Literature DB >> 25221691

Prosthodontic approach to treat obstructive sleep apnea.

K Annapurna1, S Suganya1, R Vasanth1, P Ranjith Kumar1.   

Abstract

Sleep disordered breathing represents a continuum, ranging from simple snoring sans sleepiness, upper-airway resistance syndrome, obstructive sleep apnea (OSA) syndrome, to hypercapnic respiratory failure. Fifty seven articles formed the initial database and a final total of 50 articles were selected to form this review report. Four months were spent on the collection and retrieval of the articles. Articles were selected based on accuracy and evidence in the scientific literature. Oral appliances (OAs) are indicated for use in patients with mild to moderate OSA who prefer them to continuous positive airway pressure (CPAP) therapy, or for those who do not respond to, are not appropriate candidates for, or for those who have failed treatment attempts with CPAP. OAs protrude the mandible and hold it in a forward and downward position. As a consequence, the upper airway enlarges antero-posteriorly and laterally, improving its stability. Although OA are effective in some patients with OSA, they are not universally suitable. Compliance with OAs depends mainly on the balance between the perception of benefit and the side effects. In conclusion, marked variability is illustrated in the individual response to OA therapy and hence the treatment outcome is subjective.

Entities:  

Keywords:  Mandibular advancement; Oral appliances; Sleep apnea

Year:  2014        PMID: 25221691      PMCID: PMC4160667          DOI: 10.4103/2141-9248.139275

Source DB:  PubMed          Journal:  Ann Med Health Sci Res        ISSN: 2141-9248


Introduction

Obstructive sleep apnea (OSA) is a sleep disordered breathing disease involving repeated obstruction of the upper airway during sleep. The occlusion of the upper airway is caused by sleep-induced physiologic change in muscle activity superimposed with various structural defects of upper airway, sleeping in supine position, upper airway edema caused by smoking, hypothyroidism, acromegaly and nasal obstruction.[12345678910] Various terms are used to describe OSA [Table 1]. OSA is a serious systemic disorder, when untreated may cause hypertension, severe hypoxemia, ventricular and supra-ventricular cardiac arrhythmias.[1112131415]
Table 1

Terms used to describe OSA

Terms used to describe OSA

Methods of Literature Search

The Google search engine was used to search for keywords such as OSA, oral appliances (OA), and snoring appliances. Fifty seven articles formed the initial database and a final total of 50 articles were selected to form this review report. Four months were spent on the collection and retrieval of the articles.

Method of Article Selection

Summary of Key Articles

Treatment Options for OSA

There are various surgical and non-surgical treatment modalities currently available for OSA[1617] [Table 2]. The most commonly followed medical intervention includes nasal continuous positive airway pressure (N-CPAP), which was introduced by Sullivan et al. (1981) as a pneumatic splint to prevent collapse of the pharyngeal airway and has become the first choice therapy for OSA.[181920212223] OSA symptoms, such as snoring and daytime somnolescence, are well known. Snoring appears to affect 35-40% of adults and is related to OSA. The treatment options for OSA include positive airway pressure devices, OAs, medications (such as nasal steroids and decongestants) and surgical techniques such as, tracheostomy, nasal surgery (septoplasty, turbinectomy, polypectomy), uvulopalatopharyngoplasty (UPPP) and laser assisted uvulopalatoplasty. The recent approaches include electrical pacing, radio-frequency ablation and rapid maxillary expansion.[242526272829303132] OA therapy has proved effective over the past 10 years in treating patients with OSA, by reducing the apnea and hypopnea index (AHI), improving oxygen saturation during sleep, reducing snoring and more recently, reducing arterial pressure. The efficacy of an OA depends on its retention and the amount of mandibular protrusion.
Table 2

Treatment modalities for OSA

Treatment modalities for OSA

Historical Perspective

George Cattlin was the first person to relate the influence of sleep quality on daytime function. He stated that native North American Indians were healthier than their immigrant counterparts and attributed it to the habit of breathing through their nose rather than the mouth.[33] Following his work; there were many patented devices to promote nasal breathing. However, documented clinical work began in 1903, when Pierre Robin first described his device “monoblock”, for the treatment of glossoptosis.[34] Fifty years later, Cartwright and Samelson (1982) described the tongue retaining device (TRD).[35]

Types of Appliances

The OAs used for OSA are still under research and growing [Table 3]. The three general groups of appliances are soft palate lifters (SPL) [Figure 1], TRD [Figure 2] and mandibular advancement appliance (MAA) [Figures 3 and 4]. The OA most commonly in use today is MAA. It protrudes the mandible forward, thus preventing or minimizing upper airway collapse. The amount of protrusion can be either fixed or variable.
Table 3

Examples of oral appliances

Figure 1

Soft palate lifting appliance

Figure 2

Mandibular advancement with tongue retention device

Figure 3

Mandibular advancement appliance with anterior window

Figure 4

Monoblock appliance

Examples of oral appliances Soft palate lifting appliance Mandibular advancement with tongue retention device Mandibular advancement appliance with anterior window Monoblock appliance

Mechanism of Action of OAs

Upper airway obstruction can occur between the nasopharynx and the larynx. The most common sites of obstruction are behind the base of the tongue (retroglossal) and behind to the soft palate (retroplalatal). Neuromuscular decontrol is speculated as the cause for airway obstruction. The pathological repetitive narrowing (or complete obstruction) of the upper airway is due to the combination of abnormal anatomy and the abnormal physiology.[3637] Battagel et al. and Ng et al. conducted various studies to determine the selection criteria for patients to receive OAs. They concluded that oropharyngeal collapse, rather than the velopharyngeal collapse, was predictive of a more beneficial response to OAs.[3839] According to Banabilh et al., 96% increase in the area associated with the downward displacement of the hyoid bone was detected in patients with OSA.[40] The presumed mechanism of action for OAs is that anatomical changes in the oropharynx, produced by MAA, result in an alteration of the intricate relationships between different muscle groups controlling the upper airway caliber.[41] There is currently no reliable method for the selection criteria and for the treatment outcome.

Clinical Trials

The clinical studies on OAs started with Cartwright and Samelson (1982). The most commonly used criterion in clinical studies is the nocturnal monitoring of respiration with and without OAs. In some investigations, formal in-hospital polysomnography was performed, while in others, only at-home monitoring of oxygen saturation, oxygen desaturation index and apnea index were recorded. In recent investigations AHI, or respiratory disturbance index were used.[42] The first step in analyzing the results of individual investigations is to decide on which outcome variable to analyze. The following four variables are an apparent choice for OSA: (1) Baseline index for respiration (AHIbase), (2) “With appliance” index of respiration, (3) Success rate defined as the reduction of AHIbase to a value less than the defining value for sleep apnea and response rate defined as the reduction of AHIbase by >50% while still remaining higher than the defining value for OSA. Bloch et al. (2000) compared the effectiveness and side-effects of a novel, single piece MAA device (OSA-Monobloc) with a two piece, lateral Herbst attatchments (OSA-Herbst) appliance and concluded that OSA-Monobloc relieved symptoms to a greater extent than OSA-Herbst.[43] Ferguson et al. (1997) conducted a prospective cross-over study to compare efficacy, side-effects, patient compliance and preference between MAA and N-CPAP in patients with symptomatic mild to moderate OSA and concluded that MAA is a better treatment option with greater patient satisfaction.[44] Gale et al. (2000) evaluated the effect of a MAA on minimum pharyngeal cross-sectional area (MPCSA) in 32 conscious, supine subjects with OSA and concluded that the MAA significantly increased MPCSA.[45] Barthlen et al. (2000) compared three different OAs: A MAA (snoreguard), a TRD and a SPL appliance for the treatment of severe OSA syndrome and stated that MAA is an effective treatment alternative in some patients.[46] Kyung et al. (2005) studied the pharyngeal size and shape difference between pre- and post-trials of MAAs, using cine computerized tomography and revealed that the MAA appeared to enlarge the pharynx to a greater degree in the lateral than in the sagittal plane at the retropalatal and the retroglossal levels of the pharynx, suggesting a mechanism for the effectiveness of the OA.[47] Almeida et al. studied the long-term sequelae of OA therapy and found that after a mean of 7.4 years, OAs induce clinically relevant changes in the dental arch and the occlusion.[48] MAA devices may have no effect on obstruction associated with cranial base morphology, nasal obstruction or retropalatal obstruction. Furthermore, the application of MAAs may not be a good choice for subjects with Class III malocclusion where the jaw is already protruded. A possible alternative to MAAs might be the use of a maxillary OA. Maxillary OAs putatively induce renewed midfacial development and provide an alternative approach to managing OSA, by permitting non-surgical remodeling of the upper airway.[4950]

OAs vs Other Treatment

Continuous positive airway pressure (CPAP) prevails as the “gold standard” of treatment for OSA. Hence, any other newer approach has to be compared against it. There are almost seven randomized controlled studies that compared OAs with CPAP. In all studies, CPAP showed better results than OAs in bringing the AHI <10. Smith and Stradling substituted OA for CPAP for a month and stated that OA produced similar reduction in hypopneas (number of times/hour of sleep that the blood's oxygen level drops by 3% or more from the baseline) from 29 to 4.[41] Since 1988, there are several studies comparing the efficacy of different OAs. The summary of the studies shows that the efficiency of each OA depends on the design and the degree of MAA. There were several clinical studies that compared OA with UPPP and demonstrated the superiority of OA with 78% reduction in OSA in OA group and 51% in the UPPP group.

Conclusion

Compliance with OA depends mainly on the balance between the perception of benefit and the side effects. OAs used till date constitute a relatively heterogeneous group of devices for the treatment of OSA and non-apneic snoring, which accounts for variability in benefits and side-effects. To conclude from the vast reviews and in compliance with the recent review by the American Academy of Sleep Medicine, marked variability is illustrated in the individual response to OA therapy and hence the treatment outcome is subjective.

Summary of Key Articles

  47 in total

1.  Polygraphic study of the episodic diurnal and nocturnal (hypnic and respiratory) manifestations of the Pickwick syndrome.

Authors:  H Gastaut; C A Tassinari; B Duron
Journal:  Brain Res       Date:  1966-02       Impact factor: 3.252

2.  An individually adjustable oral appliance vs continuous positive airway pressure in mild-to-moderate obstructive sleep apnea syndrome.

Authors:  Winfried J Randerath; Markus Heise; Rolf Hinz; Karl-Heinz Ruehle
Journal:  Chest       Date:  2002-08       Impact factor: 9.410

3.  Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares.

Authors:  C E Sullivan; F G Issa; M Berthon-Jones; L Eves
Journal:  Lancet       Date:  1981-04-18       Impact factor: 79.321

4.  Cranial base and airway morphology in adult malays with obstructive sleep apnoea.

Authors:  Saeed M Banabilh; A H Suzina; Sidek Dinsuhaimi; G D Singh
Journal:  Aust Orthod J       Date:  2007-11

5.  Effect of oral appliance therapy on upper airway collapsibility in obstructive sleep apnea.

Authors:  Andrew T Ng; Helen Gotsopoulos; Jin Qian; Peter A Cistulli
Journal:  Am J Respir Crit Care Med       Date:  2003-04-30       Impact factor: 21.405

6.  Sleep apnea syndrome caused by acromegalia and the treatment with a reduction plasty of the tongue. Case report.

Authors:  L E Afzelius; D Elmqvist; S Laurin; A M Risberg; M Aberg
Journal:  ORL J Otorhinolaryngol Relat Spec       Date:  1982       Impact factor: 1.538

7.  A comparative study of treatments for positional sleep apnea.

Authors:  R Cartwright; R Ristanovic; F Diaz; D Caldarelli; G Alder
Journal:  Sleep       Date:  1991-12       Impact factor: 5.849

8.  Sleep apnoea in acromegaly.

Authors:  W H Perks; P M Horrocks; R A Cooper; S Bradbury; A Allen; N Baldock; K Prowse; W van't Hoff
Journal:  Br Med J       Date:  1980-03-29

9.  Long-term sequellae of oral appliance therapy in obstructive sleep apnea patients: Part 2. Study-model analysis.

Authors:  Fernanda Ribeiro de Almeida; Alan A Lowe; Ryo Otsuka; Sandra Fastlicht; Maryam Farbood; Satoru Tsuiki
Journal:  Am J Orthod Dentofacial Orthop       Date:  2006-02       Impact factor: 2.650

Review 10.  Review of oral appliances for treatment of sleep-disordered breathing.

Authors:  Victor Hoffstein
Journal:  Sleep Breath       Date:  2007-03       Impact factor: 2.816

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