Sleep Apnea - AAO · PDF file1.Current Sleep Apnea Protocols Manage Rather than Prevent AAP guidelines omit orthodontics Focus should be the 4 year old; ... reM sleep. stages 1-2 are

Sleep Apnea:What Every Othodontist Needs to Know

www.coredentistry.com

Jeff Rouse, DDS

[email protected]

210.828.3334

6 Important Airway Issues

Sleep Dentistry- study of a mandibular advancement appliance's impact on the airway

Sleep Prosthodontics- study of the airway's impact on the stomatognathic system

1. Current Sleep Apnea Protocols Manage Rather than Prevent

AAP guidelines omit orthodonticsFocus should be the 4 year old; AOO guidelines omit the child

2. Problem is Bigger than Apnea

Sleep Apnea Facts- see Terminolgy Handout for de!nitions

Children OSA 2-3%, increase with obesity, UARS most common

Men OSA middle age 22%, elderly 42%- increase weight and lost muscle tone

Women OSA levels low until aer menopause- progesterone key

UARS- <5 AHI, >5 RERA; young "t females, children- impact from SNS activity

3. Airway must be Managed Awake and Asleep

Airway Prosthodontics- must maintain the airway 24/7 including during eating

Airway Occlusion- chewing patterns loose harmony when stressed to breath

Nocturnal- wear

Diurnal bruxism and function- wear, fracture

4. Age and Sex Creates Different Issues and Significance

Young, fit females- UARS, sleep onset insomnia, sleep maintenance insomnia, TMD/myofascial pain

Old, fat men- Bruxism TRAID- apnea, bruxism, reflux

5. Impact of Sleep Disordered Breathing on Children

Growth Phases (Rouse, JS Inside Dentistry 2013;7:60-80)

Early-birth to 4 (tonsil and adenoid hypertrophy) SDB due to premature birth and incomplete development or low tongue tone and weak orofacial hypotonia.

Late- 4-12, tonsils and adenoid growth created airway obstruction, adenoids are major source of abnormal breathing (mouthbreathing), tonsils lesser role

Mixed- early growth cluster that is further impacted when lymphoid tissue increases

Neurocognitive- (Bonuck, K, Freeman, K Chervin, R, Xu, L. Pediatrics 2012) Increased signi"cant effect in children with signi"cant SDB, Symptoms at 6-18 months= 40-50% increased risk at 7 years, "Worst case" SDB until 2.5 yr then resolve predictive of hyperactivity and conduct/peer issues, "Late" no problem until 4 yo= hyperactivity and anxiety/depression. Altered ENT and Pediatrian protocols for snoring children. Damage is not reversible.

Impact- Craniofacial- adenoid enlargement increases risk of mouth breathing, tonsils additive. Point of airway obstruction dictates adaptation which can alter craniofacial growth

Systemic- cardiovascular morbidity and endothelial dysfunction in children. Obesity magni"es impact

Treatment-Varies based on Age and Cooperation (See RSL Treatment Algorithm)

Main treatments in children are T&A and Orthodontics. Key is reducing AHI<1 and getting the child to close their mouth and become a nasal breather. May require re-training of old habits

Typical referrals: 1. Sleep MD and sleep laboratory- must be focused onchildren. Facility, monitoring and reading study different than with adults 2.  ENT- dedicated to pediatric airway issues, additionaltraining in sleep issues may prove valuable

3. Orthodontist- must be willing to intervene in earlycraniofacial issues, understanding of airway-based care

Timing of Care- begin process the moment the problem is discovered

6. Interdisciplinary "Multilevel" Treatment Key

1. Snoring-‐ sound typically created from the vibra6on of the soB palate due to a narrowing of the airway be-‐tween the tongue and soB palate

2. Upper Airway Resistance Syndrome (UARS)-‐ repe66ve increases in resistance to airflow in the upper airwayleading to RERAs and day6me fa6gue. SO2 levels remain normal

3. Respiratory Effort Related Arousal (RERA)-‐ arousal caused by respiratory effort not including apnea or hy-‐popnea

4. Apnea-‐ breathing stops for at least 10 seconds during sleep or a 4% drop in blood oxygen satura6on. Hypo-‐pnea-‐ par6al airway blockage or decrease in breathing; reduc6on in airflow 50% or greater, 3% or greater SO2 drop

5. Apnea-‐Hypopnea Index (AHI)-‐ average number of apneas and hypopneas per hour of sleep; mild 5-‐15,moderate 15-‐30, severe >30

6. Respiratory Disturbance Index (RDI)-‐ measure of severity of sleep apnea, including number of sleep dis-‐rup6ons and desatura6ons. Counts the number of arousals caused by respiratory effort (RERA)

7.Polysomnography (PSG)-‐ A test that records mul6ple physiological variables during sleep (including brainwaves, electrical ac6vity of muscles, eye movement, breathing rate, blood pressure, blood oxygen satura6on, and heart rhythm). The test is usually conducted in a sleep lab and involves direct observa6on of the person during sleep.

8. Pulse Oximetry-‐ a non-‐invasive method allowing the monitoring of the oxygena6on of a pa6ent's hemoglo-‐bin and pulse rate.

9. ConJnuous PosiJve Airway Pressure (CPAP)-‐ A machine supplies posi6ve air pressure to inflate the airwaylike a balloon which eliminates blockages and prevents the collapse of the upper airway during sleep. Air pres-‐sure is delivered through a hose to a mask that fits over the nose, or both nose and mouth.

10.Mandibular Advancement Appliance (MAA), Mandibular Advancement Device (MAD)-‐ oral applianceused to protrude the mandible crea6ng a 6ghtening of the oral airway and advancement of the tongue in an effort to open the airway

Terminology

Airway AlgorithmPrivate Practice Patient

Signs and Symtoms (Fatigue vs. Sleepiness)Refer to Medical Specialist or Pulse Oximetry Screening

YES NO

AHI Low, Pulse Rate VariabilityUARS Signs/Symptoms

NOT CONFIRM

AHI High, With or Without VariabilityApnea Signs/Symptoms

1. Re-test 2-5 years, Weight or Medical Change2. Re-test Immediately - Results Did Not Match Expectations

TMDSplint DesignProvisional ApplianceOrtho, Orthognathics, Oral MyologistEval Results with HRPOENT Consult-Nasal

CHILDT&AENT-Nasal SurguryRPE-Orthodontics/OrthognathicWeight LossNasal SteroidsAllergistCPAPOral MyologistCraniofacial TherapyRespiratory Physiologist

ADULTCPAPMAACombination CPAP/MAAOrthodontics/SFOTENT-SurgeryWeight LossAllergist, Nasal SteroidsProventOral MyologestRestore Mouth in Airway Occlusion ConceptResptratory Phystologest

ENT-SurgeryWeight LossOrthognathic SurgeryWeight - Diet/BariatricGenioglossal StimulationTracheotomy

UARS SEVERE OSA

MAINTAIN/IMPROVE RESOLVE

CONFIRMED DIAGNOSISPSG, HST, PULSE OX

ADULT/CHILDMedical Referral-PSGSleep MDENT with focus on airwayOther MD-PCP, psychiatry, Allergist, etc

MILD OSA MODERATE OSA

FATIGUE

High BerlinESS, Stop Bang Screening Exam

SLEEPY

SnoreHabitual Mouth BreatherWitnessed Apnea

CHILD

32 inside dentistry | May 2010 | insidedentistry.net

The Bruxism TriadSleep bruxism, sleep disturbance, and sleep-related GERD.By Jeffrey S. Rouse, DDS

Bruxism is defined as a diurnal and noctur-nal parafunctional activity that includes clenching, bracing, gnashing, and grinding of teeth.1 the damage

from bruxism is a reality in the everyday practice of dentistry and yet there is a great deal of confusion and controversy. dental professionals do not even agree on the relative number of people who brux. the estimates range from 5% to 95% of the population.2-4 Many dentists focus on the patients who present with wear to determine rates of bruxism. tooth wear, however, is a poor indica-tor of bruxism since attrition may play only a small role in tooth destruction and may not be indicative of an ongoing problem.5 the smaller estimates limit the patients to sleep bruxers. sleep bruxism (sB) is the grinding or clench-ing of the teeth during sleep, usually as-sociated with sleep arousals.6 to date, the pathophysiology for sB has not been definitively determined. research

points to neurochemistry, autonomic system, and sleep arousals as possible triggers.7,8 this article will restrict its focus to a unique subset of the brux-ing population: the sleep bruxer. this group is extremely destructive to their teeth and systemic health. Additionally, this article will discuss the significance of the bruxism triad: sleep bruxism, sleep disturbance, and sleep-related gastroesophageal reflux.

Tooth Weartooth wear is described in the litera-ture as the loss of the constitution of the tooth and has been classified as being caused by attrition, abrasion, erosion, or a combination of these factors.9 As it relates to sB, tooth wear is reported to additionally cause tooth mobility, tem-perature hypersensitivity, and tooth fracture.10 While sleep bruxers and non-bruxers displayed significantly dif-ferent amounts of wear over time, the contribution of tooth-on-tooth attri-tion to this wear is still controversial.11 it has been postulated that much of the wear could be erosion rather than at-trition. interestingly, those two factors are interwoven in the bruxism triad patient, magnifying the wear in this patient population (Figure 1).

the study of tooth wear is appropri-ately described as tribology: the science of interacting surfaces in relative mo-tion and associated issues of lubrication, friction, and wear. teeth sliding over each other are affected by a complex

tribological interaction. Friction is en-countered whenever there is relative motion between contacting surfaces, and it always opposes the motion. As no surface is perfectly smooth, when the teeth make contact, even under light load, it may produce the loss of tooth structure. When non-roughened surfaces contact, their coefficient of fric-tion decreases dramatically if a lubricant is introduced. tribology would suggest that a decrease in oral lubrication cou-pled with tooth-on-tooth contact would introduce friction and, thus, wear.12 in addition, elements that increase the surface roughness (eg, erosion) would unavoidably increase wear (Figure 2).

intraoral lubrication is provided pri-marily by saliva. it also lubricates and buffers the esophagus and decreases the risk of aspiration.12 salivary flow fol-lows a daily circadian variation and is significantly lower at night. during sleep, deglutination is episodic, with long peri-ods without swallowing. daytime swal-lowing averages 25 to 60 times per hour and only two to nine times at night.13 salivary flow and buffering capacity vary between individuals and may be insuf-ficient to prevent frictional tooth dam-age.14 swallowing is almost exclusively associated with microarousals (MA) during light sleep.13 these MAs play an important role in sleep bruxism.

reduced lubrication, erosive friction, and contact time play significant roles in tribologic wear of teeth in sleep brux-ers. Bruxing force is not as important as previously thought. For years the pro-fession has accepted that sB patients can exert up to six times as much force on their teeth at night than normal sub-jects.15 it has provided dentists a simple explanation to our patients as to why their teeth wear and restorations break. interestingly, the facts simply do not support that conclusion. Gibbs et al

wrote that the bite strength in some bruxer-clenchers can be as much as six times that of the non-bruxer.15 the study evaluated daytime bite strength, not nocturnal bruxing force. it also did not provide groups for bruxing subjects and a non-bruxing control. in fact, the conclusion of the study should have read that only one patient in the study during the day could produce six times greater force on biting than the aver-age dentate patient. studies monitor-ing muscle activity during sleep have confirmed that the elevator muscles are rarely, if ever, contracted to their maximum. in fact, when the eMG levels are evaluated during nocturnal bruxing activity, the muscle response is only half of the maximum voluntary contraction.16,17 Only 66% of the brux-ism episodes are at a force level equal to or greater than the force generated during chewing. While it is true that pa-tients with greater jaw muscle size may generate more total force with the same eMG activity, the amount of force is well within daily norms and definitely not six times greater.

Sleep Stages and Arousal ResponseGood-quality sleep is important for physical recovery, biochemical re-freshment, memory consolidation, and emotional regulation.18 A typical sleep cycle is 90 to 110 minutes of sleep with three to five cycles per night. sleep is

JeffRey S. RouSe, DDSPrivate Practice ProsthodontistClinical Adjunct Associate ProfessorDepartment of Graduate Prosthodonticsuniversity of Texas Health Science Center San Antonio Dental SchoolSan Antonio, Texas

AbSTRACTsleep bruxers are a difficult subset of patients to manage predictably. they damage teeth and restorations at a higher rate than normal stress-related bruxers. the adverse effect of their sleep bruxism does not stop just with tooth damage. these patients are more prone to sleep disturbances including apnea and gastric reflux symptoms. it appears that these three sleep issues are interwoven in a triad of factors that create a uniquely detrimental environment for teeth.

•describeanormalsleepcycleandlistthreesleepdisturbances,includingthetestingparametersforeach.

•listthefactorsinvolvedinthebruxismtriadandunderstandtheinfluenceofeach.

•discusstreatmentoptionsforpatientsdiagnosedwiththebruxismtriad.

Logontowww.insidedentistryCE.comtotaketheFREECEquiz.

InSIDE continuing EDucation REStoRativEPERioDonticS

Learning Objectives


inSiDE continuing EDucation

composed of two distinct states: non-reM (quiet sleep) and reM (active sleep). there are four stages of non-reM sleep. stages 1-2 are light sleep and stages 3-4 are deep sleep. in the first third of total sleep, non-reM stage 3-4 is the longest stage and de-creases or disappears in the last third. reM sleep increases in the last third. While dreams may occur in any stage of sleep, they are more common and more vivid in reM sleep.20

A micro-arousal (MA) is a shift in sleep occurring during deeper sleep. these 3- to 10-second rises in eeG activity cre-ate an increase in heart rate and muscle tone. MAs occur 8 to 15 times in an hour. Bruxism is an oromotor manifestation secondary to MA. eighty-six percent of bruxism occurs in non-reM stage 2 sleep and MA.19 A smaller percentage of bruxism events occur in reM sleep.20 More destructive bruxers, however, have a greater number of episodes and time of bruxism in reM sleep than controls.21

Sleep Disturbancesrespiratory disturbances during sleep fall into three categories: snoring, upper airway resistance syndrome (UArs), and sleep apnea-hypopnea syndrome. snoring is defined as sounds produced in the upper airway from soft tissue

vibration induced by air turbulence. it is reported in 40% of men and 24% of women. the incidence is 10% in chil-dren.22 snoring is a risk factor for ob-structive sleep apnea (OsA). A medical consultation is appropriate before mak-ing an oral appliance for snoring and is mandatory when snoring is accompa-nied by daytime sleepiness, insomnia, sleep disruption, or hypertension.

UArs is an increased inspiratory effort creating increased MAs and nar-rowing of the pharynx without oxygen desaturation below 4%.23 it is character-ized by repetitive partial collapse of the upper airway during sleep. UArs have been linked with increased bruxism, headaches, and tMd, and are thought to be an intermediate form of disorder between snoring and OsA.22

Apnea is the repetitive absence of ventilation with cessation of breathing for 10 seconds and oxygen desaturation exceeding 4%. sleep apnea may be ob-structive sleep apnea (most common) resulting from a blockage of the upper airway or central sleep apnea demon-strated by no chest movements result-ing from a lack of neural drive.18 Patients may have both types simultaneously. Hypopnea is a decrease in airflow of more than 50% or a decrease of airflow by 30% with an oxygen desaturation of

more than 3%. the level of OsA is re-lated to the number of apnea-hypopnea events per hour of sleep. the apnea-hy-popnea index (AHi) considers persons with 5 to 15 events per hour of sleep as mild, 15 to 30 as moderate, and > 30 as severe. the severity of sleep apnea is judged by a composite of the symptoms including AHi, daytime sleepiness, and % desaturation. risk factors for OsA in-clude being male, overweight, over 40, large neck size, large tonsils, and family history (Figure 3).24 it is estimated that 1 in 5 adults has at least mild obstructive sleep apnea (OsA) and 1 in 15 has at least moderate.25 Unlike the bruxism prevalence, OsA increases with age and can affect 70% of men and 56% of women over the age of 65, a three-fold increase from middle age.26 While be-yond the scope of this article, OsA is a risk factor for hypertension, cardiovas-cular morbidity, and daytime sleepiness to name just a few.25

Sleep bruxismA sleep bruxer is different than a pa-tient who occasionally bruxes during sleep. By definition, a sleep bruxer must have > 4 episodes of bruxing per hour of sleep, > 25 bruxing bursts per hour, and at least one episode per night must make noise.27 sB is higher in children

and decreases with age. sB occurs in up to 30% of children from 5 to 6 years old, 13% in respondents 18 to 29 years of age, and decreasing to 3% in patients over 60 years old.28 Unlike stress-triggered bruxing subjects, sleep bruxing episodes are unrelated to experienced and antici-pated stress.29 in addition, sB has little variability in the bruxing episodes and bursts per hour of sleep over months and years.30 in moderate to severe sB, grinding was present every night.31

sleep bruxism episodes are related to disturbances in sleep. Kato and col-leagues induced MAs during the sleep of sleep bruxers and controls.32 tooth grinding followed the experimentally induced MA in more than 71% of the trials. interestingly, this reaction was only produced in sleep bruxism pa-tients and never in controls, indicating a heightened responsiveness to sleep arousals. therefore, anything that in-duces a greater number of MAs has the ability to increase the amount of tooth grinding in these subjects.

Airwayresearchers observe that the frequency of sleep apnea increased as the frequency of bruxism increased. Given the link be-tween MA and sB, it may be more cor-rectly stated that the frequency of sB

CLINICAL EXAMPLES (1.) Classic presentation of the bruxism triad. Lateral wear pattern, generalized buccal tooth loss from erosion and abrasion, and history of sleep disruption. (2.) Asymmetric tooth wear in a bruxism triad patient as a result of friction from bruxing, poor salivary lubrication as a byproduct of medication, and roughened surfaces created as a result of erosive reflux. (3.) In addition to the traditional sleep apnea risk factors (over 40 years old, male, overweight, >17 inch neck size), practi-tioners should add the tooth wear and erosion components of the bruxism triad.

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increases with an increase in sleep apnea-induced arousals.22,33 At least one third of patients with bruxism in the general pop-ulation may also have sleep-disordered breathing conditions such as sleep apnea, periodic leg movement during sleep, and headache.22,34 the rate of OsA may be as high as 30% in a tMd population.(18, unpub-

lished data) in addition to OsA, close to 50% of UArs patients complain of bruxism.22 Prospective evaluations and case studies of sB and apnea indicate that bruxism events may be directly correlated to ap-nea episodes.35 While a causal relation-ship cannot be made, obstructive sleep apnea (OsA) syndrome has been called the highest risk factor for tooth grinding during sleep.36

Bruxism and airway appear to be re-lated to the patient’s attempt to develop a patent airway during a desaturation

episode. the majority of sB episodes occurs in a supine position and may be associated with either a reduction in the airway passage or increase in its resis-tance. during resumption of ventilation following apnea, a co-activation of both jaw-opening and jaw-closing muscles produce dilation of the upper airway. this permits a rise in inspiratory flow and reduces upper airway resistance.37 it has been reported that 99% of all rhythmic masticatory muscle activi-ties were associated with a change in the respiratory amplitude and frequency.19 Changes in lateral tongue contours, long associated with nocturnal brux-ers, can now be explained. the patient attempts to provide a patent airway by activating the tongue muscles and forc-ing the tongue off the airway and against the teeth (Figure 4).

Bruxism is greatest in 5- to 6-year-olds and slowly declines with age. Ad-enoid tonsil hypertrophy in the 5- to 6-year-old patient may account for the airway obstruction and, thus, a greater incidence of bruxism.28 As the airway improves with age, the bruxism decreas-es in the general population but in the triad group it continues. if bruxism is a reflexive mechanism to improve or protect an airway, then greater brux-ism could lower the apnea. sjöholm con-cluded that there is limited correlation between bruxing and apnea because mild apnea patients had more bruxing events than moderate apnea patients.38 However, if bruxism is a protective re-flex, clinicians might be able to predict the possibility in a young patient popu-lation that bruxism would be linked to less severe apnea. Aggressive bruxism

in 20- to 40-year-old subjects may sim-ply be an attempt to open their airway. As the sleep bruxer ages, their neuro-chemical ability to brux decreases, or it cannot overcome the additional airway obstructions due to a loss of muscle tone, weight gain, etc.

gERD Gastroesophageal reflux disorder (Gerd) is a medical condition where the stomach contents leak to the esoph-agus. it affects approximately 40% of Americans.39 Gerd is commonly as-sociated with heartburn or indigestion, although > 50% of people complain-ing of frequently clearing their throat, hoarseness, or trouble swallowing were found to have silent Gerd. Poor qual-ity of sleep may be the sole presenta-tion of silent Gerd in asymptomatic subjects.40 Medical consultation is recommended. differential diagnosis would include peptic ulcer, angina, and Barrett esophagus (possible precursor to adenocarcinoma).41

some of the acid content of the stom-ach may reach the oral cavity. this is an extremely destructive acid with a pH of 1 to 2. in comparison, dietary acids are greater than pH 3. the most common site for damage is the palatal surface of the maxillary molars (Figure 5 and Figure 6). reflux symptoms present mostly in a supine position. the dor-sum of the tongue pushes the acid to the maxillary molar palatal surface when swallowing to buffer the acid.42 While the palatal surface is the most common site of destruction, the pattern of dam-age will be dictated by the sleep posi-tion of the patient during the episodes. tongue activity associated with airway patency coupled with regurgitation may also create wear on the lingual surfac-es of teeth resembling bulimia but are not limited to the maxillary anteriors (Figure 7). Gerd patients have a sig-nificantly higher risk of xerostomia and oral burning sensation.43 this lack of lu-brication paired with acid-roughened surfaces increase the risk of frictional wear associated with sleep bruxism.

bruxism Triad: Sleepbruxism, Sleep Disturbance, and Sleep-Related GeRDthe bruxism triad coupled with noctur-nal hyposalivation or xerostomia appre-ciably increases the risk of frictional and erosive tooth wear.12,18 the bruxism triad is composed of arousal-induced tooth

SYMPTOMS Of THE TRIAD (4.) Indentations on tongue caused by forceful pressing of tongue on lingual surfaces. By pushing the tongue anteriorly, the airway is opened. (5.) The red, irregular surface on the palatal surface of a maxillary molar can be an early sign of reflux. (6.) Continued damage from erosion produced by GERD. Other areas of erosive damage will be dictated by the sleep posture of the patient.

RESULTS Of THE TRIAD (7.) Patients who combine tongue pressure to clear the airway and GERD can produce wear on the lingual sur-faces resembling bulimia. It is not restricted to maxillary anteriors. (8.) Young adult with signs and symp-toms of the bruxism triad: Lateral tooth wear, erosive and abrasive damage to the teeth, and a history of moderate apnea. (9.) Extensive erosive wear. Airway improvement can reduce GERD and GERD resolu-tion can reduce sleep bruxism.

RECOgNIzINg TRIAD PATIENTS (10.) Extensive wear on stabilizing splint. It has been postulated that continued bruxism on splints is patho-pneumonic for the bruxism triad. (11.) Continued wear on splints is indepen-dent of the design of the prosthesis. (12.) Childhood presentation of the bruxism triad. Patient had erosive and attritional wear on deciduous teeth, constricted dental arches, and deep class II bite. Physician examina-tion revealed significant GERD paired with enlarged adenoids and tonsils.

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grinding, airway-associated sleep disor-ders, and sleep-related Gerd (Figure 8 and Figure 9). While a causal relation-ship has not been established, significant correlation makes it important for den-tists to evaluate their patient population.

sleep bruxism is concomitant with sleep apnea. therefore, if the level of ap-nea can be artificially reduced, a resul-tant decrease in bruxism would be an-ticipated. Oksenberg and Arons found that during continuous positive airway pressure (CPAP) treatment, apneas were eliminated and only a few hypop-neas were seen. A complete disappear-ance of all bruxism events occurred.35 Mandibular advancement appliances (MAA) have reported to reduce bruxism events 50% to 83%.44 the variability appears to be related to the appliances’ ability to reduce desaturation episodes, which is more inconsistent than CPAP therapy. the MAA may also be used in sB patients without respiratory distur-bances. A statistically significant reduc-tion (39% and 47%) of sB episodes per hour was recorded with the MAA at pro-trusion of 25% and 75%, respectively,45

providing further evidence that im-proving airway patency is an important treatment strategy for bruxism even in a normal patient population.

One important note is that traditional occlusal stabilizing splints may have a deleterious effect on sB-OsA patients. A prospective study of 10 mild to mod-erate OsA patients was conducted with multiple nights recorded with and with-out a stabilizing splint. results indicated that six of the 10 subjects had a signifi-cant increase in their AHi with splint therapy.46 Further, OsA patients with complete dentures have significantly improved airways when sleeping with their dentures than without them.47 Both studies highlight that OsA patients have an improved airway when the mandible is placed and held in a protruded posi-tion. efforts which prevent that abil-ity may worsen the airway and increase sleep bruxism. this could account for the severity of wear found on some oc-clusal splints. the author has noted that patients with airway and Gerd issues have notably more wear on their orthosis regardless of design (Figure 10 and 11).

Gerd can be linked to the other mem-bers of the triad. Patients with Gerd had higher AHi scores and shorter pe-riods in restful stage 2 sleep.48 research has also demonstrated that more severe OsA was accompanied by more severe

Gerd.49 While the link is still contro-versial, one explanation is that during apnea episodes, there is an increase in negative intrathoracic pressure. this in-creased negative pressure could cause the gastric acids to be expelled from the stomach and into the esophagus. As the esophageal pH decreases, patients’ brux-ing episodes were significantly higher. Miyawaki studied 10 sB and 10 controls presenting without Gerd symptoms. esophageal pH was monitored during an evening of sleep. results showed that when the esophageal pH reached 4 or lower there was a simultaneous bruxism episode ending in a tonic burst representing a swallow.50 this is appar-ently an attempt to buffer the esopha-geal acid content. interestingly, the pH 4 threshold was reached exclusively by sB patients. no control patient had an esophageal pH low enough to trigger a bruxism episode.

Proton-pump inhibitors are a group of drugs that reduce gastric-acid production. Administration of a proton-pump inhibi-tor to Gerd-sB patients demonstrated a commensurate 40% reduction of sB episodes.50 Another family of Gerd medication, the H2 blocker anti-acids, showed a reduction in MAs, respiratory disturbances, and daytime somnolence. it did not, however, reduce the AHi.51 reducing the intrathoracic pressure with CPAP reduces Gerd parameters in pa-tients with and without OsA.51,52 studies with MAA have not been conducted but similar results would be anticipated giv-en their impact on the airway.

Recognizing the Triad Patientdentists should to be able to recognize the bruxism triad patient at all stages of life. early diagnosis can alter poor growth, improve physical well-being, and reduce tooth wear. the following are some of the distinguishing features of each of the stages of the triad.

Childhood 3–12Adenoid and tonsil hypertrophy pro-duces sleep disturbances including OsA. the magnitude of hypertrophy required for obstruction is smaller in obese children compared to non-obese children.53 Gerd will be found fre-quently in children with adenotonsil-lar hypertrophy and OsA and should be evaluated.54 Five-year-old children with OsA will commonly display dif-ferences in growth when compared to matched controls. this can include

a mandibular posterior inclination, greater anterior face height, and ret-roclined incisors (Figure 12).55

Adolescent 13–19dentists commonly tell parents that most children “grow out of bruxism” when they reach puberty. More accu-rately, many children grow enough to overcome the impact of the adenoids and tonsils, or orthodontic intervention expands the palate enough to create an adequate airway. Any signs of patho-logic wear due to attrition or erosion at this stage should elicit questions about sleep disturbances, sleep bruxing, and reflux symptoms (Figure 13).

Young Adult 20–40Pathologic tooth wear or significant relapse of orthodontic correction is usually addressed by fabrication of an

occlusal orthosis. Continued grind-ing on the appliance is a hallmark for the bruxism triad. self-reports of high stress may be due to repeated sleep dis-turbance and should not be disregarded. evidence of Gerd may be present on the teeth or maxillary palatal tissue. Bruxism may be acting as a protective reflex for the airway (Figure 14). there is a statistically significant association between childhood wear of the decidu-ous mandibular molars and canine teeth and the degree of whole-mouth wear ob-served 20 years later56 (Figure 15). For sleep bruxers with episodic sleep distur-bances and reflux symptoms, this author has been using an anterior reposition-ing splint with success. the appliance is fabricated at < 40% of the patient’s maximum protrusion, minimizing the occlusal risk associated with advance-ment appliances (Figure 16 and Figure

EARLY SIgNS AND TREATMENT (13.) Adolescent triad: A 16-year-old with pathologic wear on incisors and a loss of tooth texture from erosion and abrasion. Medical history was indicative of the triad. (14.) Bruxism triad in a young adult. The pathologic wear, once limited to the anterior teeth, is beginning to appear on the posteriors as guidance is lost. Patient reported sleep issues that became exacerbated with pregnancy. GERD was inter-mittent until pregnancy then it increased. (15.) Patient demonstrates wear on deciduous molars increasing the risk of bruxing as an adult. Another explanation may be the triad. Constricted dental arch, crowded lower ante-riors, and a deep bite with a lifetime of airway-related issues. GERD history coupled with erosive wear on teeth. (16.) Ramp of the anterior repositioning appliance demonstrating the path of the incisors from centric closure to anterior closure. (17.) Patient positioned at 40% of voluntary protrusion.

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17). the maxillary orthosis directs the patient’s closure into a protruded pos-ture that opens the airway without being as bulky and restrictive as most MAAs.

Middle Adult 40–65Bruxism will begin to wane as the risk of OsA increases. the impact of tooth grinding may be reduced but medical complications of OsA and Gerd have increased. the effects of years of tooth and restoration damage may be ap-parent. Airway management becomes more difficult given the physical chang-es of middle age (Figure 18). As the lit-erature elucidated, management of the airway during sleep improves all factors of the triad. CPAP is the gold standard for airway maintenance. For patients unwilling or unable to use CPAP, MAAs have the potential to diminish AHi, re-duce sleep bruxism, and potentially lessen Gerd (Figure 19 and Figure 20).

Mature 65 Olderthe majority of patients in the mature group will have at least mild apnea.

Medical issues related to overall health may be linked to OsA. Bruxism may be present but will be limited in its ability to clear the airway and reduce Gerd. Patients may need to address tooth wear issues that have been compound-ed through years of neglect (Figure 21 and Figure 22). Comprehensive evalua-tion for signs and symptoms of OsA and referral for polysomnographic study is recommended. Patients with dentures should be encouraged to wear their dentures at night if sleep disruption is present (Figure 23 and Figure 24).

Conclusionit has been demonstrated that a ma-jority of dental patients present with tooth wear. However, sleep bruxers are a unique subset. sleep bruxism is reflec-tively triggered by sleep microarousals. these disturbances in the sleep pat-terns are a natural occurrence but can also be caused by any disruption of air-way patency or a significant reduction of esophageal pH. the bruxism triad is an attempt to explain the interlocking

nature of bruxism, breathing, and ero-sion. these patients suffer a significant loss of tooth structure and restoration damage due to the increase in friction due to poor lubrication and roughened surfaces. Medical evaluation is key. CPAP, MAA, and Gerd medications were proposed as possible treatment options for the bruxism triad patient.

References 1. de Leeuw r. Orofacial Pain Guidelines for Assessment, Diagnosis, and Management. 4th ed. Chicago, ill: Quintessence; 2008.2. Lavigne GJ, Montplaisir Jy. restless leg syndrome and sleep bruxism: Prevalence and associations among Canadians. Sleep. 1994;17:739-743.3. Ohayon M, Li KK, Guilleminault C. risk fac-tors for sleep bruxism in the general population. Chest. 2001;119:53-61.4. Okeson JP, Kemper Jt. in: Okeson JP. Management of Temporomandibular Disorders and Occlusion. 5th ed. st Louis, Mo: CV Mosby; 2003.5 ekfeldt A, Hugoson A, Bergendal t, Helkimo M. An individual tooth wear index and an analysis of factors correlated to incisal and

occlusal wear in an adult swedish population. Acta Odontol Scand. 1990;48:343-349.6. American Academy of sleep Medicine. International Classification of Sleep Disorders. 2nd ed. American Academy of sleep Medicine; 2005.7. Lavigne GJ, Manzini C. Bruxism. in: Kryger M, roth t, dement W (eds). Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia, Pa: W.B. saunders Company; 2000:773-785.8. Lavigne GJ, Kato t, Kolta A, sessle BJ. neurobiological mechanisms involved in sleep bruxism. Crit Rev Oral Biol Med. 2003;14:30-46.9. Litonjua LA, Andreana s, Bush PJ, Cohen re. tooth wear: Attrition, erosion and abrasion. Quintessence Int. 2003;3:435-446.10. Lavigne GJ, Manzini C, Kato t. sleep Bruxism. in: Kryger M, roth t, dement W (eds). Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, Pa: W.B. saunders Company; 2005:946-959.11. Pintado Mr, Anderson GC, deLong r, douglas WH. Variation in tooth wear in young adults over a two-year period. J Prosthet Dent. 1997;77:313-320.12. thie nMr, Kato t, Bader G, et al. the significance of saliva during sleep and the relevance of oromotor movements. Sleep Med Rev. 2002;6:213-227.13. Lichter i, Muir rC. the pattern of swal-lowing during sleep. Electroencephalogr Clin Neurophysiol. 1975;38:427-432.14. Moazzez r, Bartlett d, Anggiansah A. dental erosion, gastro-oesophageal reflux disease and saliva: how are they related? J Dent. 2004;32:489-494.15. Gibbs CH, Mahan Pe, Mauderli A, et al. Limits of human bite strength. J Prosthet Dent. 1986;56:226-229.16. Clark nG, townsend GC, Carey se. Bruxing patterns in man during sleep. J Oral Rehabil. 1984;11;123-127.17. nishigawa K, Bando e, nakano M. Quan-titative study of bite force during sleep associated bruxism. J Oral Rehabil. 2001;28:485-491.18. Lavigne GJ, Cistulli PA, smith Mt (eds). Sleep Medicine for Dentists: A Practical Overview. Chicago, ill: Quintessence Publishing Co, inc; 2009.19. Khoury s, rouleau GA, rompré PH, et al. A significant increase in breathing amplitude pre-cedes sleep bruxism. Chest. 2008;134:332-337.20. Baba K, Clark Gt, Watanabe t, Ohyama t. Bruxism force detection by a piezoelectric film-based recording device in sleeping humans. J Oral Pain. 2003;17:58-64.21. Okeson JP, Phillips BA, Berry dt, et al. nocturnal bruxing events in subjects with sleep-disordered breathing and control subjects. J Craniomandib Disord. 1991;5:258-264.22. Gold Ar, dipalo F, Gold Ms, O’Hearn d. the symptoms and signs of upper airway resistance syndrome: a link to the functional somatic

ADvANCED TRIAD (18.) Middle-adult triad patient. Pathologic wear from sleep bruxism and erosion damage on multiple tooth surfaces. Patient had a history of GERD treated with a proton-pump inhibitor medication. Patient reported a decrease in bruxism but bed partner noticed an increase in snor-ing and apnea events. Polysomnography revealed an AHI of 34. (19.) Thorn-ton Adjustable Positioner 3 (TAP). Custom made MAA for the treatment of sleep disturbances. Anterior connector allows adjustment for titration of the airway. (20.) TAP 3 engaged. (21.) Mature patient with the bruxism triad. Lifetime history of bruxism, snoring, intermittent poor sleep, and GERD symptoms. Sleep study results indicate severe apnea. (22.) Incisal view dem-onstrates the damage from sleep bruxism and the erosive wear associated with GERD and tongue position.(23.) Retracted tongue position in edentu-lous patients limits the available airway. Wearing their dentures at night may allow for a more favorable airway. (24.) Many dentures worn at night demon-strate the same lateral wear facets indicative of the bruxism triad patient. A complete history of bruxism, sleep, and GERD should be obtained.

fIg. 18 fIg. 19

fIg. 24

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fIg. 21 fIg.23fIg. 22


syndromes. Chest. 2003;123:87-95.23. Guilleminault C, stoohs r, Clerk A, et al. A cause of excessive daytime sleepiness: the up-per airway resistance syndrome. Chest. 1993;104:781-787.24. young t, Peppard Pe, Gottlieb dJ. epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165:1217-1239. 25. shamsuzzaman AsM, Gersh BJ, somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. 2003;290:1906-1914.26. redline s. epidemiology of sleep-disor-dered breathing. Semin Respir Crit Care Med. 1998;19:113-122.27. Lavigne GJ, rompré PH, Montplaiser Jy. sleep bruxism: Validity of clinical research diagnostic criteria in a controlled polysom-nographic study. J Dent Res. 1996;75:546-552.28. Lavigne GJ, Manzini C. Bruxism. in: Kryger M, roth t, dement W (eds). Principles and Practice of Sleep Medicine. 4th ed. Philadelphia, Pa: W.B. saunders Company; 2005:946-959.29. van selms MK, Lobbezoo F, Wicks dJ, et al. Craniomandibular pain, oral parafunctions, and psychological stress in a longitudinal case study. J Oral Rehabil. 2004;31:738-745.30. Lavigne GJ, Guitard F, rompré PH, Montplaisir Jy. Variability in sleep bruxism activity over time. J Sleep Res. 2001;10:237-244.31. Camparis CM, Formigoni G, teixeira MJ, et al. sleep bruxism and temporomandibular disorder: clinical and polysomnographic evalu-ation. Arch Oral Biol. 2006;51:721-728.32. Kato t, Montplaisir Jy, Guitard F, et al. evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res. 2003;82:284-288.33. Ohayon MM, Li KK, Guilleminault C. risk factors for sleep bruxism in the general popula-tion. Chest. 2001;119:53-61.34. Bader GG, Kampe t, tagdae t, et al. descriptive physiological data on a sleep brux-ism population. Sleep. 1997;20:982-990.35. Oksenberg A, Arons e. sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure. Sleep Med. 2002;3:513-515.36. Kobayashi y, shiga H. the relationship between sleep apnea, bruxism, and the time it took the patient to seek for treatment in tMd patients. J Oral Rehabil. 2002;29:885.37. yoshida K. A polysomnographic study on masticatory and tongue muscle activity during obstructive and central sleep apnea. J Oral Rehabil. 1998;25:603-609.38. sjöholm tt, Lowe AA, Miyamoto K, et al. sleep bruxism in patients with sleep-disordered breathing. Arch Oral Biol. 2000;45:889-896.39. the Gallup Organization: A Gallup survey on heartburn across America. Princeton, nJ: Gallup; 1988.40. Fass r, dickman r. Clinical consequences of silent gastroesophageal reflux disease. Curr Gastroanterol Rep. 2006;8:194-200.

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41. shaheen n, ransohoff dF. Gastroesophageal reflux, barrett esophagus, and esophageal cancer: scientific review. JAMA. 2002;287:1972-1981.42. Lazarchik dA, Frazier KB. dental erosion and acid reflux disease: an overview. Gen Dent. 2009;57:151-156.43. Campisi G, lo russo L, di Liberto C, et al. saliva variations in gastro-esophageal reflux disease. J Dent. 2008;36:268-271.44. Landry ML, rompré PH, Manzini C, et al. reduction of sleep bruxism using a mandibular advancement device: an ex-perimental controlled study. Int J Prosthodont. 2006;19:549-556.45. schönbeck AL, de Grandmont P, rompré PH, Lavigne GJ. effect of an adjustable man-dibular advancement appliance on sleep brux-ism: a crossover sleep laboratory study. Int J Prosthodont. 2009;22:251-259.46. Gagnon y, Mayer P, Morisson F, et al. Aggravation of respiratory disturbances by the use of an occlusal splint in apneic patients: a pilot study. Int J Prosthodont. 2004;17:447-453.47. Arisaka H, sakuraba s, tamaki K, et al. effects of wearing complete dentures during sleep on the apnea-hypopnea index. Int J Prosthodont. 2009;22:173-177.48. Guda n, Partington s, Vakil n. symptomatic gastro-oesophageal reflux, arousals and sleep quality in patients undergoing polysomnog-raphy for possible obstructive sleep apnea. Aliment Pharmacol Ther. 2004;20:1153-1159.49. demeter P, Visy KV, Magyar P. Correlation between severity of endoscopic findings and apnea-hypopnea index in patients with gastro-esophageal reflux disease and obstructive sleep apnea. World J Gastroenterol. 2005;11:839-841.50. Miyawaki s, Lavigne GJ, Mayer P, et al. Association between sleep bruxism, swallowing-related laryngeal movement, and sleep posi-tions. Sleep. 2003;26:461-465.51. ing AJ, ngu MC, Breslin AB. Obstructive sleep apnea and gastroesophageal reflux. Am J Med. 2000;108:120s-125s.52. tawk M, Goodrich s, Kinasewitz G, Orr W. the effect of 1 week of continuous positive airway pressure treatment in obstructive sleep apnea patients with concomitant gastroesopha-geal reflux. Chest. 2006;130:1003-1008.53. dayyat e, Kheirandish-Gozal L, san Capdevila O, et al. Obstructive sleep apnea in children: rela-tive contributions of body mass index and adeno-tonsillar hypertrophy. Chest. 2009;136:137-144.54. noronha AC, de Bruin VM, nombre e souza MA, et al. Gastroesophageal reflux and obstruc-tive sleep apnea in childhood. Int J Pediatr Otohinolaryngol. 2009;73:383-389.55. Zettergren-Wijk L, Forsberg CM, Linder-Aronson s. Changes in dentofacial morphology after adeno-tonsillectomy in young children with obstructive sleep apnoea—a 5-year follow-up study. Eur J Orthod. 2006;28:319-326.56. Knight dJ, Leroux BG, Zhu C, et al. A longitudinal study of tooth wear in orthodonti-cally treated patients. Am J Orthod Dentofacial Orthop. 1997;112:194-202.

60 inside dentistry | July 2013 | www.insidedentistry.net

Sleep Prosthodontics: A New Vision for DentistryPart 1 of this 2-part series focuses on the snoring child Jeffrey S. Rouse, DDS

InsideContinuing eDuCation eSthetiCS | ReStoRative

• Describethedifference betweensleepprosthodontics andsleepdentistry.

• Explaintheuniqueimpactofsleep fragmentationandobstructive apneaonchildren.

• Correlatedentalabnormalities toairwaydeficienciesin pediatricpatients.

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abstraCt

the purpose of this article is to introduce a new term, sleep prosthodontics, to the den-tal community and to differentiate airway analytics from sleep dentistry. sleep dentistry may be thought of as the study of an oral appliance and its impact on the airway. sleep prosthodontics is the study of airway and its impact on the stomatognathic system. in other words, sleep dentistry addresses the how (ie, how does an appliance assist noctur-nal breathing?), whereas sleep prosthodontics addresses the why (ie, why are patients developing malocclusions, creating myofacial pain symptoms, and wearing their den-tition?) this article will focus on the impact of sleep disordered breathing on the grow-ing child and the unique role dentistry plays in screening and treating these patients.

S leep disordered breath-ing (sdB) encompasses a spectrum of dysfunctional sleep breathing, including occasional snoring, habitu-al snoring, upper airway re-sistance syndrome (UArs),

sleep apnea, and hypoventilation. the medi-cal community has traditionally focused on obstructive sleep apnea (OsA) and obesity hypoventilation syndrome. Unfortunately, many sleep-related breathing disorders, es-pecially those predominately found in women

Jeffrey S. rouSe, DDSPrivate Practice ProsthodontistSan Antonio, Texas

uArS and oSA: A Comparison Although many clinicians describe UArs and OsA as the same disease with a slight variance in severity, their pathophysiologies appear to be different.4 OsA is characterized by com-plete upper airway obstructions lasting longer than 10 seconds with an associated 4% oxygen desaturation. it is most commonly attribut-ed to a hypotonia of the soft palate or base of tongue. Partial airway obstructions that lead to desaturation or brief awakenings from sleep are classified as hypopneas. Continued desatu-rations over time may cause excessive daytime sleepiness and hypertension. they have been correlated to endothelial dysfunction, myo-cardial infarction, and cerebrovascular acci-dents. the level of severity of OsA has been associated with an increased mortality.5,6

Anatomic irregularities or minor breath-ing impairments can create UArs.7 Patients with UArs may have a more collapsible air-way because of abnormal inspiratory flow dynamics8 or increased collapsibility on expiration due to atypical anatomy.9 UArs patients have more sensitivity to restricted breathing or negative oropharyngeal pres-sure. the airway constriction is recognized

and children, have been ignored because of the focus on OsA.

snoring typically occurs when air passes between the tongue and soft palate, caus-ing a vibration of the soft palate. A snor-ing sound may also be produced from the nose during inhalation. Children can pro-duce the same loud snoring sound as an adult, but typically their snoring is more of an effortful breathing, making recogni-tion and diagnosis more challenging in this population.

the consequences of snoring can be seri-ous. Habitual snoring, defined as three times per week or more, has been associated with hyperactive behavior in children as young as 3 years of age1 and poor academic perfor-mance.2 sleep fragmentation or disruption caused by snoring appears to play a role as important as hypoxia in causing dysfunction. Benign snoring in adults has been implicat-ed in an increase risk of stroke.3

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for OsA, women with UArs and the majority of children are eliminated from the purview of the dental practitioner.

Sleep Prosthodonticssleep dentistry can be thought of as the study of an OA and its impact on the airway. sleep prosthodontics is the study of the airway and its impact on the stomatognathic system. the stomatognathic system encompasses the mouth, jaws, and the closely related struc-tures of the oro-pharynx and fauces. dentists deal with this system during its development and maintain it throughout a lifetime.

Although a physician must make the diag-nosis of sdB, the dentist plays a critical “diag-nostic” role. Many times the lack of witnessed apneic episodes or the lack of particularly egregious daytime symptoms may lead to a delay in care by the medical community. the impact of a poor airway can many times be detected in the patient’s craniofacial devel-opment, oral impairment, and occlusal dys-function well before the clinical presentation of systemic disease.15

sleep prosthodontics is not restricted to an appliance, but instead has a single-minded focus on the patient’s health. it also encour-ages a patient-centered, interdisciplinary so-lution that includes a wide range of options, including orthodontics, oral mycology, nutri-tion/diet counseling, orthognathics, CPAP, MAA, and otolaryngologic surgeries.

The Snoring Child in the general population, 2% to 3% of chil-dren have apnea.16 that proportion is grow-ing given the increase in childhood obesity.17 Apneas and hypopneas are defined in chil-dren as events lasting longer than two missed breaths and most commonly associated with some change in oxygen saturation or end tidal CO2 increase. UArs presents in children dur-ing polysomnography (PsG) as an increased respiratory effort with no apnea and little oxy-gen saturation change (Figure 2). the charac-teristic signs and symptoms of UArs vary with the age of the child, as will treatment options.18

the prevalence of snoring in children rang-es from 10% to 21% from 6 to 81 months.19 Habitual snoring has been reported in 9% of infants aged 0 to 3 months.20 in a general pediatric clinic, habitual snoring was docu-mented in 17% of patients, with that rising to 29% of the children reporting for neurolog-ic indications such as headaches and 56% of the children diagnosed with psychiatric dis-orders (half with anxiety/mood disorders).21,22 in a 2-year follow-up on habitually snoring children, 30% of subjects had worsened from baseline. OsA developed more often in boys, especially if adenotonsillar hypertrophy or an increase in waist circumference was present.23

snoring and mouth breathing in children were initially thought of as unreliable markers for OsA and not as potential problems in their own right. More recently, it is believed that snor-ing independent of OsA may cause neurocogni-tive dysfunction and impaired daytime perfor-mance.24,25 Habitually snoring children are at higher risk for social problems, poor academic performance, decreased attention, and anxiety/depression issues.26-28 Children who are chron-ic snorers have abnormal slow-wave sleep pat-terns and experience more fragmentation. this sleep instability may explain the detrimental effects of non-apneic snoring.29 studies of oc-casionally snoring children who otherwise have normal sleep demonstrated altered brain func-tion and more delayed and effortful processing. these children also experienced more behav-ioral problems than non-snoring children.30

Children who snore are not likely to “grow out of it” without experiencing cognitive impairment.

and responded to more quickly, preventing obstruction. these respiratory effort–related arousals (rerAs) and sleep fragmentations lead to activation of the autonomic nervous system—in particular, increased sympathetic nerve activity.10

Sleep DentistryContinuous positive airway pressure (CPAP) was introduced in 1981.11 CPAP is still the standard of care today for OsA.12 even with significant improvements in CPAP technol-ogy, it is unpopular with patients, rarely worn throughout an entire night,13 and has less than optimal long-term compliance.14

Oral appliances (OA) were introduced in the 1980s in an attempt to provide an alter-native to the unpopular CPAP. OAs act by protruding the mandible and attempting to position the tongue out of the oropharyn-geal region. OAs are currently divided by their manner of therapy. tongue-retaining devices utilize negative pressure from a bulb attached to the tip of the tongue to reposition the tongue. Mandibular advancing appliances (MAAs) are attached to the dental arch (Figure 1). the mandible is held in a protruded posi-tion. the protrusion is either fixed or titratable.

Although the quest to create an alternative to CPAP is understandable, sleep dentistry has become single-minded in its treatment of adult apnea with an appliance. if dentistry compartmentalizes itself on OA fabrication

DisorDereD sleep (1.) Titratable mandibular advancing appliance. (2.) Preparing for polysomnography (PSG). Monitoring and scoring is unique for pediatric sleep studies.

fig. 1 fig. 2

inside Continuing eDuCation


the neurocognitive and behavioral damage from snoring in children appears to be related to the fact that their brains are still developing. A confounding issue is that the impact of the snoring may not be detected for years, even after the snoring has resolved. the genesis of the long-term neurocognitive effect in snor-ing children may be during a critical devel-opmental period—at or before 3 years of age.

Bonuck and colleagues31 examined 7 years of epidemiologic data from more than 11,000 children followed from birth. Cognitive and behavioral assessments were conducted when the children reached 4 and 7 years of age. By 4 years old, children who had a history of sdB were 20% to 60% more likely to exhib-it behavioral difficulties; by 7 years, they were 40% to 100% more likely. the more severe sdB was linked to the poorest behavioral out-comes. the “Worst Case” cluster had a peak

of sdB symptoms at 30 months that abated. nonetheless, at 7 years the cluster displayed hyperactivity and conduct and peer difficul-ties. inclusion in the “Later sdB symptom” cluster, with a peak at 42 through 69 months, was predictive of emotional difficulties and hyperactivity at both 4 and 7 years.

Bonuck’s work underscores that the pres-ence of irregular sleep breathing may not be directly linked to the academic and behavior-al symptoms. instead, sdB during periods of brain development is very predictive of later damage. the neurocognitive damage in areas such as academic performance and executive functioning is not reversible, so early iden-tification and treatment are paramount.32-34

Metabolic ConsequencesBecause of the close link between sleep, the immune system, and inflammation, children

with sdB are prone to many of the same sys-temic inflammatory conditions that as adults lead to high blood pressure, arrhythmias, and congestive heart failure.35 sleep disturbances in children lead to aberrant sympathetic ner-vous activation that creates cardiovascular and metabolic injury.36 Pediatric apnea is connect-ed with endothelial microvascular dysfunction: a marker of subclinical cardiovascular disease, systemic hypertension, pulmonary hyperten-sion, and myocardial left ventricular remodel-ing.37 in the presence of obesity, the metabolic consequences are exacerbated. treatment of the sdB is mandatory to prevent complica-tions.38 if the child’s sdB is resolved, the sys-temic inflammation in non-obese subjects appears to be reversible.39 the unanswered question is whether the childhood autonom-ic disturbance promotes metabolic morbid-ity later in life even after sdB resolution.35

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early presentation (3.) Three-year-old with a history of snoring, bruxing, and thumbsucking. Her father and brother were both diagnosed with OSA. (4.) Pa-tient presents bilateral crossbite and sig-nificant attrition. Father assists in retrac-tion. (5.) Class 3 tonsils and an enlarged uvula. The impact on the child rather than the physical size should be key for surgi-cal intervention. (6.) Radiographic evalua-tion of tonsils. Intraoral examination may not clearly portray the volume of tissue. (7.) Enlarged adenoidal tissue. Increasing the size of the adenoids reduces the child’s ability to breath through the nose.

fig. 3 fig. 4 fig. 5

fig. 6 fig. 7

Abnormal Craniofacial GrowthsdB and abnormal craniofacial development are bidirectional. sdB may create craniofacial changes. these skeletal alterations can further exacerbate the sdB difficulty. treating the breathing issue as early as possible prevents the continuation or the worsening of the cra-niofacial problems. it may also lead to an im-provement in growth and development if ad-dressed soon enough in the process. Before the age of 4 years, 60% of craniofacial maturity is completed. Approximately 90% is finished by the age of 12 years.41 tonsils and adenoids be-gin hypertrophying at 2.5 years, reaching their greatest dimensions around 5 or 6 years. early and late growth clusters exist in children with sdB. the early cluster will have sdB without tissue hypertrophy. the late cluster will react to the additional airway blockage.

Early Growth Clusterthe pattern for bone growth resides not in the bone itself but rather in the soft tissue and muscle that encase the bone.42 Oral-facial muscle tone and tongue tonicity create a framework for normal development of the

nasomaxillary complex and mandible.43 sdB is noted in children with pathologic hypotonia of facial and tongue muscles. Children born with a normal palate and oral-facial hypotonia will develop a high, narrow palate over the first year of life (Figure 3 and Figure 4). Children born with a high, narrow palate have hypoto-nia at birth. these myofunctional changes may be detected in utero.43

Premature children suffer from sdB and OsA due to the lack of completion of cranio-facial development in utero. they typically have a narrow, hard palate, abnormal na-sal resistance, and mouth breathing. these changes promote the development of an ab-normally long lower third of the face.44 Kin and colleagues concluded that if nothing is done in these premature infants, sdB and OsA will develop.44

instinctively, clinicians have concentrated on the mandible when discussing airway di-mensions. However, the maxilla appears to be the more important arch in determining up-per airway dimensions in OsA patients.45 the distance from A point (most posterior point in the concavity of the anterior maxilla) to

Sleep Prosthodontics and the Snoring Childthe American Academy of Pediatrics (AAP) guidelines for the diagnosis and management of childhood OsA syndrome40 call for every child/adolescent to be screened for snoring at each office visit. A PsG should be ordered on children who snore and have neurocogni-tive, behavioral, or medical issues indicative of OsA. the goal of the guidelines is to screen for more sdB, but there are two diagnostic problems. Although PsG is the gold standard for diagnosis of OsAs, there is a shortage of sleep laboratories with pediatric expertise and equipment.40 in addition, the worst-case chil-dren have no behavioral issues when the snor-ing is occurring. it is not until years later that the hyperactivity and emotional issues arise, after the snoring has abated.31 Physicians fol-lowing the AAP guidelines will not discover the worst sdB children. dentists and dental hygienists have a unique role in early identi-fication of sdB in children. Beginning sleep prosthodontic indicators of sdB are cranio-facial anomalies resulting in malocclusions and sleep-related bruxing.



Porion vertical (vertical line drawn from the most superior part of the external auditory me-atus) was the most contributory cephalometric marker for airway patency. Appropriate posi-tioning of the maxilla opens the velopharyn-geal and orophayngeal airways. Additionally, proper maxillary positioning enhances man-dibular growth. thus, the lack of facial mus-cle activity and ideal tongue tone constrains the premaxilla, producing an abnormal airway dimension and amplifying the threat of sdB.

Late and Mixed Growth Clustertonsils and adenoids occupy space, increase airway resistance, and create turbulent na-sal airflow. the period of tissue hypertrophy is especially damaging to mixed cluster pa-tients. these children are undiagnosed early growth cluster children who become further compromised due to enlargement of oral and nasal tissues.

tonsils and adenoids should be judged against the relative size of the airway rather than the absolute size of the lymphoid tis-sue46 (Figure 5 and Figure 6). Adenoids are located at the posterior of the nasal cavity on

the roof of the nasopharynx (Figure 7). the normal distance from the adenoids to the soft palate for an acceptable airway should be at least 12 mm. For each millimeter de-crease, the odds of the child snoring increase 1.61 times. Mouth breathers typically show a smaller upper airway dimension as well.47 the adenoid and tonsillar obstruction cre-ates the trigger, but the deviate facial and neck muscle recruitment and tongue hypo-tonia cause the maldevelopment.48

the point of obstruction tends to determine the type of skeletal impact. nasal obstruc-tion from enlarged turbinates, blocked osti-um maxillare, deviated septum, or nasal valve stenosis creates Angle occlusions of Class i, ii, and iii equally (Figure 8). the maxilla in these cases is positioned posteriorly and the mandible is posterior-inferior. the facial type is most commonly dolicocephalic. Blockage of the airway predominately by the adenoids will create growth patterns that yield mostly Class ii occlusions and anterior open bite with both jaws located posterior-inferiorly. Facial type is again dolicocephalic with the typical long-thin “adenoidal” face49 (Figure 9 through

Figure 12). if the tonsillar tissue is responsi-ble for the airway obstruction, the tongue will have an abnormal resting posture. Class iii occlusions will be more common with the maxilla normal or posterior placed (Figure 13 through 15). the tongue may direct the mandible anteriorly or, because the tongue is not in the roof of the mouth driving A point anterior, the maxilla will become bimaxillary retrusive.50 in some cases, the anterior pos-ture of the tongue will create an open bite. this is incorrectly referred to as a tongue thrust. the impact from a thrust does not alter the tooth position. Long-term, low forces cause tooth movement. the posture of the tongue against or between the anterior teeth due to the excessive tonsillar size creates the open bite (Figure 16 and Figure 17). Facial types in this group are more brachyfacial. Lastly, if the airway is blocked through a combination of factors, the Angle classification will be either Class ii or iii. the maxilla will be in a normal location and the mandible will be the affected arch (Figure 18). these craniofacial changes are not restricted to OsA; all sdB will create unique alterations depending on the patient

aDenoiDal obstruction (8.) Exam should include nasal anatomy and func-tion. Inferior nasal turbinates occupy the lateral wall of the nose and are easily vi-sualized. When swollen, as in this 12-year-old child, the available airway is reduced and may lead to altered function. (9.) An “adenoidal” face is long, thin, and dolico-cephalic (Case courtesy of James Awbrey, DMD). (10.) Narrow maxilla with tooth wear and bilateral crossbite. (11.) Adenoidal tissue blocking the velopharyngeal airway. (12.) Class II Angle classification with worn dentition and anterior open bite.

fig. 11

fig. 8 fig. 10

fig. 12

fig. 9



mouth breathing with the tongue in the roof of the mouth directed ideal growth.

in some children, t&A alone may not com-pletely resolve the OsA (Figure 19 and Figure 20). the longer the airway dysfunction, the greater the structural impact on the airway. An interdisciplinary clinical study54 was con-ducted on children approximately 6.5 years old with inclusion criteria of OsA, large tonsils, vi-sually constricted airway, and high and narrow palate. Group 1 was treated with rapid maxil-lary expansion (rMe) and Group 2 with t&A. Maxillary expansion has been shown to cre-ate improved nasal resistance and an increase nasal cavity volume. in cases without exces-sive lymphoid hypertrophy, rMe can resolve significant levels of OsA.55,56 After the original therapy, only one child had been completely resolved (apnea-hypopnea index [AHi] <1). the remaining subjects switched groups and received the opposite treatment. After receiv-ing both treatments, 29 of the 31 children were cured. it can be concluded that many children must be treated with multiple therapies before resolution, especially if the sdB has previously altered the airway to a significant degree.

Sleep Bruxismnot only are dentists in the best position to detect and intercede in cases of abnormal cra-niofacial development, but they are also the best judges of aberrant tooth wear. Bruxism occurs in up to 30% of children, often around 5 and 6 years during late cluster adenoid and tonsillar hypertrophy.57 Carlsson and col-leagues58 determined in a 20-year prospec-tive study that bruxism in childhood may be a persistent trait. early tooth wear was pre-dictive of increased tooth wear 20 years lat-er. the results emphasize that the triggering mechanism for sleep bruxism is present as a child and does not develop over time.

For restorative dentists, it is significant-ly more important to locate what elicits the action than the “genetic code” that produc-es a bruxer. Historically, popular theories have postulated that the generator for brux-ism was stress, neurochemical, or occlusion. PsG-based research has disproven these theories. stress leads to awake bruxism, not sleep bruxism.59,60 Most chemical irregulari-ties in bruxers are linked to sleep fragmen-tation.61,62 Finally, bruxism is a centrally, not

compensation. Children with UArs have been reported to display high, narrow palates, doli-cofacial form, and a Class ii malocclusion, in-dicative of largely adenoidal blockage.51

dentists identifying craniofacial changes early in development may resolve the mal-occlusion by simply referring for adenoton-sillectomy (t&A). the impact of t&A on the pediatric immune system is controver-sial. A recent 5-year longitudinal, prospective study demonstrated that adenotonsillectomy does not pose adverse short- or long-term im-pact on the cellular or humoral immunity.52 Cephalametric changes (eg, posterior incline to the mandible, anterior incline to the maxil-la, longer anterior and shorter posterior face height, and upper and lower teeth more retro-clined than a normal matched control) were detected in 5-year-old subjects with adenoid-induced OsA.53 t&A resolved the OsA in all subjects. At the 5-year recall, cephalomet-ric evaluation demonstrated that the man-dibular plane angle and incisor relationship was similar to the control. early resolution of the sdB allowed time for the proper use of the oral-facial and tongue muscles. Closed

tonsillar obstruction (13.) Seven-year-old brachyfacial child with high body mass index (Case courtesy of James Awbrey, DMD). (14.) Angle Class III occlusion with constricted maxilla. (15.) Cephalometric evaluation demonstrates significant tonsillar blockage of the airway and bimaxillary retursion. (16.) Tongues with poor tone and posture may move the teeth over time and open the bite (Case courtesy of James Awbrey, DMD). (17.) Moderate adenoid swelling and significant tonsillar obstruction.

fig. 16

fig. 13 fig. 15

fig. 17

fig. 14


peripherally, mediated event.63 idealizing oc-clusions may control the impact of bruxism and improve chewing function, but it will not resolve sleep bruxism.64

Bruxism occurs during microarousals from regular sleep patterns.64,65 Many fac-tors may introduce microarousals, including reflux and tactile and auditory stimuli.66,67 the most common reason for these brux-ism-related microarousals appears to be re-spiratory effort. it is the author’s assertion that sleep bruxism serves a functional role in protecting and improving the airway during episodes of inspiratory flow limitation and obstruction. the activity of increasing ge-nioglossal and infrahyoid muscle tone along with the lateral movement of the mandible

dilates the upper airway, raises inspiratory flow, and reduces upper airway resistance.68

sleep bruxism is classified as a sleep-related movement disorder similar to restless leg syn-drome and is routinely referred to as a possi-ble indicator of sdB. the majority of bruxism occurs during light non–rapid eye movement sleep.69 With traditional PsG, 80% or more of the bruxing episodes have related respirato-ry events.68,70 Linking bruxism and airway re-sistance causally is difficult, given that many abnormal breathing patterns are not neces-sarily conspicuous on PsG. sleep apneas are more easily recognized, but the rerAs can be a challenge to identify, especially in children who do not desaturate like adults. Additionally, bruxism minimizes the degree of obstruction

and flow restriction.71,72 A healthy autonomic nervous system of a bruxing child can fix the airway before it can be detected within the framework of a normal PsG.

Without esophageal pressure monitoring to demonstrate the increase respiratory ef-fort, bruxism activity may not be recognized as being associated with a respiratory event.71,72 this rerA-related phenomenon was verified in a study of 50 pediatric subjects with an in-clusion criteria of sleep-related tooth wear.73 no significant statistical association was found between AHi and the severity of brux-ism. However, when respiratory effort–related arousals were added to the AHi, a statistically significant association was found. the bruxing events acted to protect the airway rather than

bruxism (18.) Tonsils and adenoids impeding breathing. (19.) Five-year-old child with significant attrition. Mother reports a his-tory of sleep bruxism (Case provided by Kathy French, DDS). (20.) Maxillary anterior tooth wear. Adenotonsillectomy (T&A) per-formed and postoperative apnea-hypopnea index (AHI) was 6.1. Continued therapy recommended for resolution. (21.) Six-year-old male presents nocturnal bruxism, habitual snoring, and behavioral issues. PSG reports an AHI of 9.6/hr and respiratory effort–related arousal (RERA) of 14.2/hr (Case provided by Kathy French, DDS). (22.) Radiograph highlights the obstructed nasal airway preopera-tively. Three months after T&A, another PSG demonstrated and AHI of 0.3 and RERA of 0.0/hr.

fig. 18

fig. 21

fig. 20

fig. 22

fig. 19




4. Bao G, Guilleminault C. Upper airway resistance syndrome—one decade later. Curr Opin Pulm Med. 2004;10(60):461-467.5. shahar e, Whitney CW, redline s, et al. sleep-disordered breathing and cardiovascular disease: cross-sectional results of the sleep heart health study. Am J Respir Crit Care Med. 2001;163(1):19-25.6. redline s. Morbidity, mortality, and public health burden of sleep apnea. in: Mcnicholas Wt, Phillipson eA, eds. Breathing Disorders in Sleep. London: WB saunders; 2002:222-235.7. Chen W, Kushida CA. nasal obstruction in sleep-disor-dered breathing. Otolaryngol Clin North Am. 2003;36(3) :437-460.8. Gold Ar, dipalo F, Gold Ms, Broderick J. inspiratory airflow dynamics during sleep in women with fibromyalgia. Sleep. 2004;27(3):459-466.9. Woodson Bt. expiratory pharyngeal airway ob-struction during sleep: a multiple element model. Laryngoscope. 2003;113(9):1450-1459.10. Walter LM, Foster AM, Patterson rr, et al. Cardiovascular variability during periodic leg movements in sleep in children. Sleep. 2009;32(8): 1093-1099.11. sullivan Ce, issa FG, Berthon-Jones M, eves L. reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet. 1981;1(8225):862-865.12. Giles tL, Lasserson tJ, smith BJ, et al. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev. 2006;19(3): Cd001106.13. somiah M, taxin Z, Keating J, et al. sleep quality, short-term and long-term CPAP adherence. J Clin Sleep Med. 2012;8(5):489-500.14. tokunaga t, ninomiya t, Kato y, et al. Long-term compliance with nasal continuous positive airway pressure therapy for sleep apnea syndrome in an otorhinolaryngological office [published online ahead of print April 9 2013]. Eur Arch Otorhinolaryngol. http://link.springer.com/article/10.1007/s00405-013-2483-3#page-1. Accessed May 23, 2013.15. rouse Js. the bruxism triad: sleep bruxism, sleep disturbance, and sleep-related Gerd. Inside Dentistry. 2010;6(5):33-44.16. Lumeng JC, Chervin rd. epidemiology of pedi-atric obstructive sleep apnea. Proc Am Thorac Soc. 2008;5(2):242-252.17. Chervin rd, Clarke dF, Huffman JL, et al. school performance, race, and other correlates of

sleep-disordered breathing in children. Sleep Med. 2003;4(1):21-27.18. Guilleminault C, Khramtsov A. Upper airway resistance syndrome in children: a clinical review. Semin Pediatr Neurol. 2001;8(4):207-215.19. Bonuck KA, Chervin rd, Cole tJ, et al. Prevalence and persistence of sleep disordered breathing symp-toms in young children: a 6-year population-based cohort study. Sleep. 2011;34(7):875-884.20. Piteo AM, Lushington K, roberts rM, et al. Prevalence of snoring and associated factors in in-fancy. Sleep Med. 2011;12(8):787-792.21. Archbold KH, Pituch KJ, Panahi P, Chervin rd. symptoms of sleep disturbances among chil-dren at two general pediatric clinics. J Pediatr. 2002;140(1):97-102.22. ivanenko A, Crabtree VM, Obrien LM, Gozal d. sleep complaints and psychiatric symptoms in chil-dren evaluated at a pediatric mental health clinic. J Clin Sleep Med. 2006;2(1):42-48.23. Li AM, Au Ct, ng sK, et al. natural history and predictors for progression of mild childhood obstruc-tive sleep apnoea. Thorax. 2010;65(1):27-31.24. O’Brien LM, Mervis CB, Holbrook Cr, et al. neurobehavioral correlates of sleep-disordered breathing in children. J Sleep Res. 2004;13(2):165-172.25. Barnes Me, Huss eA, Garrod Kn, et al . impairments in attention in occasionally snoring children: an event-related potential study. Dev Neuropsychol. 2009;34(5):629-649.26. Blunden s, Lushington K, Lorenzen B, et al. neuropsychological and psychosocial function in children with a history of snoring or behavioral sleep problems. J Pediatr. 2005;146(6):780-786.27. O’Brien LM, Mervis CB, Holbrook Cr, et al. neurobehavioral implications of habitual snoring in children. Pediatrics. 2004;114(1):44-49.28. Urschitz Ms, eitner s, Guenther A, et al. Habitual snoring, intermittent hypoxia, and impaired behavior in primary school children. Pediatrics. 2004;114(4): 1041-1048.29. Lopes MC, Guilleminault C. Chronic snoring and sleep in children: a demonstration of sleep disruption. Pediatrics. 2006;118(3);e741-e746.30. Barnes Me, Huss eA, Garrod Kn, et al . impairments in attention in occasionally snoring children: an event-related potential study. Dev Neuropsychol. 2009;34(5):629-649.31. Bonuck K, Freeman K, Chervin rd, Xu L. sleep-disordered breathing in a population-based cohort:

to resolve an obstruction. Bruxism should rise with UArs, habitual snoring, and occasion-al snoring, because negative pressure and respiratory effort drives the action. the re-searchers concluded that pediatric sleep-re-lated tooth wear could be used as a marker for sdB. Currently, no other healthcare provider is more equipped to evaluate and monitor pe-diatric nocturnal tooth wear than the dental practitioner (Figure 21 and 22).

Conclusionthe impact of sdB on the growing, snoring child can be serious, and sleep prosthodon-tics plays a unique role in screening and treat-ing these patients. dentists should screen children based on history and pediatric sleep questionnaire, as well as physical, intraoral, airway, and radiographic examination. it is important to note that dentists should not consider treatment in these children with-out a medical evaluation and possibly a sleep study. interdisciplinary treatment options must be reviewed within the context of the particular sleep breathing disorder, age of the patient, and level of cooperation of the child and the parents. Given its focus on MAAs, sleep dentistry is limited in treating the snor-ing child. sleep prosthodontics screens possi-ble OsA/UArs in children and acts as a con-duit of care, placing the patient in the proper medical, orthodontic, orthognathic, nutri-tionist/dietician, and/or oral mycology care for the best possible results. dentistry has a bigger role to play in sdB, and sleep prosth-odontics encapsulates that role.

References 1. Gill Ai, schaughency e, Galland BC. Prevalence and factors associated with snoring in 3-year olds: early links with behavioral adjustment. Sleep Med. 2012;13(9):1191-1197.2. Kurnatowski P, Putyński L, Lapienis M, Kowalska B. neurocognitive abilities in children with adeno-tonsillar hypertrophy. Int J Pediatr Otorhinolaryngol. 2006;70(3):419-424.3. Cho JG, Witting PK, Verma M, et al. tissue vibra-tion induces carotid artery endothelial dysfunction: a mechanism linking snoring and carotid atheroscle-rosis? Sleep. 2011;34(6):751-757.


behavioral outcomes at 4 and 7 years. Pediatrics. 2012;129(4):e857-e865.32. Gozal d, Pope dW Jr. snoring during early child-hood and academic performance at ages thirteen to fourteen years. Pediatrics. 2001;107(6):1394-1399.33. Bhattacharjee r, Kim J, Kheirandish-Gozal L, Gozal d. Obesity and obstructive sleep apnea syn-drome in children: a tale of inflammatory cascades. Pediatr Pulmonol. 2011;46(4):313-323. 34. Bhattacharjee r, Kheirandish-Gozal L, Pillar G, Gozal d. Cardiovascular complications of obstructive sleep apnea syndrome: evidence from children. Prog Cardiovasc Dis. 2009;51(5):416-433. 35. Kim J, Hakim F, Kheirandish-Gozal L, Gozal d. inflammatory pathways in children with insuf-ficient or disordered sleep. Respir Physiol Neurobiol. 2011;178(3):465-474.36. Hakim F, Gozal d, Kheirandish- Gozal L. sympathetic and catecholaminergic alterations in sleep apnea with particular emphasis on children. Front Neurol. 2012;3:7.37. Gozal d, Kheirandish-Gozal L, Bhattacharjee r, spruyt K. neurocognitive and endothelial dys-function in children with obstructive sleep apnea. Pediatrics. 2010;126(5):e1161-e1167.38. spicuzza L, Leonardi s, La rosa M. Pediatric sleep apnea: early onset of the ‘syndrome’? Sleep Med Rev. 2009;13(2):111-122. 39. Gozal d, serpero Ld, sans Capdevila O, Kheirandish- Gozal L. systemic inflammation in non-obese children with obstructive sleep apnea. Sleep Med. 2008;9(3):254-259. 40. Marcus CL, Brooks LJ, draper KA, et al. diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(5):576-584. 41. Guilleminault C, Khrammtsov A. Upper airway resistance syndrome in children: a clinical review. Semin Pediatr Neurol. 2001;8(4):207-215.42. enlow dH, Hans MG. Basic growth concepts. in: enlow dH, Hans MG, eds. Essentials of Facial Growth. Philadelphia, PA: WB saunders Company; 1996:18-38.43. Huang ys, Guilleminault C. Pediatric obstructive sleep apnea and the critical role of oral-facial growth: evidences. Front Neurol. 2012;3:1-7. 44. Kim JH, Guilleminault C. the nasomaxillary complex, the mandible, and sleep-disordered breath-ing. Sleep Breath. 2011;15(2):185-193.45. dempsey JA, skatrud JB, Jacques AJ, et al. Anatomic determinants of sleep-disordered breath-ing across the spectrum of clinical and nonclinical

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male subjects. Chest. 2002;122(3):840-851.46. ruoff CM, Guilleminault C. Orthodontics and sleep-disordered breathing. Sleep Breath. 2012;16 (2):271-273.47. Juliano ML, Machado MA, de Carvalho LB, et al. Polysomnographic findings are associated with cephalometric measurements in mouth-breathing children. J Clin Sleep Med. 2009;5(6):554-561.48. Harvold eP, tomer Bs, Vargervik K, Chierici G. Primate experiments on oral respiration. Am J Orthod. 1981;79(4):359-372.49. solow B, skov s, Ovesen J, et al. Airway dimensions and head posture in obstructive sleep apnoea. Europ J Orthod. 1996;18(6):571-579.50. Güray e, Karaman Ai. effects of adenoidectomy on dentofacial structures: a 6-year longitudinal study. World J Orthod. 2002;3(1):73-81.51. Guilleminault C, stoohs r, Kim yd, et al. Upper airway sleep-disordered breathing in women. Ann Intern Med. 1995;122(7):493-501. 52. Marcus CL, Brooks LJ, draper KA, et al. diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(5):576-584.53. Zettergren-Wijk L, Forsberg CM, Linder-Aronson s. Changes in dentofacial morphology after adeno-/tonsillectomy in young children with obstructive sleep apnoea—a 5-year follow-up study. Eur J Orthod. 2006;28(4):319-326.54. Guilleminault C, Monteyrol PJ, Huynh nt, et al. Adeno-tonsillectomy and rapid maxillary distraction in pre-pubertal children, a pilot study. Sleep Breath. 2011;15(2):173-177.55. Oliveira de Felippe nL, da silveira AC, Grace Viana G, et al. relationship between rapid maxillary expansion and nasal cavity size and airway resistance: short- and long-term effects . Am J Orthod Dentofacial Orthop. 2008;134(3):370-382.56. Pirelli P, saponara M, Guilleminault C. rapid maxillary expansion in children with obstructive sleep apnea syndrome. Sleep. 2004;27(4):761-766.57. Lavigne GJ, Manzini C, Kato t. sleep Bruxism. in: Kryger MH, roth t, dement WC, eds. Principles and Practice of Sleep Medicine. Philidelphia, PA: saunders; 2005:946-959.58. Carlsson Ge, egermark i, Magnusson t. Predictors of bruxism, other oral parafunctions, and tooth wear over a 20-year follow-up period. J Orofac Pain. 2003;17(1):50-57.59. van selms MK, Lobbezoo F, Wicks dJ, et al. Craniomandibular pain, oral parafunctions, and

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Rehabil. 2011;38(9):635-642.70. Kato t, thie nM, Huynh n, et al. topical review: sleep bruxism and the role of peripheral sensory influ-ences. J Orofac Pain. 2003;17(3):191-213.71. simmons JH, Prehn r. Airway protection: the missing link between nocturnal bruxism and obstructive sleep apnea. Paper presented at: 23rd Annual Meeting of the Associated Professional sleep societies; June 6-11, 2009; seattle, WA. Abstract A218.72. simmons JH, Prehn r. nocturnal bruxism as a protective mechanism against obstructive breathing during sleep. Paper presented at: 22rd Annual Meeting of the Associated Professional sleep societies; June 7-12, 2008; Baltimore, MA. Abstract A199.73. singh n, Chandwani B, Finkelmann M, et al. sleep bruxism-related tooth wear as a clinical marker for pediatric sleep-disordered breathing. Paper pre-sented at: 21st Annual American Academy of dental sleep Medicine Meeting; June 8, 2012; Boston, MA. Poster #015.

psychological stress in a longitudinal case study. J Oral Rehabil. 2004;31(8):738-745.60. Pierce CJ, Chrisman K, Bennett Me, Close JM. stress, anticipatory stress, and psychologic mea-sures related to sleep bruxism. J Orofac Pain. 1995;9 (1):51-56.61. seraidarian P, seraidarian Pi, das neves Cavalcanti B, et al. Urinary levels of catecholamines among individuals with and without sleep bruxism. Sleep Breath. 2009;13(1):85-88.62. Zhang J, Ma rC, Kong AP, et al. relationship of sleep quantity and quality with 24-hour urinary cate-cholamines and salivary awakening cortisol in healthy middle-aged adults. Sleep. 2011;34(2):225-233.63. Gastaldo e, Quatrale r, Graziani A, et al. the excitability of the trigeminal motor system in sleep bruxism: a transcranial magnetic stimula-tion and brainstem reflex study. J Orofac Pain. 2006;20(2):145-155.64. Lavigne GJ, Khoury s, Abe s, et al. Bruxism

physiology and pathology: an overview for clinicians. J Oral Rehabil. 2008;35(7):476-494. 65. Khoury s, rouleau GA, rompré PH, et al. A signifi-cant increase in breathing amplitude precedes sleep bruxism. Chest. 2008;134(2):332-337.66. Miyawaki s, Lavigne GJ, Pierre M, et al. Association between sleep bruxism, swallowing-related laryngeal movement, and sleep positions. Sleep. 2003;26(4):461-465.67. Kato t, Montplaisir Jy, Guitard F, et al. evidence that experimentally induced sleep bruxism is a consequence of transient arousal. J Dent Res. 2003;82(4):284-288.68. Krieger J. Breathing in normal subjects. in: Kryger MH, roth t, dement WC, eds. Principles and Practice of Sleep Medicine. 3rd ed. Philadelphia, PA: WB saunders Company; 2000:229-241. 69. Carra MC, rompré PH, Kato t, et al. sleep brux-ism and sleep arousal: an experimental challenge to assess the role of cyclic alternating pattern. J Oral


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Sleep Prosthodontics: A New Vision for DentistryJeffrey S. Rouse, DDS

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sleep disordered breathing (sDb) encompasses a spectrum of dysfunctional sleep breathing, including:

a. habitualsnoring. b. upperairwayresistancesyndrome(UARS). C. sleepapnea. D. alloftheabove.

Osa is characterized by complete upper airway obstructions:

a. lastinglongerthan4secondswith10%oxygendesaturation. b. lastinglongerthan10secondswith4%oxygendesaturation. C. lastinglongerthan6secondswith6%oxygendesaturation. D. lastinglessthan15secondswith5%oxygendesaturation.

according to the author, sleep dentistry can be thought of as the study of:

a. anoralappliance(OA)anditsimpactontheairway. b. polysomnography(PSG). C. thewayocclusionaffectssleep. D. continuouspositiveairwaypressure(CPAP).

sleep prosthodontics is the study of:

a. UARS,butnotOSA. b. occlusionandcentricrelation. C. theairwayanditsimpactonthestomatognathicsystem. D. SDBinwomen.

in the general population, what percentage of children has apnea?

a. 2%to3% b. 4%to5% C. 6%to7% D. 8%to10%

Habitually snoring children are at higher risk for:

a. socialproblems. b. pooracademicperformance. C. decreasedattention. D. alloftheabove.

sleep disturbances in children lead to sympathetic nervous activation that creates:

a. cardiovascularandpulmonaryproblems. b. cardiovascularandmetabolicinjury. C. metabolicandpulmonarydevelopmentaldelays. D. growthproblemsandsocial-emotionalissues.

beginning sleep prosthodontics indicators of sDb are craniofacial anomalies resulting in:

a. alow,narrowpalate. b. congenitaledentulism. C. malocclusions. D. ankyloglossia.

the normal distance from the adenoids to the soft palate for an acceptable airway should be:

a. atleast15mm. b. between8and10mm. C. nomorethan10mm. D. atleast12mm.

With traditional Psg, what percentage of bruxing episodes is related to respiratory events?

a. 80% b. 65% C. 50% D. 35%


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Sleep Prosthodontics: Understanding Myofascial Pain A new paradigm for examining temporomandibular disorderJeffrey S. Rouse, DDS

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epistemic uncertainties are those that result from a lack of knowledge. Often reso-lution is achieved for these types of uncertainties by testing alternative explanations that lie outside current unsatisfactory paradigms. sleep prosthodontics, the study of the airway and its impact on the stomatognathic system, is a new concept that may help to explain many uncertainties that remain within the field of dentistry in terms of myofascial pain. Dentistry has historically concluded that myofascial discomfort has a mechanical explanation, with the most predominant areas of interest being mal-occlusion and bruxism. this article presents the airway as an alternative source for problems with myofascial pain.

I n dentistry, it is often said, “you cannot diagnose what you cannot see”; in statistics, this concept is re-ferred to as epistemic uncertainty. epistemic uncertainty results from a lack of knowledge, and can occur when available information is in-

complete or imprecisely evaluated. improving knowledge acquisition is one way to avoid epistemic uncertainties. As part of this pro-cess, alternative explanations for a problem can be envisioned and experimental data can be gathered to support or refute them.

Prevalence and SymptomstMDs are a varied group of conditions that may affect the tMJ, the masticatory muscles, or both, and are the leading cause of nonden-tal pain in the orofacial region. A classic pre-sentation includes muscle or joint pain, joint sounds, and restricted or altered motion.2

in an attempt to create a standard for com-paring findings from different tMD stud-ies, the research Diagnostic Criteria for temporomandibular Disorders was estab-lished in 1992.3 Patients with known tMD are grouped by diagnostic criteria: muscle disorders (myofascial pain and myofascial pain with limited opening), disc displace-ments (with reduction, without reduction with limited opening, and without reduc-tion without limited opening), or arthral-gia/arthritis/arthrosis (arthralgia, osteoar-thritis, and osteoarthrosis).2 in a systematic review, the prevalence of each group was as follows: muscle disorders, 45.3%; disc dis-placements, 41.1%; and arthralgia/arthritis/arthrosis, 30.1%.2 the most common of the subgroups was myofascial pain without lim-ited opening and with more than three sites of pain on palpation.

in dentistry, there is considerable epis-temic uncertainty surrounding temporoman-dibular disorders (tMDs), especially the myofascial pain subtype. the hypothesis that dysfunctional sleep breathing may elicit tem-poromandibular joint (tMJ) pain will be ex-amined as an alternative to traditional me-chanical explanations, which focus on malocclusion and bruxism.

A previous article introduced the concept of sleep prosthodontics to differentiate it from sleep dentistry.1 sleep prosthodontics is the study of the airway and its impact on the stomatognathic system, which encompasses the mouth, jaws, and the closely related struc-tures of the oropharynx and fauces. Dentists become familiar with this system during its development, and assist in its maintenance throughout a patient’s life. this article will address the connection between sleep frag-mentation and airway maintenance and the signs and symptoms of tMDs.

Peer Reviewed

Jeffrey S. rouSe, DDSPrivate Practice San Antonio, Texas

36 insiDe Dentistry | December 2013 | www.insidedentistry.net

low baseline somatization scores continued to diminish over the 12-month period. those with higher somatization scores at baseline had a measured relapse of complaints. it ap-pears that somatization plays a role in the eti-ology and recurrence of M-tMD. this is in-teresting, given that many patients with tMD have functional somatic syndromes such as fi-bromyalgia, irritable bowel syndrome, and in-terstitial cystitis. these conditions are more associated with a generalized central nervous system hyperexcitability.10

etiologic Theories for Myofascial PainMechanical Theoriesthe mechanical explanations for myofas-cial pain that predominate the dental liter-ature include malocclusion and bruxism. A prevailing etiologic theory is the connection between occlusion and tMD. the concept is that if the teeth are not in harmony with a cen-tered condylar position in the fossa and/or if the guidance in function to a maximum inter-cuspal position has interferences, the muscle of mastication must reposition the mandible to allow proper function. this constant effort will create muscle dysfunction and M-tMD. treatment options include occlusal adjust-ment, orthodontics, and orthognathic surgery.

Although 90% of the population does not have harmonious centric relation/maximum intercuspation positioning, and the major-ity have functional interferences, very few

people have tMD.11 in addition, no system-atic review has found evidence to indicate that occlusal adjustment leads to a greater degree of tMD resolution than placebo ad-justment.12 Orthodontic interventions per-formed to improve occlusal relationships have also proved to not routinely resolve M-tMD and should not be considered a pre-ventive measure or treatment option.13

Although there are many malocclusions that do not lead to tMD symptoms, those such as unilateral cross bite, deep bite, in-creased overjet, and anterior open bite have been correlated with an increased risk of tMD.13 the underlying mechanism con-necting these malocclusions with tMD may be the airway, given the bidirectional nature of the disorder. Many dentofacial physical risk indicators for malocclusion and tMD are also identified as indicators of increased risk for sleep-disordered breathing (Figure 1 through Figure 3). Measures aimed at pre-vention, reversal, and/or adequate treatment of malocclusion early in development might also help preclude negative health outcomes often associated with sleep−airway issues.

Another common mechanical theory is that force from bruxism is the pathogenic factor in myofascial pain. it seems that some patients also hold this belief. A recent study showed the self-reported rate of nighttime bruxism in patients with M-tMD (55.3%) to be higher than that of the general popula-tion (15.2%).14 However, polysomnography

As expected, prevalence of tMD was found to be lower in the general population, with 10.5% having myofascial pain subtype of tMD (M-tMD).2 Other studies have showed that the risk for tMDs is significantly elevated among women, especially black women.4 this article’s focus is limited to M-tMD, given that it is a common subtype of myofascial pain seen in patients presenting to restorative practices.

M-tMD is characterized by a dull, aching pain that worsens with palpation and func-tion. Physical examination reveals hypersensi-tive regions or “trigger points” of taut skeletal muscle fiber. Cairns5 identified patients with M-tMD who complained of pain as exhibit-ing a localized hyperexcitability of the central nervous system when challenged with painful stimuli. the population seeking treatment for M-tMD comprises mostly women (3.8:1 ratio of women to men).6 the age of those diagnosed with M-tMD has been shown to range from 25 to 40 years, with prevalence decreasing with advancing age.7 this subtype of tMD has been shown to have variable pain intensity, as well as self-limiting and vacillating character-istics, making it difficult to create a framework for the natural progression of the disorder.8

A study was conducted by van selms and colleagues9 to determine whether predictive factors for M-tMD pain could be identified over time. Patients were assessed before tMD treatment was initiated and were followed up for 12 months after resolution of pain symp-toms. the pain complaints of patients with


fig. 1 fig. 3fig. 2

(1.) Patients with sleep-disordered breathing demonstrate many of the malocclusions associated with temporomandibular disorders, including anterior open bite and unilateral cross bite. The scalloped tongue is indicative of an airway issue. (2.) A patient with the myofascial pain subtype of temporomandibular disorder presenting with an adenoid facial type, high mandibular angle, and retrog-nathic mandible. (3.) Anterior open bite and increased overjet can be airway-directed malocclusions.


data failed to confirm this higher rate, and higher rates of bruxism were actually found in patients with less myofascial pain and in control subjects (Figure 4).

Biologic Theory: UARS A biologic theory that serves as an alterna-tive to the traditional mechanical theories is that hyperresponsive management of a more collapsible airway creates spontaneous pain and hyperalgesia. Within the fields of sleep medicine and sleep dentistry, recent focus has been placed on obstructive sleep apnea (OsA), which is characterized by complete upper air-way obstruction lasting longer than 10 seconds with an associated 4% oxygen desaturation.1 it is most commonly attributed to a hypotonia of the soft palate or base of the tongue. Partial airway obstructions that lead to desaturation or brief awakenings from sleep are classified as hypopneas. Continued desaturation over time may cause excessive daytime sleepiness and medical comorbidities.

Upper airway resistance syndrome (UArs) was first described in the literature in 1993.15 Although many clinicians describe UArs and OsA as being the same disease with a slight variance in severity, their pathophysiologies in fact appear to differ.16 Anatomic irregulari-ties or minor breathing impairments can cause UArs.17 Patients with UArs may have a more collapsible airway because of abnormal inspi-ratory flow dynamics18 or increased collaps-ibility on expiration due to atypical anatomy.19

Patients with UArs also differ from those with OsA in their responsiveness to the in-duction of an airway event. in patients with OsA, repetitive closures of the upper airway appear to dull the sensory receptors, caus-ing an absence of activation of the dilator muscles in the airway.20 therefore, patients with OsA may exhibit hyporesponsiveness or nonresponsiveness to upper airway collapse. Patients with UArs have more sensitivity to restricted breathing or negative oropharyn-geal pressure, however, and airway constric-tion is recognized and responded to more quickly, preventing obstruction.

these respiratory effort–related arousals (rerAs) and sleep fragmentations lead to

activation of the autonomic nervous system, particularly increased sympathetic nerve ac-tivity.21 this, in turn, causes a release of cate-cholamine (epinephrine and norepinephrine) into the bloodstream, creating a transient in-crease in pulse rate, blood pressure, and res-piration. Catecholamine levels remain abnor-mally high for 24 hours after the event.22 this

“fight-or-flight” response may be responsible for many of the damaging aspect of UArs.23

Polysomnography indicators for UArs include an apnea-hypopnea index score of 5 or less, five or more rerAs, and a minimum oxygen saturation level greater than 92%.24

Although some symptoms of UArs overlap with those of OsA, there are important dis-tinctions between the two disorders. the typi-cal patient with UArs is not overweight, for example. Women (typically aged 25-50 years) are three times more likely to be affected than men.24-26 it appears that women are more hy-perresponsive to airway challenges because of the hormones progesterone and, to a slight degree, estrogen. Progesterone is a pharynge-al dilator and respiratory stimulator and also generates tongue muscle tone.27 Menstrual cycle phases alter hormone levels; one study found that more women complained of

fatigue during the follicular phase, whereas there was a higher level of apnea (as measured by the apnea-hyponea index) in women dur-ing the luteal phase.28 the authors found that hormonal contraceptive use appeared to be associated with a reduced risk of airway dys-function, improved sleep efficiency, and in-creased sleep duration.28 Most likely because of hormonal changes, postmenopausal wom-en are more likely to snore and experience witnessed apneas, gasping, and frequent awakenings.29 in many cases, UArs devel-ops into OsA in postmenopausal women.30

Chronic sleep-onset insomnia and sleep-maintenance insomnia are more common in patients with UArs.16 in a recent pilot study, 90% of the nocturnal awakenings ex-perienced by patients with chronic insomnia were sleep breathing events, the majority of which were rerAs.31 All of the awakenings that lasted 5 minutes or longer, a duration that predisposes toward an insomnia epi-sode, were preceded by a sleep-disordered breathing event.31 Adults with UArs may complain of fatigue rather than sleepiness.24 Higher incidence of sleepwalking, sleep ter-rors, myalgia, depression, and anxiety have been seen in patients with this disorder.25

(4.) Higher rates of bruxism are not seen in patients with myofascial pain.

fig. 4


Patients with UArs often present with a functional somatic syndrome misdiagno-sis, including migraine/tension headaches, irritable bowel syndrome, chronic fatigue syndrome, tMD, and fibromyalgia.26 Many young women with sleep-disordered breath-ing are mistakenly treated with hypnotics, antidepressants, pain medication, attention-deficit/hyperactivity disorder medication, eugeroics, and muscle relaxants.32

The Link Between Pain and Sleep-Disordered Breathingsleep fragmentation may be culpable in cas-es of both allodynia, in which a normally in-offensive stimulus causes pain, and hyper-algesia, in which an increased response to a painful stimulus is experienced. Fragmented sleep profiles increase spontaneous pain or sensitize mechano-insensitive nociceptors with catecholamine, contributing to sympa-thetically maintained pain,33 and further im-pair natural pain-control mechanisms that are thought to play a key role in the devel-opment, maintenance, and exacerbation of chronic pain.34 Polysomnography reports on 25 consecutive patients who reported head-ache or palpable muscle pain revealed that 100% were diagnosed with UArs (J. Metz, personal communication, 2011).35

the phase of sleep that is reduced or elimi-nated by sleep fragmentation may also be im-portant for maintaining homeostasis. rapid eye movement (reM) sleep is a normal stage of sleep that usually accounts for 20% to 25% of total sleep time. it is considered the light-est level of sleep and is responsible for non-declarative memory consolidation, anxiety/depression regulation, and pain control. sleep deprivation, especially deprivation of reM sleep, induces spontaneous pain and hyper-algesia.35 During reM sleep, the only muscles that maintain normal tone are the diaphragm and those of the eyes. the remaining muscles are hypotonic, including the muscles that pro-tect the airway. this is the first time during the evening that a hyperresponsive patient with UArs cannot adequately protect his or her airway. Many patients wake with a large re-lease of adrenaline and cannot return to sleep.

in this case, a patient may lose the majority of reM sleep for the evening.

Women are more likely to experience sleep-disordered breathing during reM sleep (40.8%) than men (21.0%).36 As women age, the number of reM sleep disturbances they experience decreases, falling by 26.7% per de-cade; tMD proclivity data mimic reM sleep disturbance data.37 Postmenopausal women have been shown to experience more apnea and awakenings than premenopausal women.38

inspiratory flow limitation with rerAs (ie, UArs) is associated with an increase in low-frequency sympathetic nervous system modulation.38 Apnea triggers awakenings but is associated with high-frequency parasym-pathetic activity, and does not create a sym-pathetic tone and pain response similar to UArs. research that used cardiopulmonary coupling revealed that the ratio of damaging low-frequency to benign high-frequency spec-tral power was higher in the tMD group.39 Patients with tMD had greater sympathet-ic activation and patients with M-tMD were shown to have nocturnal heart rate variability and augmented sympathetic activity.39

Treatment Although a full discussion of treatment proto-cols is beyond the scope of this article, the res-olution of sleep-disordered breathing is criti-cal because of all the negative effects it has on patient health and quality of life. Continuous positive airway pressure, mandibular ad-vancement devices, neuromuscular onlays, and anterior repositioning splints have all been shown to be effective in the treatment of M-tMD, possibly due to the airway improve-ments they facilitate.40-43 Biofeedback and muscle exercises appear to be as effective.44,45

traditional stabilization splint designs are routinely used in restorative dental practic-es. Despite their reparative advantages, they do not appear to be helpful in cases of sleep-disordered breathing. in fact, many patients with airway difficulties may experience an exacerbation of their condition when using a splint.46,47 Future studies are needed, but this may explain why many patients experience unsuccessful treatment or increased bruxing with their use, as well as why many remove the splint during the night.

ConclusionA lack of knowledge, or the inaccurate inter-pretation of available data, can create epis-temic uncertainty, a state of understanding that invites new approaches and addition-al research. the objective of this article was to explore sleep-disordered breathing as an alternative explanation for M-tMD, which had not been completely understood and ad-dressed through current models in dentistry.

Data indicate that there is considerable overlap between patients with M-tMD and patients with UArs in terms of both demo-graphics and signs and symptoms. Further research in the area of sleep prosthodontics represents an opportunity for innovative thinking. if dentistry begins to recognize that M-tMD could be a biologic problem rath-er than, or in addition to, a mechanical one, treatments could be designed to equilibrate to a systemic balance instead of an occlusal one.

References1. rouse Js. A new vision for dentistry. Inside Dentistry. 2013;9(7):60-78.2. Manfredini D, Guarda-nardini L, Winocur e, et al. research diagnostic criteria for temporomandibular disorders: a systematic review of axis i epidemiologic findings. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2011;112(4):453-462.3. Dworkin sF, Leresche L. research diagnostic criteria for temporomandibular disorders: review, criteria, examinations and specifications, critique. J Craniomandib Disord. 1992;6(4):301-355.4. Janal Mn, raphael KG, nayak s, Klausner J. Prevalence of myofascial temporomandibular disorder in Us community women. J Oral Rehabil.


“Sleep fragmentation may be culpable in cases of both allodynia and hyperalgesia.”


2008;35(11):801-809.5. Cairns Be. Pathophysiology of tMD pain—basic mechanisms and their implications for pharmaco-therapy. J Oral Rehabil. 2010;37(6):391-410.6. Michelotti A, Cioffi i, Festa P, et al. Oral parafunc-tions as risk factors for diagnostic tMD subgroups. J Oral Rehabil. 2010;37(3):157-162.7. Machado LP, nery Cde G, Leles Cr, et al. the preva-lence of clinical diagnostic groups in patients with tem-poromandibular disorders. Cranio. 2009;27(3):194-199.8. deLeeuw r, ed. Orofacial Pain: Guidelines for Assessment, Diagnosis, and Management. 4th ed. Chicago, iL: Quintessence Publishing Co; 2008:129-204.9. van selms MK, Lobbezoo F, naeije M. time courses of myofascial temporomandibular disorder complaints during a 12-month follow-up period. J Orofac Pain. 2009;23(4):345-352.10. Balasubramaniam r, Laudenbach JM, stoopler et. Fibromyalgia: an update for oral health care pro-viders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2007;104(5):589-602.11. reider C. the prevalence and magnitude of mandibular displacement in a survey population. J Prosthet Dent. 1978;39(3):324-329.12. List t, Axelsson s. Management of tMD: evidence from systematic reviews and meta-analyses. J Oral Rehabil. 2010;37(6):430-451.13. Leite rA, rodrigues JF, sakima Mt, sakima t. relationship between temporomandibular disor-ders and orthodontic treatment: a literature review. Dental Press J Orthod. 2013;18(1):150-157.14. raphael KG, sirois DA, Janal Mn, et al. sleep bruxism and myofascial temporomandibular disor-ders: a laboratory-based polysomnographic inves-tigation. J Am Dent Assoc. 2012;143(11):1223-1231.15. Guilleminault C, stoohs r, Clerk A, et al. A cause of excessive daytime sleepiness. the upper airway resistance syndrome. Chest. 1993;104(3):781-787. 16. Bao G, Guilleminault C. Upper airway resistance syndrome—one decade later. Curr Opin Pulm Med. 2004;10(6):461-467.17. Chen W, Kushida CA. nasal obstruction in sleep-disordered breathing. Otolaryngol Clin North Am. 2003;36(3):437-460.18. Gold Ar, Dipalo F, Gold Ms, Broderick J. inspiratory airflow dynamics during sleep in wom-en with fibromyalgia. Sleep. 2004;27(3):459-466.19. Woodson Bt. expiratory pharyngeal airway ob-struction during sleep: a multiple element model. Laryngoscope. 2003;113(9):1450-1459.

20. Petrof BJ, Hendricks JC, Pack Ai. Does upper air-way muscle injury trigger a vicious cycle in obstructive sleep apnea? A hypothesis. Sleep. 1996;19(6):465-471.21. Walter LM, Foster AM, Patterson rr, et al. Cardiovascular variability during periodic leg move-ments in sleep in children. Sleep. 2009;32(8):1093-1099.22. Zhang J, Ma rC, Kong AP, et al. relationship of sleep quantity and quality with 24-hour urinary cate-cholamines and salivary awakening cortisol in healthy middle-aged adults. Sleep. 2011;34(2):225-233.23. Gozal D, Hakim F, Kheirandish- Gozal L. Chemoreceptors, baroreceptors, and autonomic deregulation in children with obstructive sleep ap-nea. Respir Physiol Neurobiol. 2013;185(1):177-185.24. exar en, Collop nA. the upper airway resis-tance syndrome. Chest. 1999;115(4):1127-1139.25. Guilleminault C, Kirisoglu C, da rosa AC, et al. sleepwalking, a disorder of nreM sleep instability. Sleep Med. 2006;7(2):163-170.26. Gold Ar, Dipalo F, Gold Ms, O’Hearn D. the symptoms and signs of upper airway resistance syn-drome: a link to the functional somatic syndromes. Chest. 2003;123(1):87-95.27. Popovic, rM, White DP. Upper airway muscle activity in normal women: influence of hormonal status. J Appl Physiol. 1998;84(3):1055-1062.28. Hachul H, Andersen ML, Bittencourt L, et al. A population-based survey on the influence of the menstrual cycle and the use of hormonal contracep-tives on sleep patterns in são Paulo, Brazil. Int J Gynaecol Obstet. 2013;120(2):137-140. 29. tantrakul V, Park Cs, Guilleminault C. sleep-disordered breathing in premenopausal women: dif-ferences between younger (less than 30 years old) and older women. Sleep Med. 2012;13(6):656-662. 30. Jonczak L, Pływaczewski r, sliwiński P, et al. evolution of upper airway resistance syndrome. J Sleep Res. 2009;18(3):337-341.31. Krakow B, romero e, Ulibarri VA, Kikta s. Prospective assessment of nocturnal awakenings in a case series of treatment-seeking chronic insomnia patients: a pilot study of subjective and objective causes. Sleep. 2012;35(12):1685-1692.32. tantrakul V, Guilleminault C. Chronic sleep com-plaints in premenopausal women and their association with sleep-disordered breathing. Lung. 2009;187(2):82-92.33. Jørum e, Ørstavik K, schmidt r, et al. Catecholamine-induced excitation of nociceptors in sympathetically maintained pain. Pain. 2007;127(3):296-301. 3 4 . s m i t h M t, e d w a r d s r r , M c C a n n U D,

Haythornthwaite JA. the effects of sleep depriva-tion on pain inhibition and spontaneous pain in women. Sleep. 2007;30(4):494-505.35. roehrs t, Hyde M, Blaisdell B, et al. sleep loss and reM sleep loss are hyperalgesic. Sleep. 2006;29(2):145-151.36. Koo BB, Patel sr, strohl K, Hoffstein V. rapid eye movement-related sleep-disordered breathing: influ-ence of age and gender. Chest. 2008;134(6):1156-1161.37. schwartz DJ, Moxley P, Barker A, Longman M. On a characteristic of cortical arousals in individuals with obstructive sleep apnea. J Clin Sleep Med. 2005;1(1):35-40.38. Chandra s, sica AL, Wang J, et al. respiratory effort-related arousals contribute to sympathetic modulation of heart rate variability [published online ahead of print February 18, 2013]. Sleep Breath. 39. eze-nliam CM, Quartana PJ, Quain AM, smith Mt. nocturnal heart rate variability is lower in temporo-mandibular disorder patients than in healthy, pain-free individuals. J Orofac Pain. 2011;25(3):232-239.40. Goksan B, Gunduz A, Karadeniz D, et al. Morning headache in sleep apnoea: clinical and polysomnograph-ic evaluation and response to nasal continuous positive airway pressure. Cephalalgia. 2009;29(6):635-641. 41. Giannasi LC, Almeida Fr, Magini M, et al. systematic assessment of the impact of oral ap-pliance therapy on the temporomandibular joint during treatment of obstructive sleep apnea: long-term evaluation. Sleep Breath. 2009;13(4):375-381.42. Cooper BC, Kleinberg i. establishment of a tem-poromandibular physiological state with neuromus-cular orthosis treatment affects reduction of tMD symptoms in 313 patients. Cranio. 2008;26(2):104-117.43. Brown Dt, Gaudet eL Jr. temporomandibular dis-order treatment outcomes: second report of a large-scale prospective clinical study. Cranio. 2002;20(4):244-253.44. niemelä K, Korpela M, raustia A, et al. efficacy of stabilisation splint treatment on temporomandibular disorders. J Oral Rehabil. 2012;39(11):799-804.45. shedden Mora MC, Weber D, neff A, rief W. Biofeedback-based cognitive-behavioral treatment compared with occlusal splint for temporomandibu-lar disorder: a randomized controlled trial [published online ahead of print February 26, 2013]. Clin J Pain.46. nikolopoulou M, naeije M, Aarab G, et al. the effect of raising the bite without mandibular protrusion on ob-structive sleep apnoea. J Oral Rehabil. 2011;38(9):643-647.47. Gagnon y, Mayer P, Morisson F, et al. Aggravation of respiratory disturbances by the use of an oc-clusal splint in apneic patients: a pilot study. Int J Prosthodont. 2004;17(4):447-453.


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Sleep Prosthodontics: Understanding Myofascial Pain Jeffrey S. Rouse, DDS

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Sleepprosthodonticsisthestudyof:

a. oralappliancetherapyforthetreatmentofapnea. b. sleepdisordersrelatedtomalocclusion. C. bruxismanditsimpactonsystemichealth. D. theairwayanditsimpactonthestomatognathicsystem.

Themyofascialpainsubtypeoftemporomandibular disorder(M-TMD)compriseswhatpercentageofthe generalpopulation?

a. 10.5% b. 30% C. 45.5% D. 75%

M-TMDischaracterizedby:

a. reducedresponseofthecentralnervoussystem. b. dull,achingpainthatworsenswithpalpationandfunction. C. higherprevalenceinmen. D. increasedprevalenceinolderage.

ThepopulationseekingtreatmentforM-TMDcomprises whatratioofwomentomen?

a. 3.8:1 b. 5:1 C. 7.2:1 D. 10:1

Whichofthefollowingmalocclusionshavebeencorrelated withanincreasedriskofTMD?

a. Unilateralcrossbite b. Increasedoverjet C. Anterioropenbite. D. Alloftheabove.

Obstructivesleepapneaischaracterizedbyanupper airwayobstruction:

a. lastinglongerthan5secondswithnochangeinoxygenation. b. lastinglongerthan10secondswith10%oxygendesaturation. C. lastinglongerthan10secondswith4%oxygendesaturation. D. lastinglongerthan20secondswithnochangeinoxygenation.

Inpatientswithupperairwayresistancesyndrome(UARS):

a. obesityisarecognizedcause. b. airwayconstrictionisrespondedtomorequickly, preventingobstruction. C. thereislesssensitivitytonegativeoropharyngealpressure. D. sensoryreceptorsintheairwayaredulled.

Womenaremorehyperresponsivetoairwaychallengesbecause:

a. ofthehormoneprogesterone. b. ofthehormonetestosterone. C. theytendtohavehigh-stresslifestyles. D. oftheuseoforalcontraceptives.

Aswomenage,thenumberofsleepdisturbancesduring rapideyemovementsleep:

a. remainsthesame. b. decreasesby26.7%perdecade. C. increasesby26.7%perdecade. D. increasesby40.8%.

Whichofthefollowingtreatmentshavebeenshowntobe effectiveinthetreatmentofM-TMD?

a. Continuouspositiveairwaypressure b. Neuromuscularonlays C. Anteriorrepositioningsplints D. Alloftheabove


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Sleep Apnea - AAO · PDF file1.Current Sleep Apnea Protocols Manage Rather than Prevent AAP guidelines omit orthodontics Focus should be the 4 year old; ... reM sleep. stages 1-2 are