediated inhibition of genioglossus activity. As a result, there is a greater risk of upper airway collapse [7,8].

Furthermore, OSA events during REM sleep are usually longer, more frequent, and associated with higher oxyhemoglobin desaturation than those during non-REM (NREM) sleep. Furthermore, REM sleep is linked to increased sympathetic activity and myocardial demand, as well as significant hemodynamic variability [9]. Apneas and/or hypopneas occur exclusively during REM sleep in 10-37 percent of individuals submitted for OSA examination. OSA during REM sleep has been linked to objective drowsiness in a few clinic-based investigations, and therapy may improve subjective sleepiness and quality of life [9].

REM sleep is linked to OSA and has been linked to both prevalent and incident hypertension as well as glucose metabolism problems. While hypertension and metabolic dysfunction can increase the risk of cardiovascular disease, the impact of REM sleep-specific OSA on endpoints like myocardial infarction, stroke, coronary revascularization, and congestive heart failure is yet unknown [9].

Figure 2: Risks Of Obstructive Sleep Apnea

Prevalence: OSA is characterized by recurrent bouts of upper airway blockage during sleep, which are generally accompanied by a drop in blood oxygen saturation [10]. The apnea-hypopnea index (AHI), which is defined as the number of apneas plus hypopneas per hour of sleep, is commonly used to assess the presence and severity of OSA (or hour of recording for home tests). OSA affects 4% of men and 2% of women

differ significantly between patients. Impaired pharyngeal dilator muscle function, premature waking to modest airway restriction (low respiratory arousal threshold), and unstable control of breathing (high loop gain) are non-anatomical contributions [1].

Impairment in one or more of these non-anatomical factors can sustain OSA severity when paired with a pharyngeal airway that is vulnerable to closure during sleep. Given that OSA only occurs while sleeping, the interaction of an anatomical predisposition with state-dependent changes in non-anatomical components is critical in causing this common disorder [1]. 

Upper airway collapsibility: The Pharyngeal Critical Closing Pressure (PCRIT) is a well-known method for measuring upper airway collapsibility while sleeping. PCRIT is a term that has been used to describe changes in upper airway collapsibility across the spectrum of sleep disordered breathing (from snoring to OSA). It is widely regarded as the gold standard method for determining “functional anatomy” during sleeping. When compared to wakefulness, the PCRIT approach permits the pharyngeal airway to be evaluated under conditions of reduced, but not nonexistent, neuromuscular input.

Once a therapeutic Continuous Positive Airway Pressure (CPAP) level that prevents airway obstruction or narrowing is established, brief reductions (5 breaths) in the holding pressure are applied during stable sleep. This procedure is repeated at different levels of mask pressure until airflow limitation and closure occur [1].

Respiratory Arousal Threshold: Because most respiratory events are coupled with cortical arousal, arousals have long been thought to be essential for reopening the upper airway after a respiratory event in OSA. However, about 20% of respiratory episodes end without cortical arousal, and another 20% happen after the upper airway has already been reopened and the airflow has been restored. Indeed, 75% of adults with OSA have respiratory episodes that end without arousal or arousal that occurs after airway closure at some point throughout the night. As a result, airway reopening can take place without arousal. [1] 

Loop gain: The phrase "loop gain" refers to the stability of a feedback control

to OSA increases directly with the number of affected relatives [22,23].

Craniofacial and maxillofacial anomalies: Craniofacial and maxillofacial anomalies can both play a role in obstructive sleep apnea instances. Patients with a receding chin and bimaxillary or mandibular retrognathism are more likely to develop indications of obstructive sleep apnea.

Smoking and alcohol consumption: Cigarette smoking and alcohol intake have both been identified as risk factors for OSA. Smoking is linked to an increased risk of snoring and sleep-disordered breathing [24,25].

Clinical Features: some of the common signs and symptoms associated with obstructive sleep apnea are given in Table 1.

Table:1 Signs and Symptoms of Obstructive Sleep Apnea 

Figure 3: Symptoms of Obstructive Sleep Apnea

The most sensitive symptom of OSA is snoring. To distinguish between simple snoring and OSA, patients should be asked about their snoring. Patients with OSA report loud, nightly snoring that is disturbing to others. Extreme daytime drowsiness is a generic characteristic that is important in determining therapeutic options and monitoring therapy response [26]. 

Due to the lung-to-finger circulation duration, the nadir oxygen saturation is delayed relative to the apnea. Normal breathing and oxygen saturation return following EEG arousals returning to sleep after each arousal causes upper airway collapse and recurrent obstructive apnea [29].

2. The multiple sleep latency test (MSLT) is used to establish how rapidly the patient falls asleep to distinguish it from narcolepsy.

3. The Epworth sleepiness scale is an 8-item scale that quantifies the propensity for dozing off during everyday activities. [26,30].

4. The Mallampati score (grade 1-4) can be used as a predictor of sleep apnea, particularly in cases where an enlarged tongue seems to be the cause of airway obstruction [31].

5. Lateral cephalometric radiographs reveal the diversion of the airway column, position of hyoid bone and craniofacial skeleton for any maxillo-mandibular deficiencies.

6. Fibro optic naso-pharygoscopy to examine the three-dimensional structure of the airway revealing any anatomic site of obstruction.

Dental diagnostics: A dentist is also the first healthcare professional to recognise an individual with a sleep disorder, as the sleep disorder's distinctive signs and symptoms are frequently observable in the dental office [2].

The following are common clinical findings: 

1. Excess fat accumulation in the palate, tongue, and pharynx (potentially resulting in true macroglossia) — restricting the airway.

2. Those who have small (micrognathia) or retrognathic jaws.

3. Macroglossia with decreased functional space that is driven posteriorly toward the pharyngeal wall and superiorly above the occlusion plane.

4. Because the soft palate is extended and expanded and posteriorly positioned during phonation, the uvula is hidden beneath the base of the posteriorly positioned tongue.

With 3D reconstructed models from computed tomography (CT) data, researchers investigated the influence of the tongue and mandible size ratio (T/M ratio) on the upper airway, concluding

of symptomatic OSA. Through a mask worn over the nose or the nose and mouth, PAP devices apply pressure to the airway. This pressure works as a splint during inspiration, preventing the airway from collapsing [29]. Nasal CPAP preserves the patency of the upper airway during sleep using a pneumatic stent. It is the most frequently prescribed treatment for moderate to severe instances of OSA [36]. While wearing the device, CPAP normalises AHI in more than 90% of patients. Benefits are contingent upon therapeutic adherence, with more hours of use per night related to better symptom alleviation and blood pressure reduction. Although subjective, acceptable adherence is typically described as using PAP for at least four hours per night for at least five nights per week, a requirement that the Center for Medicare & Medicaid Services uses to authorise continuing funding for PAP after the initial 90 days of therapy [29]. Factors that contribute to improved PAP adherence include education about the risks of OSA and the expected benefits of CPAP therapy; monitoring of CPAP use with reinforcement and support for technical difficulties; and behavioural interventions, such as cognitive behavioural therapy and motivational enhancement therapy. Each of these factors boosts PAP adherence by more than 30 minutes per night, with behavioural intervention having a mean effect of up to 80 minutes per night [29].

The ability of most contemporary CPAP machines to broadcast adherence data over cellular networks for remote viewing simplifies monitoring PAP adherence. Earlier PAP devices delivered a constant positive pressure and required pressure titration in the laboratory to determine the ideal treatment pressure. Automatic titrating PAP devices, which monitor airflow and alter the pressure in response to variations in flow, have enabled the beginning of PAP therapy without a titration study, lowering costs and enhancing convenience without compromising efficacy or adherence to therapy [29].

Auto-titrating CPAP systems detect flow restriction as a surrogate for upper airway narrowing and adjust pressure automatically to maintain therapeutic levels. In terms of patient adherence and drowsiness reduction, auto-titrating CPAP is comparable to fixed-pressure CPAP. It is not recommended for people with Cheyne–Stokes breathing and has not been well-researched in patients with concomitant pulmonary disease.

Figure: 5 Tongue retaining devices ( TRD) 

Design consideration of OSA [38, 39]

Over 40 distinct OSAs have been patented to date. Variations in design are determined by the following factors:

• method of retention
• material flexibility
• adjustability
• vertical opening
• freedom of jaw movement

These appliances can be manufactured of polyvinyl vacuum moulded thermoplastic or hard acrylic, depending on the material utilised. These may be fixed or adjustable in terms of adjustability. Fixed oral appliances are typically made of one piece and are adjustable in the anteroposterior plane.

One of the recognised designs is a one-piece, non-adjustable soft vinyl vacuum formed mandibular repositioning device made of a thermoplastic material that covers the maxillary and mandibular arches in the appropriate anteroinferior position. A wax bite, silicon bite, or anterior jig with inter-occlusal registration is used to establish and record the occlusal position [40].

Mandibular Repositioning appliance non-adjustable

In the two-part Herbst-style device, the arches are joined by pivoting bars that can be changed in length to taper down the protrusive mandibular posture for the best effectiveness and comfort. Occlusal registration is less necessary with these two-part devices since mandibular repositioning can indeed be gradually increased from the inter-cuspal position [40]. 

rates (equivalent to uvulo-palato-pharyngoplasty but also less effective than CPAP), high compliance, a more benign adverse effect profile, quick effect, and easy cessation without sequelae [42]. In an outpatient situation, OA insertion can be accomplished in a single stage. These can be used effectively for simple snoring and mild to moderate OSA, as recommended by the American Academy of Sleep Medicine [43], but according to a study by Jeffery Pancer, oral appliances appear to be an effective treatment alternative for selected patients with snoring and varying degrees of sleep apnea, including those with severe OSA [44].

In 20% to 75% of patients, OSA improves blood oxygen saturation levels by relieving apnea. They reduce the AHI to ten incidents per hour or achieve a 50% reduction in the AHI. Additionally, they return AHI to normal in 50-60% of patients.

According to a recent study conducted by Kazvya Yoshida, appliance therapy resulted in a significant decrease in mean arterial pressure of approximately 3.7mmHg in a selected cohort [45].

Blood pressure response was substantially linked with AHI reduction, demonstrating oral appliance therapy's efficacy. Reduced blood pressure results in a decreased risk of coronary heart disease and stroke. Oral appliances often have modest side effects, which include excessive salivation, muscle and tooth soreness, and, on rare occasions, temporomandibular joint discomfort. However, symptoms typically improve over time [46]. 

Surgery as a treatment option

Surgery should be considered a last option in the treatment of OSA. Patients who have difficulty with CPAP tolerance owing to anatomical abnormalities may benefit from nasal surgery like septoplasty or turbinate reduction [26]. Although uvulo-palato-pharyngoplasty (UPPP) is a well accepted procedure for managing snoring and sleep apnea, it is only effective in less than half of all patients. Repositioning the hyoid bone is another therapy strategy. Maxillo-Mandibular Advancement (MMA) surgery is another effective method that involves enlarging the upper airway by roughly 10 mm using LeFort I maxillary and bilateral mandibular osteotomies combined with forward stabilisation of the facial bone. Although it is an invasive surgery with a lengthy postoperative recovery period, it cures more than 90% of non-obese

Prognosis: OSA treatment often improves sleep apnea and associated behavioural impairment. The degree of improvement is dependent on adherence to therapy. An optimal response is obtained when CPAP therapy is used for more than 6 hours every night. Residual sleepiness is observed in approximately 9% to 20% of people with OSA who use PAP for at least 6 hours per night. This is not much more than the population without OSA and is therefore most likely due to reasons other than OSA, such as sleeping less than the recommended minimum of seven hours per night [29].

CPAP and oral appliances are not curative. Without sufficient weight loss to promote disease remission, lifetime treatment is frequently required. While compliance is not required for surgical procedures, OSA may recur or worsen with additional weight gain [29].

This examination is not without limitations. To begin, it was restricted to English-language articles and sourced mostly from previously published systematic reviews, meta-analyses, and clinical practice guidelines. Second, it is probable that some relevant papers were omitted during the literature search. Third, not all aspects of OSA were addressed. Fourth, certain topics are not adequately covered due to a lack of high-quality data.