Sleep apnea and bruxism

Transcription

1 Sleep disordered breathing (SDB) Sleep apnea and bruxism CAPD-ACDP 2014 Annual Meeting, Montreal Increasing upper airway collapsibility Occasional snoring Habitual snoring Upper airway resistance syndrome Sleep apnea Andrée Montpetit, DMD, MSc, RCDC Nelly Huynh, PhD Snoring vibration of respiratory structures and the resulting sound, due to obstructed air movement while breathing during sleep. Obstructive Sleep Apnea (OSA) «characterized by repetitive episodes of complete (apnea) or partial (hypopnea) upper airway obstruction occurring during sleep. These events often result in reductions in blood oxygen saturation and are usually terminated by brief arousals from sleep.» Central Sleep Apnea «characterized on the polysomnogram by recurrent cessation off respiration during sleep with the apnea having no associated ventilatory effort.» Sleep study Epidemiology Mild 5 to 15 events/hr Moderate 15 to 30 events/hr Severe more than 30 events/hr Snoring 3% to 12% 25% Habitual snoring??? AHI 10 and over is treated if SLEEPINESS and HBP Sleep apnea 1% to 10% 2% Huynh et al AJODO Mild 1 to 5 events/hr Moderate 5 to 10 events/hr Habitual snoring abnormal Clinically significant 5/hr due to study on elevated BP [Bixler 2008] Severe more than 10 events/hr Prevalence peak between 2-8 y.o. [Fujioka 1979, Jeans 1981, Sahin 2009] 34% mouth breathers Dayyat 2007; AASM

2 Seasonal incidence Consequences As early as perinatal period Woman with OSA have increased risks for: 1.8% for low birth weight 2.3% for preterm birth 1.3% for small size for gestational age 1.7% for cesarian section 1.6% for preeclampsia/eclampsia Chen et al Am J Obstet Gynecol Walter et al Arch Dis Child Consequences Cardiovascular Metabolism Growth Cognition Can SDB grow an ADHD child? Following treatment: TNF-α (inflammatory cytokines) [Gozal 2010] Hypoxic stress sympathetic activation Insulin resistance (Type 2 Diabetes) nocturnal cortisol Hypersomnolence Growth delay Growth catch-up after T&A [Montgomery-Downs 2010; Ungkanont 2006; Liu 2005, Nimubona 2000; Trachtenbard 1998; Commare 1993; Breton 1993; Stradling 1990] [Kiris 2010; Aydogan 2007; Bar 1999] Controversial Execute functions and behavior [Lewin 2002, O Brien 2004, Beebe 2004, Halbower 2006, Honaker 2009, Calhoun 2009, Kohler 2009, Sahin 2009, Ting 2010] Constantin et al., 2014 Behav Sleep Med By 4 y.o., children with mouthbreathing, snoring and/or witnessed apnea were 20-60% more likely to exhibit behavioral difficulties consistent with clinical dx. By 7 y.o., they were % more likely. Bonnuck et al., 2012 Pediatr Consequence mortality in adults Risk factors Although there is no available data in children, untreated apnea leads to greater mortality in adults. Children 1. Nasal obstruction 2. Skeletal morphology 3. Soft tissues 4. Obesity Adults 1. Obesity 2. Nasal obstruction 3. Skeletal morphology 4. Soft tissues He et al., 1988 Chest Growth Aging 2

3 Nasal obstruction Risk factors Seasonal allergic rhinitis Deviated septum Hypertrophy of turbinates Children 1. Nasal obstruction 2. Skeletal morphology 3. Soft tissues 4. Obesity Adults 1. Obesity 2. Nasal obstruction 3. Skeletal morphology 4. Soft tissues Growth Aging RisksSymptomsSymptoms TreatmentsScreening Role of Dentist Dentist s rôle Clinical Treatments Evaluation PANIC study 6-8 years old with and without SDB Questionnaires Abnormal palatal morphology (Mallampati III or IV) Thick neck Adipose tissue under the chin Cross bite Open bite Convex facial profile Increased lower facial height Mandibular retrusion Tonsilar hypertrophy Ikavalko et al., 2012 PANIC study 6-8 years old with and without SDB Questionnaires Abnormal craniofacial morphology, but not excess body fat, is associated with an increased risk of having SDB in 6-8-year-old children Ikavalko et al., 2012 Craniofacial morphologies Strong association between OSA and congenital craniofacial malformations Mandibular hypoplasia Pierre-Robin Prader-Willi Treacher-Collins Marfant Maxillary hypoplasia Down syndrome Cleft palate Apert, Crouzon or Pfeiffer syndromes Authors Marino 2009 Pirila- Parkkinen 2009 Pirila- Parkkinen 2010 Tsuda 2010 Risk factors Studies 21 OSA pts (mean age 4.5 y.o.) Ceph 41 OSA pts (mean age 7.2 y.o.) vs 41 controls Dental casts 70 snorers/symptomatic OSA pts, 70 controls (mean age 7.2 y.o.) 173 children (20% strong snorers) OSA-18 and ceph Craniofacial morphology in children with OSA Long and narrow face Narrow width (high arch palate, narrow maxillary) Mandibular retrognatia 3

4 Predisposing factors/risks Risk factors Children Adults Sleep disordered breathing Craniofacial imbalances 1. Nasal obstruction 2. Skeletal morphology 3. Soft tissues 4. Obesity 1. Obesity 2. Nasal obstruction 3. Skeletal morphology 4. Soft tissues Growth Aging Soft tissues - airway Age tonsils and adenoids Controls OSA Narrowest at A+T A adenoids; T tonsils; A+T overlap; E epiglottis Arens et al In snoring children: T&A hypertrophy persists Papaioannou et al J Pediatr Soft tissues Tonsils classification: Macroglossy Often in association with a syndrome 4

5 Soft tissues Long soft palate Airway obstruction from soft tissues Risk factors Children 1. Nasal obstruction 2. Skeletal morphology 3. Soft tissues 4. Obesity Growth Adults 1. Obesity 2. Nasal obstruction 3. Skeletal morphology 4. Soft tissues Aging Obesity Obese children have a (4.5x) increased risk of developing obstructive sleep apnea [Redline 1999] Incidence of SDB: Obese children 46% [Marcus 1996] Morbidly obese children 55% [Kalra 2005] Possible causes: Adipose tissue deposited in pharyngeal area (fat pads) [Shelton 1993, Schwab 2003] Tissus adipeux viscéral [Vgontzas 2008, Makino 2009] Risk factors Breastfeeding and snoring Children 1. Nasal obstruction 2. Skeletal morphology 3. Soft tissues 4. Obesity Growth Adults 1. Obesity 2. Nasal obstruction 3. Skeletal morphology 4. Soft tissues Aging Breastfeeding for at least one month reduced the risk of parent reported snoring and witnessed apneas. In this study, no children breastfed more than 3 month had witnessed apneas at age 8. Brew et al PLOS one 5

6 Mouth breathing Growth Septal deviation/chronic rhinitis Often associated with upper airway obstruction Tonsils & Adenoids hypertrophy Nasal congestion Associated with habitual snoring Nasal airway resistance Mouth breathing If present during growth, it can alter the development of the canial and jaw morphology. Alters position of tongue (stays low) Deep and narrow palate Sleep in OSA children Pre-school age children s sleep is not affected as much as school age children. But they have more central apeas Mouth breathing is associated with a clockwise mandibular rotation, increased lower face hight, cl.ii malocclusions and high arch palates. Harari 2010, D Ascanio 2010, Peltomäki 2007, Mattar 2004 Walter et al Sleep Med Daytime signs and symptoms Hyperactivity Behaviour problems Attention deficit Sleepiness Nightime signs and symptoms Agitated sleep Sweating Nocturia / enuresis Nightmares Bruxism 6

7 Bruxism Bruxism - prevalence 1997 AASM published ICSD-1 Classified as parasomnia 2005 AASM published ICSD-2 Classified as movement disorder 2013 International consensus (and ICSD-3) Repetitive jaw-muscle activity characterized by clenching or grinding of the teeth and/or by bracing or thrusting of the mandible < 40% 13% Sleep bruxism is the 3rd most frequent parasomnia [Ohayon 2001] 6-8% < 12 y.o y.o. Adults > 60 y.o. Reding 1966; Goulet 1992; Lavigne 1994; Ohayon 2001; Laberge 2000; Cheifetz % Bruxism ground, clenched, tapped or made noise with their teeth during sleep or any time in their life (n=1019) Bruxism parental reports Rhythmic masticatory activity (quantitative) associated to parental reports (qualitative): Prevalence with questionnaires 12.5% Sleep recording (complete PSG) Prevalence with PSG 7.4% Qualitative + quantitative Questionnaire + PSG 5.5% Maluly et al., Bruxism risk factors Moderate daytime fatigue OR 1.3 Stress/anxiety (OR 1.3) Snoring (OR 1.2) Bruxism and OSA In patients with bruxism: 4.8% in bruxers vs. 1.4% in non-bruxers Apnea 2-3x more frequent in bruxers Reduction of bruxism with mandibular advancement appliances [Landy 2006; Carra 2013] Nicotine (OR 1.3) Selfreported Bruxism Sleep apnea (OR 1.8) In patients with OSA: 50% of children with OSA will develop bruxism [Lamberg 2008] Bruxism decreases or disappears in 75% of children following adenotonsillectomy [DiFrancesco 2004] Daily caffeine (OR 1.4) Daily alcohol (OR 1.5) Ohayon et al., 2001 Sleep bruxism Bruxism may help to reestablish airway opening OSA 7

8 Sleep testing type I in-lab attended polysomnography [EEG, EOG, EMG, EKG, breathing, oxymetry, audio-video] In-lab attended Unattended (usually at home) Type I Type II Type III Type IV Info derived: Sleep EEG arousals Hypoxia Respiratory events EKG arrhythmia Leg movements RisksSymptomsSymptoms TreatmentsScreening Role of Dentist Dentist s role Clinical Treatments Evaluation type IV limited home polysomnography [3 channels: breathing (efforts), oxymetry] Info derived: Hypoxia as a screen for sleep apnea Screening and referral to pediatric sleep specialist or ENT Provide craniofacial assessment and growth follow-up ROLE OF THE DENTIST (pedodontist/orthodontist) Treat or refer to address craniofacial anomalies Role Diagnostic by a sleep physician Sleep disordered breathing Craniofacial imbalances Medical history Physical exam Sleep study 8

9 Medical history Family genetic predisposition Sleep bruxism was more frequently observed in monozygotic twins [Lindqvist 1974; Hublin 1998] Increased sibling risk of OSA in children, which may be due to heritable genes and/or shared environment [Friberg 2009] Lifestyle and/or behavior modification Positive airway pressure Medication Oral devices Surgery Dento-facial orthopedics Weight loss Avoid alcohol, sedatives and hypnotics Positional therapy Continuous positive airway pressure (CPAP) Auto-titrating CPAP Bi-level PAP Nasal corticosteroids Leukotriene receptor antagonist Tongue-retaining device Palatal-lifting device Mandibular advancing device Nasal surgery Tonsillectomy Uvulopalatopharyngoplasty (UPPP) Lingualplasty Genioglossus and hyoid advancement Sliding genioplasty Maxillo-mandibular advancement osteotomy (MMA) Laser-assisted uvulopalatoplasty (LAUP) Radiofrequency volumetric tissue reduction Tracheostomy Bariatric surgery Rapid Maxillary Expansion Surgically-Assisted Rapid Maxillary Expansion Myofunctional Device (mandibular) If left untreated? Author Study Development Marcus 1998 Topol 2001 Anuntaseree 2005 Li 2010 N=20 (2-15y.o.) Primary snoring 1-3 yrs F/U with PSG N=13 children Primary snoring 3 yrs F/U with PSG N=755 children (questionnaires) N=7 children (PSG) Snoring/OSA 3 yrs F/U N=45 (6-13y.o.) Mild OSA (1-5/hr) 2 yrs F/U with PSG Majority do not develop OSA 10% have moderate OSA after 3 yrs No difference between patients and controls Only youngest child developed OSA 65% 9 to of snorers 29% of stopped children with SDB 9% of children will continue/aggravate developed OSA Moderate improvement 29% aggravate (male, regular snoring, hypertrophy of tonsils, waist circumference) Weight loss (obesity) With a loss of 32% of their BMI, a success rate of 71% 12 of 49 patients (24%) have persistent OSA even following weight loss Van Hoorenbeeck et al., 2012 Sleeping position In 3-5y.o., no difference in AHI associated with position Nasal corticosteroids 6 weeks 25 children between 1 and 10 y.o. In 6-10y.o. and 11-13y.o., side-sleeping is associated with a decreased AHI vs. on their back Zhang et al., 2007 Brouillette et al.,

10 Montelukast Singulair : leukotriene receptor antagonist for asthma and seasonal allergies First-line treatments 1. Adenotonsillectomy 2. Positive airway pressure 2. Maxillary expansion 4-5 mg/d for 12 weeks Goldbart et al., 2012 Adenotonsillectomy Friedman et al., 2009 AHI <1 post-op (meta-analysis of 23 studies) 60% success AHI <5 post-op 66% success Adenotonsillectomy Hypoxemia (4 studies) Improvement of nocturnal oxygen saturation Blood pressure (3 studies) Mixed results, although increased BP associated with recurrent OSA Carvalho et al., 2012 Adenotonsillectomy, is curative in approximately 80% of pediatric cases of pediatric OSA 20 to 40% cases are not resolved Cardiovascular control (4 studies) Decrease in sympathetic activity Inflammation and endothelial function (8 studies) C-reative protein (marker of inflammation) decreased Altered endothelial function reversed Cardiac function and structure (3 studies) Echocardiographic findings return to normal Vlahandonis et al., 2013 Persistent apnea PSG1 pre-op PSG2 post-op Persistent apnea Recurrent SDB is reported in teenagers after over 10 yrs following adenotonsillectomy 13 symptomatic children (27%) PSG3 1.5yr F/U PSG3 confirms persistent apnea in 9 children (18.4%) 70% have adenoids regrowth Tagaya et al., 2012 Guilleminault et al., 1999; Tasker et al.,

11 Craniofacial analyses 20 non-operated children (mdx) vs. 20 children with adenotonsillectomy In children with adenotonsillectomy: Mandibular posterior position Backward rotation of the mandible Rotation postérieure de la mandibule Class II Stenosis/narrowing of the nasopharyngeal airway Elongated soft palate high probability of the necessity of adenotonsillectomy when a morphological factor played a major role for OSA Positive airway pressure Some craniofacial changes midface hypoplasia (nasal mask) Case-report: CPAP worn between 5 to 15 y.o. * Mostly used in children with complicating medical disorders Sato et al., 2012 Li et al., 2000 Orthodontics Improvement in dento-facial morphology can have a positive impact on SDB and OSA. Rapid maxillary expansion Maxillary expansion Role in OSA treatment in children Widens nasal fossa Reduces nasal airway resistance Pirelli 2004 Villa 2007 Miano 2008 Pirelli 2010 Villa 2011 Orthopaedic maxillary advancement Orthopaedic mandibular advancement Pirelli P et al., Prog Ortho Baseline AHI Post-expansion AHI 4 short term studies+ 1 long term study (2 years) Pirelli 2004, Pirelli 2005, Miano 2009, Villa 2007, Villa 2011 Rapid maxillary expansion Caution with expansion Sleep disordered breathing Craniofacial imbalances 15 OSA children underwent RPE: 8 improved 7 stationary or worsened Iwasaki et al AJODO Marino et al., 2012 Eur J Paediatr Dent 11

12 More than one treatment? More than one treatment? 31 OSA patients Group 1 T & A surgery RPE Baseline Severe OSA in both groups T&A: AHI 4.9 RPE: AHI 5.4 Final: AHI 0.9 in both groups Group 2 RPE T & A surgery Guilleminault et al., 2008 Guilleminault et al., 2008 More than one treatment? Persistent apnea Resolved Adenotonsillectomy 25 children Pre-PSG AHI 17 Post-PSG AHI 1.8 Rapid palatal expansion 22 children Pre-PSG AHI 5 Post-PSG AHI 2.6 Adenotonsillectomy + Rapid palatal expansion 5 children Pre-treatment PSG AHI 10.1 Post-treatment PSG AHI 0.9 Villa et al., 2013 Functional appliances Study Population Methods Results Cozza OSA patients (4 8 y.o.) vs 20 CTL Villa OSA patients (4 10 y.o.) with malocclusion PSG; Cephalometric Rx; MONOBLOC APPLIANCE (for 6 months) PSG; JAW POSITIONING APPLIANCE (for 6 months) Differences in craniofacial morphology between groups (at baseline) Reduction of AHI in the OSA group following tx with monobloc Reduce daytime sleepiness Reduction in AHI/resolution of OSA in the treated group compared with non treated patients Improve snoring, oral breathing, sleep quality, sleepiness, irritability and tiredness Cozza et al., 2004; Villa et al., 2002 To extract or not Exo (n=20) vs. Non-ex (n=20) Where to refer Pediatric Dental Sleep Apnea (PDSA) network Multicentre incidence study of craniofacial morphology in children assessed in sleep clinics followed from 12 to 15 y.o. similar growth was seen for Oropharyngeal volume Minimal Axial Area Valiathan et al.,