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Breathing, malocclusion as well as obstructive sleep apnoea / for orthodontists by Almuzian

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Breathing, malocclusion as well as obstructive sleep apnoea / for orthodontists by Almuzian

  1. 1. Mohammed Almuzian dr_muzian@hotmail.com 13 Breathing and malocclusion as well as Obstructive sleep apnoea
  2. 2. Mohammed Almuzian, University of Glasgow 1 Contents Respiration is controlled by the followings ...............................................................................2 Breathing and the upper airway system....................................................................................2 Causes of upper airway obstruction ..........................................................................................2 Consequences of nasal obstruction........................................... Error! Bookmark not defined. Head posture or position ...........................................................................................................4 Treatment option for nasopharyngeal and oropharyngeal obsrtuction ...................................4 Sleep related sleeping disorders OSA........................................................................................4 Types of sleeping disorders........................................................................................................8 Definition of OSA........................................................................................................................9 Pathophysiology.......................................................................................................................11 Prevalence................................................................................................................................11 Classification of OSA ................................................................................................................11 Aetiological factors ..................................................................................................................11 Sign and Symptoms, Jurdya 2004, Coborune 2011 .................................................................13 Complications...........................................................................................................................15 Diagnosis..................................................................................................................................15 Treatment ................................................................................................................................17 Ideal Features of MAA .............................................................................................................20 Classification of MAA ...............................................................................................................21 Advantages of MAA .................................................................................................................23 Disadvantage of MAA...............................................................................................................23 Breathing and malocclusion as well as Obstructive Sleep Apnoea
  3. 3. Mohammed Almuzian, University of Glasgow 2 Respiration is controlled by the followings: 1. Sensors:  Central chemoreceptors, which respond to changes in the chemical composition of the blood or other fluid around it (found in the ventral surface of the medulla)  Peripheral chemoreceptors in the carotid bodies which respond to decreases in arterial 02 and pH levels  Lung receptors - stretch receptors, irritant receptors and others 2. Other reflex mechanism  Nasal and upper airway (mechanical and chemical)  Gamma systemin inter-costals muscles (detect stretching)  Joint and muscle (stimulate breathing in exercise)  Arterial baroreceptors (detect blood pressure levels)  Pain and temperature Breathing and the upper airway system In the nose, the nasal passages contain three conchae which are lined with mucous membranes that aid in: 1. Air warming, within 37 degree of body temperature. 2. Air humidifying through the mucous within 2-3% of the maximum humidification. 3. Air filtering by the mechanism of nasal hair filteration, turbinlation mechanisim as well as the cilia of the pseudostratified columnar epithelium. 4. The turbinate bone - the conchae - also aids to increase the size of the surface area of the nasal passage. When breathing is done through a tube (as for example, in a tracheostomy), this effect will be absent and so the drying effect on the lower lung can lead to serious lung crusting and infection (Guyton and Hall, 1996). Causes of upper airway obstruction A. Nasal
  4. 4. Mohammed Almuzian, University of Glasgow 3 1. Soft tissue  Allergies  Hyperplasia 2. Hard tissue  Nasal anomalies  Deviated nasal septum Trauma B. Nasopharyngeal Allergy or infection of:  Tubular Tonsils  Pharyngeal Tonsils or called Adenoids C. Oropharyngeal  Large tongue  Low / posterior tongue position  Lingual tonsil Waldeyer's tonsillar ring • Waldeyer's tonsillar ring is an anatomical term collectively describing the arrangement of lymphoid tissue in the pharynx. Waldeyer's ring was named after the nineteenth century German anatomist Heinrich Wilhelm Gottfried von Waldeyer-Hartz. • The ring consists of the (from posterior to anteriro): A. One pharyngeal tonsils (or nasopharyngeal tonsil(s), due to the location; also known as 'adenoid(s)' when inflamed/swollen B. Two tubal tonsil (bilaterally, where each Eustachian tube opens into the nasopharynx) C. Two palatine tonsils (commonly called "the tonsils" located in the oropharynx) D. One (or many) lingual tonsils (on the posterior tongue).
  5. 5. Mohammed Almuzian, University of Glasgow 4 Head posture or position Represent the relationship of the head to H or V lines and mainly the position or angulation of the cranial base in relation to vertebral axis. It is very reproducible position. It depends on: 1. Visual axis 2. Hearing 3. Balance 4. Breathing 5. Swallowing 6. Gravity Treatment option for nasopharyngeal and oropharyngeal obsrtuction 1. Pharmacological 2. Turbinectomy 3. Nasal septoplasty 4. Tonsileectomy or adenictomy ( no evidence) 5. Tongue reduction 6. BSSO advancement 7. RME (no evidence) 8. MAA Functions of sleep 1. Fatigue reversal: Sleep allows the individual to recover and reenergize. 2. Biochemical refreshment • Sleep promotes synaptic efficiency, protein synthesis, neurogenesis, metabolic (eg, glycogen) restoration, growth (secretion of growth hormone peaks during sleep), etc. • Immune function and Reset or protection. 3. Memory • Daytime learning needs sleep for memory consolidation. • Sleep seems to facilitate encoding of new information.
  6. 6. Mohammed Almuzian, University of Glasgow 5 4. Psychologic well-being • Dreams occur in all sleep stages. REMdreams are more vivid. • Lack of sleep presents a risk of mood alteration to depression. Sleep efficiency it is defined as the amount of time asleep divided by the amount of time spent in bed, expressed as a percentage. Sleep efficiency greater than 90% is an indicator of good sleep. Sleeping cycle • Sleep Rechtschaffen and Kales introduced a standardization of human sleep that divides it into five distinct stages, the first four belonging to slow-wave (non-REM) sleep and the last one being REM sleep. • The duration of a sleep cycle is about 90 minutes, and the first cycles are shorter than the last ones. • There are in general four to six sleep cycles during a night, depending on the total sleep time. • The first two cycles are generally complete with successive attendance in all sleep stages. • During the later cycles the contribution of stages 3 and 4 diminishes gradually, and sleep bounces between stage 2 and REMsleep. • The REM episodes are generally short (5 minutes) in the early cycles but can attain 1 hour during the last cycle. A. Non-REM sleep: • During non-REM sleep the muscular tone remains present in the EMG. • Ocular and axial muscular movements are absent, with the exception of occasional postural adjustments.
  7. 7. Mohammed Almuzian, University of Glasgow 6 1. Sleep begins with stage 1, which is a transitory epoch of about 1 to 10 minutes, characterized by a slight increase in the EEG amplitude and appearance of scattered triangular waveforms called vertex waves (they are most evident in the vertex leads). 2. Deepening of non-REM sleep toward stage 2 is announced by increased amplitude of the EEG. Vertex waves increase in amplitude and are termed K-complexes also termed sigma waves; generally 10 to 14 Hz 3. Stage 3 is generally equivalent to the beginning of deep sleep. Between 20% and 30% of the EEG activity consists of high-amplitude (greater than 50 μV) slow waves (less than 4 Hz, termed delta waves). 4. Sleep stage 4 is recognized when more than 50% of the EEG activity is spent in delta waves. The amplitude of the waves reaches the highest values (around 100 μV). In clinical recordings, stages 3 and 4 are usually reported as one sleep state. B. Transition to REM sleep • Stage 4 is ended by a return to lighter sleep (stages 3 and 2) and subsequent entrance into REM sleep. • Major features are specific for REM sleep: 1. Very low EMG activity, 2. Axial muscular hypotonia, 3. Rapid eye saccades that trigger large deflections in the EOG. Elements of the medical and social history and clinical examination to include in the patient’s medical record A. History 1. Symptoms related to insomnia: - Sleep duration (when the patient goes to sleep and when the patient awakens) - Number of awakenings - Trouble falling or staying asleep (number of nights per week)
  8. 8. Mohammed Almuzian, University of Glasgow 7 - Number of times the patient gets up in the night to go to the bathroom - Use of medication or alcohol to fall asleep - Use of pain or anxiety-related medication 2. Symptoms related to sleep-disordered breathing: - Snoring - Cessation of breathing - Choking - Awakening gasping for breath - Tendency to fall asleep during the daytime (Epworth sleepiness scale) - History of hypertension and other cardiovascular disorders (eg, ischemic heart disease, stroke, night sweating, loss of memory, morning headache, difficulty concentrating) - Nocturia/enuresis 3. Symptoms related to movement disorders: - Tooth grinding sounds during sleep (sleep bruxism) - Tooth tapping (faciomandibular myoclonus or sleep-related epilepsy) - Leg or arm movement during sleep, with or without injuries (periodic limb movement, REM behavior disorder) - Body rocking or head banging 4. Other symptoms: - Eating during the sleep period (may exacerbate insomnia or sleepd isordered breathing) B. Clinical examination • Weight, height, and body mass index • Neck circumference (at risk if greater than 41cm [women] or 43 cm [men]) • Retrognathia (Class II) • Deep palate • Narrow dental arches • Tongue size (macroglossia) • Tongue indentation (tongue thrusting habit or tic) • Adenoids and tonsil size • Oropharyngeal size, viewed through the mouth (Mallampati classification). Modified Mallampati Scoring:[3] I. Class I: Soft palate, uvula, fauces, pillars visible.
  9. 9. Mohammed Almuzian, University of Glasgow 8 II. Class II: Soft palate, uvula, fauces visible. III. Class III: Soft palate, base of uvula visible. IV. Class IV: Only hard palate visible. • Nose shape (narrowing) and obstruction • Usual body position (supine is a risk factor for respiratory disorders and bruxism) • Tooth wear or damage or use of oral splint (bruxism or orofacial pain) • Absence of tooth or protrusive mandibular movement (precludes use of oral appliance to treat sleep-disordered breathing) Sleep related sleeping disorders OSA Types of sleeping disorders 1. Sleep bruxism 2. upper airway resistance syndrome (UARS) 3. Habitual snoring
  10. 10. Mohammed Almuzian, University of Glasgow 9 4. Obstructive sleep apnoea (OSA) 5. Central sleep apnea UARS It is characterized by partial collapse of the upper airway, without the occurrence of obstructive apneas and hypopneas.3 It is thought to be an intermediate form of sleep- related breathing disorder, between snoring and frank OSA. Sleep bruxism (tooth grinding)  It is a repetitive activity (repeated at least 3 times per episode) in the jaw muscles (rhythm at 1 Hz, of bursts lasting more than 0.5 and upto 2.0 seconds) that generates tooth grinding sounds and occasional jaw clenching (a sustained muscle contraction of more than 2.0 seconds). As is the case with snoring,generally sleep partners are the ones who complain of tooth grinding sounds.  Prevalence: in infants 14% to 18%. And in adult 8%  The consequences of sleep bruxism may include tooth destruction (tooth wear or restoration destruction), morning headache, jaw pain, and a limited ability to open the mouth due to muscle tension or meniscus displacement Habitual Snoring  Snoring is an acoustic phenomenon produced by the vibration of the pharyngeal tissues as air passes through a narrow orifice created by the relative positions of the soft palate and the base of the tongue. It is an almost exclusively inspiring noise but can persist on expiration when there is a partial blockage of the airway as is the case with patients with OSA. It initiates when falling asleep, intensifies as sleep progresses to non-REM sleep and then weakens and discontinues during REM sleep. Snoring is one of the cardinal symptoms of OSA, but not all snorers have sleep apnea. Itappears to be the milder and initial form of upper airway dysfunction leading to OSA.
  11. 11. Mohammed Almuzian, University of Glasgow 10  Habitual snoring has been reported as occurring in up to 24% of the male population and up to 14% of the female population. The prevalence increases with age, reportedly affecting 40% - 60% of the middle-aged population”. OSA  OSA is characterized by more than 5 repetitive episodes (more than 10 seconds) of upper airway obstruction in each hour of sleeping, usually associated with a reduction in blood oxygen and associated symptoms such as daytime sleepiness, impaired cognition and fatigue an AHIof 15 or greater regardless of associated symptoms.  Before Measurement Techniques were outlined in 2010 the prevalence of OSA was varied in the literature due to different measurements used in the past. Using AHI > 5 with no other symptoms gives a prevalence of 24% of men and 9% of women whilst an AHI > 15may be found in 9% of men and 4% of women. When the second criteria of day-time sleepiness is added as required for OSAS, these figures fall to 4% and 2% for men and women respectively  The prevalence of OSA increases as Body Mass Index [BMI] increases. The prevalence ofOSA is 41% in overweigh people with a BMI over 28 and as high as 78% in morbidly obese patients. Central Sleep Apnea (CSA)  CSA is characterized by recurrent apneic episodes during sleep in the absence of an upper airway obstruction and with minimal or no respiratory effort due to cessation of respiratory drive. Similar to OSA this results in oxygen desaturations, recurrent arousal and day-time s1eepiness.  the exact prevalence remains unknown Apnea-Hypopnea Index (AHI) The Apnea-Hypopnea Index [AHI] is the average number of apneas and hypopneas perhour. The suggested AHI cut points are 5, 15, and 30 events/hour to indicate mild, moderate, and severe levels of OSA respectively
  12. 12. Mohammed Almuzian, University of Glasgow 11 Respiratory Disturbance Index (RDI) This is also measured as events per hour of sleep and takes into account the average frequency of apneas and hypopneas as well as reductions of airflow with resultant arousal but without meeting the desaturation criteria for a hypopnea Pathophysiology 1. The respiratory blockage occurs at the level of the nasopharynx or oropharynex when the tongue falls backward and blocks the airway during sleep. 2. Obstruction can occur at a single or multiple levels along the upper airway, with theoropharynx or retroglossal airway being the most common site 3. The sleep is interrupted by periods of apnoea where the patient stops breathing for up to 15-20 seconds at a time. 4. When the CO2 level in the blood rises to a certain point (hypercapncea), it causes a sudden reflex intake of breath and breathing starts again. Prevalence 1. Adult population: 2% female and 4% male. (Bixler 2009) 2. In children 0.7% in Europe & 1,2% in USA (Bixler 2009) 3. More in Afro-Caribbean than other Classification of OSA This is done according to HAI (hypopnea and apnoea index) 1) Mild (5-15) episode of apenea per hour 2) Moderate (16-30) episode of apenea per hour 3) Sever (>30) episode of apenea per hour. In people with severe OSA these apnoea can happen up to 400 times per night. Aetiological factors A. Anatomical factors 1. Genetically determined retro-positioned facial skeleton 2. Functional impairment of the upper airway dilatory muscles.
  13. 13. Mohammed Almuzian, University of Glasgow 12 3. Chronic snoring: Upper airway muscle activity decreases during sleep leading to increased collapsibility of the pharyngeal tissues.“ Oedema or inflammation of pharyngeal tissues due to heavy snoring might not only narrow the upper airway but might also impair normal function of the receptors responsible for initiating protective reflexes.” 4. Craniofacial anatomy  Congenitally reduced nasopharyngeal and /or oropharyngeal dimensions as in some syndrome like Down, hypothyrodisim, Achndroplasia, Apert & Pierr Robin syndrome  Enlarged tongue.  Enlarged tonsils.  Nasal septal deviation  Blocked nose by allergy or rhinitis B. Risk factors 1. Age: OSA prevalence increases steadily with age throughout midlife with a 2- to 3-fold higher prevalence in persons above 65 years of age compared with those between 30-64 years of age. After 65 years it seems to plateau. This is due to  Dimensional changes in the airways related to age,  increased size of the soft palate,  Posterior positioned tongue  the inferior repositioning of the hyoid bone, 2. Gender: Twice more in male than female. This may be attributed to differences in:  upper airway shape  genioglossal muscle activity during the awake state, in craniofacial morphology,  pattern of fat deposition around the pharynx. Males have greater upper-body fat distribution and fat in the neck which males make them more susceptible to upper airway collapse 3. Genetics; The association of OSA amongst family members may be a reflection of lifestyle, but there are studies supporting a genetic predisposition to OSA in relation to craniofacial structure, body fat distribution and neural control of the upper airway muscles
  14. 14. Mohammed Almuzian, University of Glasgow 13 4. Ethnicity; OSA has a greater prevalence in Asian and African—American populations according to some studies, but at present, data from studies of groups other than white subjects are too sparse to determine with confidence if prevalence differs worldwide.” 5. Obesity: It is estimated that a 10% increase in weight is associated with a 6-fold greater risk of developing OSA among persons initially free of OSA. The correlation between OSA and BMI is weak though due to the fat distribution not being homogenous among obese people 6. Alcohol Intake: Alcohol and sedatives have an acute inhibitory effect on the genioglossal activity of thetongue & upper airway dilators that leads to an increase in snoring and as well as apnea andhypopnea frequency 7. Smoking 8. Sedatives, which can relax throat muscles, contributing to the collapse of the airway at night 9. Hypothyroidism. 10. Sleeping posture: Supin-dependent OSA or positional sleep apnea refers to patients who displays higher AHI when they are sleeping on their back compared to when they are sleeping on their side and comprises of an average of 56% of patients with OSA. Positional therapy can be used to prevent a patient from sleeping in the worst sleeping position which is usually, but not exclusively, the supine position. 11. Hormonal: • increase in testosterone • reduction in progesterone or menopause • Hypothyroidism • Acromegaly • Down syndrome • Marfan syndrome Sign and Symptoms Signs and symptoms associated with OSA (mentioned by Magliocca & Helman 2005, Jordan 2005) A. Nocturnal Signs and symptoms 1. Snoring or witness snoring 2. Apnoeas or witness apnea
  15. 15. Mohammed Almuzian, University of Glasgow 14 3. Choking or gasping 4. Restless sleep 5. Notcturia 6. Drooling 7. Xerostomia B. Daytime Signs and symptoms 1. Presence of the risk factors mentioned above 2. Morning headaches assessed by Epworth sleeping Score • Sleepiness over recent times can be subjectively measured in using the Epworth Sleepiness Scale (ESS), first described by Johns 1991. • This self-reported 8 item scale assesses the likelihood of falling asleep in various scenarios commonly encountered in daily life • Subjects are asked to rate the chance of falling asleep in each circumstance from 0 (no chance of dozing) to 3 (high chance of dozing). • The scores are tallied to give a total between 0 – 24, with those above 12 indicating excessive sleepiness • The ESS focuses on levels of sleepiness over the preceding two weeks and can be used to subjectively quantify sleepiness and assess change due to treatment effects 3. Excessive sleepiness 4. Impaired concentration 5. Depression 6. Decreased libido (Sexual problem) 7. Irritability C. Cephalometric feature  Solow et al. (1993, 1996) found that OSAHS patients have a high cervico-cranial angle compared to non-OSAHS subjects. This had been explained by Hellsing (1989) who found that elevation of the head also resulted in widening of the airway at this level, and as a result it may be stated that OSAHS patients tend to hold their head in a more extended position.  The SNA and SNB are severely reduced
  16. 16. Mohammed Almuzian, University of Glasgow 15 D. If OSA developed at early age with chronic nasal obstruction the following could be occurred 1. Blockage of the nasal airway results in elevation of the head in relation to the true vertical and the cervical column, in order to allow more air into the lungs. This has been shown in a primate experiment by Solow and Talgren 1969 as well as Harvold (1981), where artificial obstruction of the nasal airway in monkeys resulted in altered mandibular posture and an anterior open bite after a year with class II tendency. However there is no strong evidence to support this hypothesis. Vig et al 1981?? 2. Pectoris excavatim where the intercostal muscle fail to develop. 3. Hearing problem due to obstruction in the Austachian tube and this could be improve by RME, since RME help to increase the drainage from the tube 4. Nocturnal enuresis because of reduced vasopressin which normal released during Rapid Eye Movement stage of sleeping (REM). In case of sever chronic nasal blockage, there will be associated repeated apnea and so the REMis not achieved. (Kurol 2008) 5. Mental development because REM is not achieved then growth hormone will not be secreted. 6. Due to the above reason there is an impact on psychology and quality health of life Complications 1. Negative influence on the physical and mental growth, since the REM not achieved which is essential to secrete growth hormone. 2. Due to poor sleep at night, consequently, drowsiness during the day with cognitive impairment, impaired ability to operate a motor vehicle, and an increased automobile accident rate. 3. Rise in CO2 levels over a long period of time can result in pulmonary hypertension, heart failure and in some cases, sudden death during sleep due to stroke. Diagnosis 1. History from patient and sleeping partner 2. Examination including  ENT visual examination and assessment.
  17. 17. Mohammed Almuzian, University of Glasgow 16  laryngoscopy,  endoscopy during wakefulness: Endoscopy during wakefulness of patients with OSA is usually performed in the supineposition to assess the level of maximum narrowing in the upper airway. The patient can beasked to perform the Muller maneuver, which consists of a forced inspiratory effort againsta closed mouth and nose. The retropalatal and retrolingual level of the pharynx can beinvestigated during this maneuver and may be used to detect collapse in these areas. Thepredictive value of this maneuver is limited though, as it does not necessarily reflect theobstructions during sleep,  nasendoscopy during sleep: Fiberoptic endoscopy performed whilst the patient is asleep is known as nasendoscopy.It is a time consuming procedure if sedation is not used, but there is a risk that sedativesmay increase OSA due to hypotonia of the genioglossus. A further disadvantage is thatvarious levels of the airway cannot be observed simultaneously and quantifying the cross-sectional area is difficult and once again semi-objective. Videotaped images of the lumen canbe digitized and the cross-sectional area calculated, but it is a very time-consuming task  Somnofluoroscopy: SomnofluoroscopyFluoroscopy is a dynamic radiographic examination of the upper airway and incombination with PSG is called somnofluoroscopy. A preliminary image is recorded of thepatient in the supine position whilst they are awake and then further images are obtainedonce an obstructive event is witnessed on the PSG. This method is not widely used due tothe significant radiation exposure and the airway only being shown two—dimensionallywithout the possibility to make cross—sectional cuts  lateral cephalography,  CT scanning,  CBCT scanning and  MRI scanning. 3. Overnight polysomnography in sleep laboratory, measurements include:  AHI  Sleep time,  Sleep stages,  Respiratory effort,  Airflow,
  18. 18. Mohammed Almuzian, University of Glasgow 17  Cardiac rhythm,  Oximetry,  Limb movements  Body position Treatment 1. Conservative treatment:  Supine dependent OSA is indicated by a difference of 50% or more in AHI between supine and non-supine positions. Positional therapy can be used to prevent patients from sleeping in the worst sleeping positions, which is usually, but not always, the supineposition. Long term compliance remains an issue, but various techniques are used to prevent patients from assuming the supine position such as positional alarms, tennis balls sown into vests, or special pillows. MRI study has found that patients with positional have wider upper airways in the lateral dimension, which may explain the maintenance of pharyngeal airway patency in the lateral sleep position  Behavioural therapy: this will aim to reduce the risk factors. Many patients are told to avoid smoking or alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night  Bariatric surgery is increasingly performed for refractory medically complicated obesity. Due to the improvement in AHI with weight loss, it is thought that bariatric surgery may play a role in the treatment of morbidly obese OSA patients as an adjunct.  Pharmacological option: according to SIGN 2003 Pharmacological therapy should not be used as first line therapy for OSAHS. 2. Surgery to widen the nasopharynx like:  Septoplasty  Turbinate surgery  Tonsillectomy  Uvulo-palato-pharyngo-plasty (UPPP or UP3) are available to address pharyngeal obstruction. According to SIGN guidelines 2003 ‘’the use of UPPP or LAUP for the treatment of OSAHS is not recommended’’.
  19. 19. Mohammed Almuzian, University of Glasgow 18  Soft palate implants: it may attempt to shrink or stiffen excess tissue in the mouth or throat; the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues, According to NICE guidelines 2007 Current evidence on soft-palate implants for obstructive sleep apnoea (OSA) raises no major safety concerns, but there is inadequate evidence that the procedure is efficacious in the treatment of this potentially serious condition for which other treatments exist. Therefore, soft-palate implants should not be used in the treatment of this condition.  Tongue advancement.  By moving the major anchor point for the tongue forward, the procedure creates more room for the tongue to relax during sleep without obstructing the throat. The result is an enlargement and stabilization of the airway.  An incision is made inside the lower lip. The chin muscle and other soft tissues are cleared away to expose the central part of the lower jaw. Small rectangular cuts (roughly 1 x 2 cm, or less than ½ x 1 inch) are made in the lower jaw below the lower front teeth to capture the area of attachment of the genioglossus muscle. This rectangle of bone is moved forward and turned slightly. A small titanium screw is used to hold the bone fragment in place by securing it to the remainder of the lower jawbone.  RISKS 1. Bleeding 2. Infection 3. Tooth injury 4. Chin and lower lip numbness 5. Change in appearance 6. Weakening of the lower jawbone The jaw’s thickest, strongest portion is along the lower edge. This procedure is designed so that this part of the bone is not disturbed. 7. Trouble swallowing.  Mandibular advancement surgery where the mandible is markedly class II (which advances the tongue forward), With MMA, all the soft-tissue structures making up the pharyngeal walls are tightened at once (including the palatophyrangeous, hyoglossus, genioglossus,) this stops them from collapsing. The tongue is also pulled forward. The result is a significant
  20. 20. Mohammed Almuzian, University of Glasgow 19 increase of posterior airway space (PAS) and the resolution of the syndrome in a high (95%) percentage of cases  Tracheostomy has proven value; due to the fact the incision by-passes the pharyngeal airway. Naturally, the procedure is reserved for very severe obstructions which fail to respond to other treatment modalities, in view of its psychosocial morbidity. 3. Non-surgical treatment I- RME II- PFM III- Class II functional appliance IV- CPAP (Continuous Positive Airway Pressure)  A CPAP device consists of a unit that generates airflow, which is directed to the airway via a mask. Positive pressure is generated by the airflow, which prevents upper airway collapse.  Should be used for at least 6 hour per day/7 days a week  According to NICE guidelines 2006 and SIGN 2003, CPAP is recommended as a treatment option for adults with mild OSAHS. V- Tongue stabilising device (TSD)  A tongue-stabilizing device (TSD) is a preformed appliance and uses suction to protrude the tongue and improve upper airway structure and function. The earlier designs were similar to a mouthguard, covering the upper and lower teeth to assist retention, with a flexible bulb into which the tongue was protruded (Cartwright, 1985). The current design has no dental coverage, reduced bulk, and has the bulb being retained in place only by suction. There are currently only limited data on the efficacy of the current device, which is commercially available.  A tongue stabilizing device attaches to the end of the tongue using gentle suction andholds the tongue in a protruding position. It increases the anteroposterior diameter of thevelopharynx by displacing the tongue and soft palate anteriorly and the velopharyngeallateral diameter is extended more with TSD than compared to MAS.  This mouthpiece is made of soft medical grade silicone that is non-irritating to the gums. Unlike many oral devices that need to be fitted either in a laboratory or by using a boil-and- bite technique, aveoTSD is ready-to-use right out-of-the-box. It is available in small,
  21. 21. Mohammed Almuzian, University of Glasgow 20 medium, and large sizes, but the manufacturer states the medium fits about 95 percent of patients. Indication and advantages:  When PD is compromised or when there is few teeth to hold MARA.  Less gag reflex  Less dental side effect  Deane and Darendeliler 2009 (RCT) Objective testing showed the MAS and TSD had similar efficacy in terms of AHI reduction. Patients reported improvements with both devices; however, better compliance and a clear preference for MAS was apparent when both devices were offered. Longer term studies are needed to clarify the role of TSD. VI- Mandibular advancement device (MAD) which are similar to functional appliances  SIGN 2003 guidelines: It is an alternative therapy for patients who are unable to tolerate CPAP.  Cochrane review: by Carvalho 2008 for apnoea in children. It found that at present there is no sufficient evidence to state that oral appliances or functional orthopaedic appliances are effective in the treatment of OSAS in children. Another recent Cochrane review evaluated randomised trials in adults with OSA (Lim 2004). The review found that oral appliances were less effective than nasal CPAP and the use of oral appliances should be restricted to OSA subjects unwilling or unable to cope with nasal CPAP. Ideal Features of MAA 1. Robust
  22. 22. Mohammed Almuzian, University of Glasgow 21 2. Adjustable 3. Minimal chair side time 4. Good retention 5. Allow non-restricted movement of the mandible when it is in use. 6. Full occlusal coverage to prevent over-eruption of the teeth 7. Clinically proven Mechanism of action  The first is that it protrudes the lower jaw forward to thrust the tongue base forward, thereby enlarging the upper airway.  Another theory is that it decreases the pharyngeal collapsibility through improved muscle tone. “ The lateral wall of the soft palate anatomically connects to the base of the tongue through the palatoglossal arch. Anterior displacement of the mandible and tongue stretches the soft palate, stiffening the Velopharyngeal segment and decreasing its collapsibility Clinical and cephalometric predictors of successful treatment within MRA 1. Clinical predictors • Younger age • Lower body mass index • Supine-dependent OSA • Supine-dependent OSA • Smaller oropharynx • Smaller overjet • Shorter soft palate • Smaller neck circumference • Lower AHI 2. Cephalometric predictors • Shorter soft palate • Longer maxilla • Decreased distance between mandibular plane and hyoid bone
  23. 23. Mohammed Almuzian, University of Glasgow 22 Activation of the appliance  In general, the maximum protrusion is around 10mm. 20% of the maximum protrusion increase in the advancement of the mandible can improve the polysomnographic variables by 20%, but the ideal scenario is to undertake 75% advancement.  The degree of vertical opening has been shown not to have a significant impact on treatment efficacy. For comfort levels, a decreased Vertical opening of 4mm compared to14mm was preferred by patients.104 One study reported a decrease in the airway lumen with increased vertical opening of the MAS most likely due to the posterior rotation of the mandible.  Follow-up appointments with a dental specialist is recommended at least annually toevaluate the health of the oral structures and integrity of the occlusion, evaluate devicedeterioration and monitor patient adherence. If there are any signs and symptoms tosuggest worsening of OSA, the patient should be referred to a sleep physician for furtherassessment Classification of MAA The currently available appliances could be broadly classified into three types, based on a succession of design modifications, which importantly permit incremental advancement of the mandible: A. First generation. (non-adjustable)These were primarily one-piece in design, with no ability to incrementally advance the mandible. B. Second generation. (semi-adjustable)This type of appliance was principally two-piece in design and offered the potential for incremental advancement. However, this would often necessitate laboratory support and potentially were more time-consuming at the chair side. C. Third generation. (fully-adjustable)These appliances may be regarded as the ‘gold standard’ in design. They not only permit incremental advancement, which is self-adjustable, but also lateral movement of the mandible, and ensure the mandible is retained in its postured state during sleep
  24. 24. Mohammed Almuzian, University of Glasgow 23 Advantages of MAA 1) Non-invasive 2) Inexpensive 3) Easy to use in case of travelling 4) Clinically proved (Johal, 2004) to:  Effective in reducing snoring (40-60%)  Improve sleep quality  Reduce blood pressure  The durability of 0A is estimated at 1.5 to 3 years,  Compliance rate of 52-100% reported (Johal 1999) Disadvantage of MAA 1) Hypersalivation 2) Muscle discomfortability 3) Change in the bite 4) TMJ problem 1.

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