Sleep Apnea and Bruxism Habitual Snoring

CAPD/ACDP Montreal 2014‐09‐13

Sleep disordered breathing (SDB)

Occasional snoring

Sleep apnea and bruxism Habitual snoring

CAPD-ACDP 2014 Annual Meeting, Montreal Upper airway resistance syndrome Sleep apnea Increasing upper airway collapsibility airway upper Increasing

Andrée Montpetit, DMD, MSc, RCDC Nelly Huynh, PhD Mechanisms RisksSymptomsSymptomsTreatmentsScreeningRole of DentistDentist’s roleClinicalTreatments Evaluation  [email protected]  [email protected]

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. »

Mechanisms RisksSymptomsSymptomsTreatmentsScreeningRole of DentistDentist’s roleClinicalTreatments Evaluation Mechanisms RisksSymptomsSymptomsTreatmentsScreeningRole of DentistDentist’s roleClinicalTreatments Evaluation

Sleep study Epidemiology

• Snoring

Mild Moderate Severe • 3% to 12% 25% 5 to 15 events/hr 15 to 30 events/hr more than 30 events/hr

Habitual snoring ??? • Sleep apnea AHI ≥ 10 and over is treated if SLEEPINESS and HBP • 1% to 10% 2% Huynh et al. 2012 AJODO

Mild Moderate Severe 1 to 5 events/hr 5 to 10 events/hr more than 10 events/hr 34% mouth breathers Habitual snoring abnormal Clinically significant ≥5/hr due to study on elevated BP [Bixler 2008] • Prevalence peak between 2-8 y.o. [Fujioka 1979, Jeans 1981, Sahin 2009]

Dayyat 2007; AASM 2005

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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. 2012 Am J Obstet Gynecol Walter et al. 2013 Arch Dis Child

Consequences Can SDB grow an ADHD child?

Cardiovascular Metabolism Growth Cognition

Hypoxic stress Growth delay Controversial ↓ ↑sympathetic activation Growth catch-up Execute functions ↓ after T&A and behavior Insulin resistance (Type 2 Diabetes) ↑ ↑nocturnal cortisol Following treatment: ↑ Hypersomnolence Constantin et al., 2014 Behav Sleep Med ↓ TNF-α [Montgomery-Downs 2010; Ungkanont 2006; Liu 2005, (inflammatory Nimubona 2000; • By 4 y.o., children with mouthbreathing, snoring and/or witnessed apnea were cytokines) Trachtenbard 1998; [Lewin 2002, O’Brien 2004, Commare 1993; Breton Beebe 2004, Halbower 2006, 20-60% more likely to exhibit behavioral difficulties consistent with clinical dx. 1993; Stradling 1990] Honaker 2009, Calhoun 2009, [Kiris 2010; Aydogan 2007; Kohler 2009, Sahin 2009, [Gozal 2010] Bar 1999] Ting 2010] • By 7 y.o., they were 40-100% more likely. Bonnuck et al., 2012 Pediatr

Consequence – mortality in adults Risk factors

Children Adults

Although there is no 1. Nasal obstruction 1. Obesity available data in children, 2. Skeletal morphology 2. Nasal obstruction untreated apnea leads to 3. Soft tissues 3. Skeletal morphology greater mortality in 4. Obesity 4. Soft tissues adults. 5. Familial predisposition 5. Familial predisposition

Growth Aging He et al., 1988 Chest

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Nasal obstruction Risk factors

Children Adults • Seasonal allergic rhinitis • Deviated septum 1. Nasal obstruction 1. Obesity • Hypertrophy of turbinates 2. Skeletal morphology 2. Nasal obstruction 3. Soft tissues 3. Skeletal morphology 4. Obesity 4. Soft tissues 5. Familial predisposition 5. Familial predisposition

Growth Aging

PANIC study PANIC study

• 6-8 years old with • 6-8 years old with and without SDB and without SDB • Questionnaires • Questionnaires

• Abnormal palatal morphology (Mallampati III or IV) • Thick neck • Adipose tissue under the chin • Abnormal craniofacial morphology, but not excess

• Cross bite body fat, is associated with an increased risk of having • Open bite SDB in 6-8-year-old children • Convex facial profile • Increased lower facial height • Mandibular retrusion • Tonsilar hypertrophy Ikavalko et al., 2012 Ikavalko et al., 2012

Craniofacial morphology Craniofacial morphologies in children with OSA • Strong association between OSA and congenital craniofacial malformations Risk factors Authors Studies • Mandibular hypoplasia Marino 21 OSA pts (mean age 4.5 y.o.) • Pierre-Robin 2009 Ceph Long and narrow face • Prader-Willi • Treacher-Collins Pirila- 41 OSA pts (mean age 7.2 y.o.) vs Narrow width • Marfant Parkkinen 41 controls 2009 Dental casts (high arch palate, narrow maxillary) Pirila- • Maxillary hypoplasia 70 snorers/symptomatic OSA pts, Parkkinen • Down syndrome 70 controls (mean age 7.2 y.o.) • Cleft palate 2010 Mandibular • Apert, Crouzon or Pfeiffer syndromes Tsuda 173 children (20% strong snorers) retrognatia 2010 OSA-18 and ceph

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Predisposing factors/risks Risk factors

Children Adults

1. Nasal obstruction 1. Obesity 2. Skeletal morphology 2. Nasal obstruction Sleep Craniofacial disordered 3. Soft tissues 3. Skeletal morphology imbalances breathing 4. Obesity 4. Soft tissues 5. Familial predisposition 5. Familial predisposition

Growth Aging

Soft tissues - airway Age – tonsils and adenoids

Controls OSA

• Narrowest at A+T

• In snoring children: T&A hypertrophy persists A – adenoids; T – tonsils; A+T – overlap; E – epiglottis Arens et al. 2003 Papaioannou et al. 2013 J Pediatr

MécanismesMechanisms RisquesRisksSymptomsSymptômesSymptomsTreatmentsTraitementsScreeningRoleRôle of duDentist dentisteDentist’s roleClinicalÉvaluationTreatments Evaluation clinique MécanismesMechanisms RisquesRisksSymptomsSymptômesSymptomsTreatmentsTraitementsScreeningRoleRôle of duDentist dentisteDentist’s roleClinicalÉvaluationTreatments Evaluation clinique

Soft tissues Macroglossy

• Tonsils • Often in association with a syndrome • classification:

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Soft tissues Airway obstruction from soft tissues • Long soft palate

Risk factors Obesity

Children Adults • Obese children have a (4.5x) increased risk of developing obstructive sleep apnea [Redline 1999] 1. Nasal obstruction 1. Obesity 2. Skeletal morphology 2. Nasal obstruction • Incidence of SDB: 3. 3. Soft tissues Skeletal morphology • Obese children– 46% [Marcus 1996] 4. Obesity 4. Soft tissues • Morbidly obese children– 55% [Kalra 2005] 5. Familial predisposition 5. Familial predisposition • Possible causes: • Adipose tissue deposited in pharyngeal Growth Aging area (fat pads) [Shelton 1993, Schwab 2003]

Mechanisms RisksSymptomsSymptomsTreatmentsScreeningRole of DentistDentist’s roleClinicalTreatments Evaluation MécanismesMechanisms• TissusRisquesRisks SymptomsadipeuxSymptômesSymptomsTreatments TraitementsviscéralScreeningRole Rôle[Vgontzas of duDentist dentisteDentist’s 2008, Makino roleClinicalÉvaluation 2009] Treatments Evaluation clinique

Risk factors Breastfeeding and snoring

Children Adults

1. Nasal obstruction 1. Obesity 2. Skeletal morphology 2. Nasal obstruction 3. Soft tissues 3. Skeletal morphology 4. Obesity 4. Soft tissues 5. Familial predisposition 5. Familial predisposition

• Breastfeeding for at least one month reduced the risk of parent reported snoring and witnessed apneas. Growth Aging • In this study, no children breastfed more than 3 month had witnessed apneas at age 8. Brew et al. 2014 PLOS one

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Growth Mouth breathing Septal deviation/chronic rhinitis

• Often associated with upper airway obstruction  Nasal airway resistance • Tonsils & Adenoids hypertrophy • Nasal congestion Mouth breathing

• Associated with habitual snoring Alters position of tongue (stays low) • If present during growth, it can alter the development of the canial and jaw morphology. 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 Walter et al. 2012 Sleep Med malocclusions and high arch palates. MécanismesMechanisms RisquesRisksSymptomsSymptômesSymptomsTreatmentsTraitementsScreeningRoleRôle of duDentist dentisteDentist’s roleClinicalÉvaluationTreatments Evaluation clinique Harari 2010, D’Ascanio 2010, Peltomäki 2007, Mattar 2004

Daytime signs and symptoms Nightime signs and symptoms

• Hyperactivity • Agitated sleep • Behaviour problems • Sweating • Attention deficit • Nocturia / enuresis • Sleepiness • Nightmares • Bruxism

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Bruxism Bruxism - prevalence

45 40 Sleep bruxism is the 3rd most 35 frequent parasomnia [Ohayon 2001] 30 2013 < 40% 25 2005 International consensus 20 AASM published (and ICSD-3) 15 1997 ICSD-2 10 13% AASM Classified as 5 3% movement “Repetitive jaw-muscle activity 6-8% published characterized by clenching or 0 ICSD-1 disorder grinding of the teeth and/or by < 12 y.o. 18-29 y.o. Adults > 60 y.o. Classified as bracing or thrusting of the Reding 1966; Goulet 1992; Lavigne 1994; Ohayon 2001; Laberge 2000; Cheifetz 2005 parasomnia mandible”

Bruxism Bruxism – parental reports

“ground, clenched, tapped or made noise with their teeth during sleep or any time • Rhythmic masticatory activity (quantitative) associated to parental reports (qualitative): in their life” (n=1019)

Prevalence with questionnaires 12.5%

Sleep recording (complete PSG)

Prevalence with PSG 7.4%

Qualitative + quantitative

Questionnaire + PSG 5.5%

Maluly et al., 2013

Bruxism – risk factors Bruxism and OSA

Moderate daytime fatigue • In patients with bruxism: OR 1.3 • 4.8% in bruxers vs. 1.4% in non-bruxers • Apnea 2-3x more frequent in bruxers Stress/anxiety Snoring (OR (OR 1.3) 1.2) • Reduction of bruxism with mandibular advancement appliances [Landy 2006; Carra 2013]

• In patients with OSA: Self- • 50% of children with OSA will develop bruxism [Lamberg 2008] reported • Bruxism decreases or disappears in 75% of children following Nicotine Bruxism Sleep apnea adenotonsillectomy [DiFrancesco 2004] (OR 1.3) (OR 1.8)

Sleep OSA Bruxism bruxism may help to re- establish Daily alcohol Daily caffeine airway (OR 1.4) Ohayon et al., 2001 (OR 1.5) opening

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type I – in-lab attended polysomnography Sleep testing [EEG, EOG, EMG, EKG, breathing, oxymetry, audio-video]

Info derived: • Sleep In-lab attended • Type I • EEG arousals • Hypoxia • Respiratory events • EKG arrhythmia • Leg movements

• Type II Unattended • Type III (usually at home) • Type IV

Mechanisms RisksSymptomsSymptomsTreatmentsScreeningRole of DentistDentist’s roleClinicalTreatments Evaluation

type IV – limited home polysomnography ROLE OF THE DENTIST [3 channels: breathing (efforts), oxymetry] (pedodontist/orthodontist)

Info derived: • Screening and referral to pediatric sleep specialist or

• Hypoxia as a ENT screen for sleep apnea • Provide craniofacial assessment and growth follow-up

• Treat or refer to address craniofacial anomalies

Role Diagnostic by a sleep physician

• Medical history

• Physical exam

• Sleep study Sleep Craniofacial disordered imbalances breathing

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Lifestyle and/or • Weight loss behavior • Avoid alcohol, sedatives and hypnotics Medical history modification • Positional therapy • Continuous positive airway pressure (CPAP) Positive airway • Auto-titrating CPAP pressure • Bi-level PAP • Family – genetic predisposition • Nasal corticosteroids Medication • Leukotriene receptor antagonist • Tongue-retaining device Oral devices • Palatal-lifting device • Sleep bruxism was more frequently observed in monozygotic • Mandibular advancing device twins [Lindqvist 1974; Hublin 1998] • Nasal surgery • Tonsillectomy • Uvulopalatopharyngoplasty (UPPP) • Lingualplasty • Increased sibling risk of OSA in children, which may be due to • Genioglossus and hyoid advancement heritable genes and/or shared environment [Friberg 2009] Surgery • Sliding genioplasty • Maxillo-mandibular advancement osteotomy (MMA) • Laser-assisted uvulopalatoplasty (LAUP) • Radiofrequency volumetric tissue reduction • Tracheostomy • Bariatric surgery • Rapid Maxillary Expansion Dento-facial • Surgically-Assisted Rapid Maxillary Expansion orthopedics • Myofunctional Device (mandibular)

If left untreated? Weight loss (obesity) Author Study Development • With a loss of 32% of their BMI, a success rate of 71% N=20 (2-15y.o.) •Majority do not develop OSA Marcus 1998 Primary snoring •10% have moderate OSA after 3 yrs 1-3 yrs F/U with PSG • 12 of 49 patients (24%) have persistent OSA even following N=13 children •No difference between patients and controls weight loss Topol 2001 Primary snoring •Only youngest child developed OSA 3 yrs F/U with PSG N=755 children •65%9 toof snorers29% of stopped children with SDB (questionnaires) •9% of childrenwill continue/aggravate developed OSA Anuntaseree 2005 N=7 children (PSG) Snoring/OSA 3 yrs F/U N=45 (6-13y.o.) •Moderate improvement Li 2010 Mild OSA (1-5/hr) •29% aggravate (male, regular snoring, 2 yrs F/U with PSG hypertrophy of tonsils, ↑waist circumference) Van Hoorenbeeck et al., 2012

Sleeping position Nasal corticosteroids

• In 3-5y.o., no difference in AHI associated with • 6 weeks position • 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., 2001

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Montelukast First-line treatments

• Singulair : leukotriene receptor antagonist for asthma 1. Adenotonsillectomy 2. Positive airway pressure and seasonal allergies

2. Maxillary expansion

• 4-5 mg/d for 12 weeks Goldbart et al., 2012

Adenotonsillectomy Adenotonsillectomy

• Hypoxemia (4 studies) • Improvement of nocturnal oxygen saturation Friedman et al., 2009 AHI <1 post-op AHI <5 post-op (meta-analysis of 23 studies) 60% success 66% success • Blood pressure (3 studies) • Mixed results, although increased BP associated with recurrent OSA

Adenotonsillectomy, • Cardiovascular control (4 studies) Carvalho et al., 2012 is curative in approximately 80% of • Decrease in sympathetic activity pediatric cases of pediatric OSA • Inflammation and endothelial function (8 studies) • C-reative protein (marker of inflammation) decreased 20 to 40% cases are not resolved • Altered endothelial function reversed

• Cardiac function and structure (3 studies) • Echocardiographic findings return to normal Vlahandonis et al., 2013

Persistent apnea Persistent apnea PSG1 pre-op • Recurrent SDB is reported in teenagers after over 10 yrs following adenotonsillectomy PSG2 post-op

• 13 symptomatic children (27%)

PSG3 1.5yr • PSG3 confirms persistent apnea in 9 children F/U (18.4%)

• 70% have adenoids regrowth Tagaya et al., 2012 Guilleminault et al., 1999; Tasker et al., 2002

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Craniofacial analyses Positive airway pressure

• 20 non-operated children (mdx) vs. 20 children with adenotonsillectomy • Some craniofacial changes • In children with adenotonsillectomy: • Mandibular posterior position • midface hypoplasia (nasal mask) • Backward rotation of the mandible • Rotation postérieure de la mandibule • Class II • Case-report: CPAP worn between 5 to 15 y.o. • Stenosis/narrowing of the nasopharyngeal airway • Elongated soft palate

high probability of the necessity of adenotonsillectomy when a * Mostly used in children with morphological factor played a major role for OSA complicating medical disorders

Sato et al., 2012 Li et al., 2000

Orthodontics Rapid maxillary expansion

20 • Improvement in dento-facial morphology can have a 18 positive impact on SDB and OSA. 16 14

12 Pirelli 2004 • Maxillary expansion 10 Villa 2007 • Role in OSA treatment in children 8 Miano 2008 • Widens nasal fossa 6 Pirelli 2010 Villa 2011 • Reduces nasal airway resistance 4 2 0 Baseline AHI Post-expansion • Orthopaedic maxillary advancement Pirelli P et al., Prog Ortho 2005 AHI 4 short term studies+ 1 “long” term study (2 years) • Orthopaedic mandibular advancement Pirelli 2004, Pirelli 2005, Miano 2009, Villa 2007, Villa 2011

Rapid maxillary expansion Caution with expansion

15 OSA children underwent RPE: Sleep Craniofacial disordered • 8 improved imbalances breathing • 7 stationary or worsened

Iwasaki et al. 2012 AJODO Marino et al., 2012 Eur J Paediatr Dent

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More than one treatment? More than one treatment?

31 OSA patients

Group T & A Baseline T&A: AHI 4.9 Final: AHI 0.9 RPE Severe OSA in RPE: AHI 5.4 in both groups 1 surgery both groups

Group T & A RPE 2 surgery

Guilleminault et al., 2008 Guilleminault et al., 2008

More than one treatment? Functional appliances

Adenotonsillectomy Rapid palatal expansion Study Population Methods Results

25 children 22 children Cozza 2004 20 OSA patients (4‐ PSG; Cephalometric Rx; • Differences in craniofacial Pre-PSG – AHI 17 Pre-PSG – AHI 5 8 y.o.) vs 20 CTL MONOBLOC APPLIANCE morphology between groups (at ↓ ↓ (for 6 months) baseline) Post-PSG – AHI 1.8 Post-PSG – AHI 2.6 • Reduction of AHI in the OSA group following tx with monobloc • Reduce daytime sleepiness Persistent apnea Villa 2002 32 OSA patients (4‐ PSG; JAW POSITIONING • Reduction in AHI/resolution of OSA Resolved 10 y.o.) with APPLIANCE (for 6 in the treated group compared with Adenotonsillectomy + Rapid palatal expansion malocclusion months) non‐treated patients • Improve snoring, oral breathing, 5 children sleep quality, sleepiness, irritability Pre-treatment PSG – AHI 10.1 and tiredness ↓ Post-treatment PSG – AHI 0.9

Villa et al., 2013 Cozza et al., 2004; Villa et al., 2002

To extract or not Where to refer

• Pediatric Dental Sleep Apnea (PDSA) network • Multicentre incidence study of craniofacial morphology in children assessed in sleep clinics Exo (n=20) vs. Non-ex (n=20)

followed from 12 to 15 y.o.

similar growth was seen for • Oropharyngeal volume • Minimal Axial Area

Valiathan et al., 2010

MécanismesMechanisms RisquesRisksSymptomsSymptômesSymptomsTreatmentsTraitementsScreeningRoleRôle of duDentist dentisteDentist’s roleClinicalÉvaluationTreatments Evaluation clinique