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INTRODUCTIONOptimal is very different than acceptable,especially if you are the patient. This casestudy will highlight the need for a structuralassessment of the 4 points of the airwayprior to treatment utilizing CBCT (i-CAT). Inaddition, this case report will demonstratehow successful resolution of severe apneawith an oral appliance on a patient forwhom continuous positive airway pressure(CPAP) had little effect on excessive fatigueuntil the nasal airway was addressed.

BackgroundSince 2004, the American Academy of SleepMedicine has formally accepted the use oforal appliances to treat obstructive sleepapnea (OSA). Consequently, there has beena dramatic increase in dentists deliveringthis type of care. This is evidenced by thegrowth of academies that provide boardcertification in dental sleep medicine suchas the American Board of Dental Sleep Med -icine and the American Board of Cranio -facial Dental Sleep Medicine. It is impor-tant that dentists treating OSA have astrong background in temporomandibulardisorders (TMDs) as OSA symptoms pre-cede the first-onset TMD as found in theNIH-funded “Orofacial Pain: ProspectiveEval uation and Risk Assessment” study,also known as OPPERA.1

This is great news for patients as moredentists are screening for OSA, and mostpeople who have OSA have not been diag-nosed (more than 80%). Extrapolated datafrom the Wisconsin Sleep Cohort Studyestimated that the overall prevalence ofOSA was 9% for women and 24% for men.2The adult prevalence of OSA in general den-tistry practices is 33% for men and 7% forwomen.3 So 40% of your adult patientshave a diagnosable OSA problem, and thatdoes not include the patients who have less-er forms such as upper airway resistancesyndrome (UARS), snoring, or are children(who have an equal or greater presentationof sleep breathing disorders). The fact thatOSA and periodontitis are significantlylinked is vital to our treatment plans forthese conditions.4-6 The fact that night-guards make OSA worse makes it impera-tive to find the origin of nocturnal brux-

ism.7-9 The Frost & Sullivan firm reportsthat the US markets for oral appliances(OAs) for OSA, both custom and non-cus-tom, will more than double by 2020.10 Themost dynamic sector, custom OAs, isexpected to see a fivefold revenue increasein that period.

Lesser forms of airway obstruction suchas UARS and mild and moderate OSAsdemonstrate Epworth scores on average of

13 out of 24 in a study of military person-nel.11 The Epworth Sleepiness Scale (ESS) isan industry standard for evaluation ofexcessive daytime sleepiness and an indica-tor of the presence of a sleep breathing dis-order. Normal controls have an ESS score of5.9 ± 2.2, demonstrating baseline. Patientswith primary snoring had ESS scoresgreater than 6 ± 3.0. Sleep disorders such asperiodic leg movement disorder, OSA syn-

Steven R.Olmos, DDS

ChaseBennett, DDS

Optimal Dental Therapy for Obstructive Sleep Apnea

CBCT 3-D soft-tissue rendering of patient. CBCT sagittal view of hard tissues and airway.

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Figure 1. Tongue posture above the occlusal plane. Figure 2. Mallampati 4, all indicating a minimal oralvolume.

Figure 3. Disc movement without perforations and consistent with inflammation. The vertical dotted line sepa-rates soft-tissue vibrations (zero to 300 Hz) from hard-tissue vibrations (> 300 Hz).

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drome, narcolepsy, and idiopathic hypersomniaall had ESS values greater than 9.12

CASE REPORTA 57-year-old white female was referred to ouroffice (on August 15, 2012) by her family physi-cian. She presented with a chief complaint offatigue, significant daytime drowsiness, an unre-freshed feeling in the morning, frequent awaken-ings and an inability to tolerate CPAP.  Her neckcircumference was 14.5 inches, height 5’ 8,”weight 200 lb, BMI 39.06, B.P. 116/117, pulse 70,respirations 16, and temperature 97.7. Her medicalhistory was lengthy: right hip replacement, rightbrain surgery toremove tissue and hip-pocampus, “oral sur-gery to correct over-and underbite,” “sev-eral changes in mouthwith appearance re -sulting in grindingrear teeth,” and L-5and S-1 disc repair. Shehad a medication regi-men for the treat-ment of hyperten-sion, epilepsy, gas-troesophageal reflex(GERD), migraines,osteo arthritis, thyroidproblems, anxiety, de -pression, and difficul-ty concentrating. HerESS score was 14.

The patient’s med-ications, upon presen-tation, were as follows:Simcor (statin drug forcholesterol) 500 mg/20mg once daily, Nuvigil(stimulant for exces-sive daytime sleepi-ness) 250 mg oncedaily, Syn throid (hypo -thyroid function) 137mcg once daily, Lev -etiradcetam (Kep pra)(anti-convulsion drugused to treat seizures)

1,500 mg twice daily, Trileptal (anti-convulsiondrug used to treat seizures) 450 mg twice daily,Viibryd (SSRI antidepressant) 40 mg once daily,Losartan (anti-hypertensive, angiotensin IIreceptor antagonist) 50 mg once daily, Nexium(proton pump inhibitor that decreases theamount of acid produced in the stomach)(GERD) 40 mg daily, Intuniv (multivitamin) 4mg daily, and aspirin 81 mg once daily.

Clinically, she had tongue posture above theocclusal plane, hyperkeratosis (B), retraction ofthe tongue into the airway, and Mallampati 4,all indicating a minimal oral volume (Figures 1and 2). This meant that a minimally invasive

oral appliance should be used to treat the OSA.She had no headaches or facial pain complaints.Muscle palpation was negligible and she hadnormal ranges of mandibular movement. Themaximum opening was 45 mm (Fig ures 1 and 2)with lateral movements of 12 and 10 mm leftand right, respectively. Normal ranges ofmandibular movement were 42 to 52 mm maxi-mum opening and 10 to 14 mm lateral move-ments.13 Dynamic evaluation of the jaw joints infunction was performed using Joint VibrationAnalysis (JVA [Bio Research]) and found to bewithin normal limits for soft tissue and withoutperforations to the discs bilaterally (Figure 3).

Figure 4. CBCT scan provided 3-D information on thecondyles.

Figure 5. 3-D imaging of the joints reveals osteogenicremodeling of the condyles and fossa indicating long-term stress to these joints.

Figure 6. Scan showing patient’s right and left gonialangle hypertrophy.

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The 3-D imaging of the joints re -vealed osteogenic remodeling of thecondyles and fossa indicating long-term stress to these joints (Fig ures 4and 5).

Hypertrophied gonial angles arethe result of frequent and continuedcontractions of the superficial mas-seter muscles bilaterally, which areassociated with increased hypercap-nea (increases CO2 in the blood).14,15

Hypercapnea is the stimulus tobreathe in OSA. The patient’s gonialangle hypertrophy was clearly seen onthe scan (Figure 6).

Occlusal analysis was Class IIwith attrition from bruxism. Stan -dard photographic records were alsocaptured (Figure 7).

The patient was diagnosed by aboard-certified sleep physician utiliz-ing polysomnography (PSG) withsevere OSA. Her apnea/hypopneaindex (AHI) was 79.9 (an AHI > 30 isconsidered severe). The results of herPSG were as follows: arousal index:21.9 (10.3 from AHI/respiratory distur-bance index [RDI], 8.5 spontaneous,3.1 snore). The patient slept supine allnight: N1 sleep: 12.3% of total sleeptime (TST); N2 sleep: 87.7% of TST; N3sleep: zero; and REM sleep: zero.

Our patient received no stage 3 orREM sleep. This meant that she hadlimited ability to produce growthhormone and had terrible memoryproblems. Growth hormone is pro-duced in stage 3 delta wave deep sleepand is essential for healing. Cognitivememory is an important function ofREM sleep and without it, memorywould be significantly affected.

Lowest O2 was 77%. She spent 37minutes or 27% of TST below 90%blood oxygen, and her CPAP titrationwas 8 cm H2O to reduce events to zero.

She tried CPAP nasal cannula for8 months; however, pressure, leaks,and the noise kept her awake. So,even though the CPAP was effective,it was impossible for her to wear. Thispoints out the most common flaw inthe evaluation and treatment of OSA.Patients are evaluated for their sleepbreathing pathology via a sleepstudy; however, rarely are patientsevaluated for the origin of theobstructions. As a result, very oftenthey have nasal obstructions and aregiven a CPAP without a physical orimaging of the airway, which leads toproblems with mask leakage.

The first step to an effective treat-ment plan for OSA must include a full-head CBCT scan to determine the 4points of obstruction. (For a detailedexplanation of the 4 points ofobstruction [Figure 8] and how toevaluate using CBCT (i-CAT), see theMarch/April 2015 edition of Ortho -dontic Practice US.16) Examina tion ofthe patient’s 4 points of obstruc-tion—nasal valve, naso-pharyngeal,velo pharynx and oropharynx—demonstrated that, in addition to herpositional apnea (base of tongue andvelopharynx), she had nasal obstruc-tion (see CBCT image in Figure 9).

Nasal airway resistance and BMI arethe most limiting factors in treatingOSA patients with oral appliance ther-apy (OAT).17 Nasal airway obstructionis directly linked to daytime fatigue.18

The i-CAT imaging softwareallows for volumetric evaluation ofthe oropharyngeal airway. This pa -tient had a severely compromised air-way with a minimum of 61.3 mm2.The color scale demonstrates that thebottom end of evaluation is 100 mm2

(Figures 9 to 11). Our treatment planincluded OAT (EMA II), ENT consult,and a follow-up sleep study. The FDA-approved orthotic was delivered onSeptember 5, 2012 (Figure 12).

The Sibilant Phoneme bite regis-tration was utilized as the startingposition for appliance fabricationbecause it is physiologic as opposedto a construction technique. It is theonly bite registration technique thathas been proven and published in apeer-reviewed journal to open the air-way, but most importantly, reducecollapse.19 Patients with OSA don’tstop breathing during wakefulness;they only stop breathing when theyare asleep. So the volume of theoropharyngeal airway is less impor-tant than the collapse. This meansthat titration is rarely necessaryusing the phonetic bite registrationas a starting point. This particularpatient is a perfect example of this, asher appliance never needed to betitrated. The oropharyngeal volumes(Figure 13) at baseline and with thebite registration show little improve-ment in wakeful breathing; however,these small changes resulted in reso-lution of her severe apnea.

Within 2 weeks of delivery of theoral appliance, her fatigue and daytimedrowsiness were reduced by 30%. Her

symptom of feeling unrefreshed uponawakening had reduced 50%.

A follow-up home sleep test wasperformed on October 20, 2012 (Brae -bon MediByte), and had these results:AHI: 6.2, RDI: 9.8, O2 below 90%: 0.5minutes or 0.1%, min O2: 87%, andsupine sleep: 100%. An AHI of 5 orless is considered normal. Success uti-lizing OAT on patients with severeapnea is defined as reducing the AHIby 50%, ESS scores less than 8, andblood oxygenation greater than90%.20 Her ESS score was 10 at thispoint, demonstrating that daytimefatigue was a significant problem.

She was reluctant to see the ENTspecialist to whom she was referredfor her nasal obstruction. She finallyrelented after we had demonstratedeffective relief of fatigue utilizingProvent nasal valves (no longer onmarket; replaced by Theravent). Shehad nasal surgery on December 20,2012, and after the 6-week healingprocess, her fatigue was resolved,multiple awakenings were 90% im -proved, and her daytime drowsinesswas resolved. 

She was seen for re-evaluation (onApril 13, 2015) with the followingresults: Simcor, Nuvigil, Keppra, andNexium had all been discontinued in2014. That meant she no longer need-ed medication for elevated choles-terol, excessive daytime sleepiness,seizure activity, or GERD. Her newESS score was a 5. Soft-tissue hyper-trophy from diet and allergies canblock the nasal airway, so we recom-mended a xylitol nasal spray (Xlear).Xylitol is a sugar that is antimicrobialand anti-inflammatory. It is used forpatients with dry mouth who are atrisk for caries and periodontal disease.

A comparison of i-CAT images of

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Figure 9. The 3-D scan showing turbinatesand septum issues.

Figure 8. Diagram of the 4 points of obstruction. (Illustration by Brett Steed.)Figure 7. Occlusal analysis: Class II with attrition from bruxism.

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the nasal passages demonstrates littlesoft-tissue hypertrophy and astraighter septum that resulted in adramatic increase in nasal airflow(Figure 14). A very interesting findingwas that the oropharyngeal airway wasgreater after the nasal surgery. The min-imum increased from 61.3 mm2 to 213mm2 (Figure 15).

CLOSING COMMENTSThis case report serves to highlightthat too much emphasis is placed ondeveloping big airways, without theunderstanding that prevention of col-lapse of the airway is most importantas well as nasal airflow.21 As demon-strated in this case, a combined orhybrid therapy of OAT and nasal sur-gery, directed by a dentist, was the

optimal treatment. The dentist isclearly in position to be the centraltriage professional for treatmentoptions with the CBCT as the vitaltool in this process. Without a CBCTscan, patients can suffer from multi-ple ineffective treatment plans.�

References1. Sanders AE, Essick GK, Fillingim R, et al. Sleep

apnea symptoms and risk of temporomandibulardisorder: OPPERA cohort. J Dent Res.2013;92(suppl 7):70S-77S.

2. Young T. Rationale, design, and findings from theWisconsin Sleep Cohort Study: toward under-standing the societal burden of sleep-disorderedbreathing. In: Bixler EO, ed. Sleep MedicineClinics: Epidemiology of Sleep Disorders: ClinicalImplications. Philadelphia, PA: Saunders;2009:37-46.

3. Levendowski DJ, Morgan T, Montague J, et al.Prevalence of probable obstructive sleep apnearisk and severity in a population of dentalpatients. Sleep Breath. 2008;12:303-309.

4. Ahmad NE, Sanders AE, Sheats R, et al.Obstructive sleep apnea in association with

perio dontitis: a case-control study. J Dent Hyg.2013;87:188-199.

5. Nizam N, Basoglu OK, Tasbakan MS, et al. Salivarycytokines and the association between obstructivesleep apnea syndrome and perio dontal disease. JPeriodontol. 2014;85:e251-e258.

6. Gunaratnam K, Taylor B, Curtis B, et al. Obstructivesleep apnea and periodontitis: a novel associa-tion? Sleep Breath. 2009;13:233-239.

7. Nikolopoulou M, Ahlberg J, Visscher CM, et al.Effects of occlusal stabilization splints onobstructive sleep apnea: a randomized con-trolled trial. J Orofac Pain. 2013;27:199-205.

8. Gagnon Y, Mayer P, Morisson F, et al. Aggravationof respiratory disturbances by the use of anocclusal splint in apneic patients: a pilot study.Int J Prosthodont. 2004;17:447-453.

9. Nikolopoulou M, Naeije M, Aarab G, et al. Theeffect of raising the bite without mandibular pro-trusion on obstructive sleep apnoea. J OralRehabil. 2011;38:643-647.

10. Industry New: US Oral Appliance Market toDouble by 2020. Sleep Review. Published onMarch 18, 2015. sleepreviewmag.com/arti-cle/us-oral-appliance-market-double-2020.Accessed on June 22, 2015.

11.Powers CR, Frey WC. Maintenance of wakeful-ness test in military personnel with upper airwayresistance syndrome and mild to moderate

obstructive sleep apnea. Sleep Breath.2009;13:253-258.

12.Johns MW. A new method for measuring daytimesleepiness: the Epworth sleepiness scale.Sleep. 1991;14:540-545.

13.Grummons D. Temporomandibular disorders:the problem and orthodontic perspectives. In:Grummons D. Orthodontics for the TMJ/TMDPatient. Scottsdale, AZ: Wright and Co.Publishers; 1994:19-20, chapter 1.

14.Hollowell DE, Suratt PM. Activation of massetermuscles with inspiratory resistance loading. JAppl Physiol (1985). 1989;67:270-275.

15.Hollowell DE, Suratt PM. Mandible position andactivation of submental and masseter musclesduring sleep. J Appl Physiol (1985).1991;71:2267-2273.

16.Olmos S. CBCT in the evaluation of airway—min-imizing orthodontic relapse. Orthodontic PracticeUS. 2015;6:34-37.

17.Zeng B, Ng AT, Qian J, et al. Influence of nasalresistance on oral appliance treatment outcomein obstructive sleep apnea. Sleep. 2008;31:543-547.

18.Hussain SF, Cloonan YK, Rahbar MH, et al.Association of self-reported nasal blockage withsleep-disordered breathing and excessive day-time sleepiness in Pakistani employed adults.Sleep Breath. 2010;14:345-351.

19.Singh GD, Olmos S. Use of a sibilant phonemeregistration protocol to prevent upper airway col-lapse in patients with TMD. Sleep Breath.2007;11:209-216.

20.Ferguson KA, Cartwright R, Rogers R, et al. Oralappliances for snoring and obstructive sleepapnea: a review. Sleep. 2006;29:244-262.

21.Ng AT, Gotsopoulos H, Qian J, et al. Effect of oralappliance therapy on upper airway collapsibilityin obstructive sleep apnea. Am J Respir Crit CareMed. 2003;168:238-241.

Dr. Olmos is an internationally recognizedlecturer and researcher, and the founder ofthe TMJ & Sleep Therapy Centres Inter -national. He graduated from the University ofSouthern California School of Dentistry, andhas dedicated the past 26 years to the fieldsof craniofacial pain, TMD, and sleep-relatedbreathing disorders. He has extensive post-graduate education and board certificationsin both craniofacial pain and dental sleepmedicine, and he is an adjunct professor atthe University of Tennessee College ofDentistry. Dr. Olmos is currently directingresearch in these fields through data collec-tion at 32 TMJ & Sleep Ther apy Cen -tres spanning 6 countries. This effort isfocused to establish protocols and bridgethe gap between dentistry and medicine foroptimal treatment outcomes. He can bereached at (877) 865-4325 or via the web-site tmjtherapycentre.com.

Disclosure: Dr. Olmos discloses that he hasbeen sponsored for courses by ImagingSciences, BioResearch, and Braebon.

Dr. Bennett is a second-generation dentistfrom Tulsa, Okla, where he attended Okla -homa State University. Dr. Bennett graduatedfrom the College of Dentistry with very spe-cial distinction while completing an extern-ship at the renowned Tufts University DentalSchool’s Craniofacial Pain and Dental SleepCenter under the direction of Dr. NoshirMehta in Boston. In 2014, Dr. Bennettbecame the youngest dentist ever to achieveDiplomate status in the American Board ofCraniofacial Pain for the disciplines ofCraniofacial Pain and Sleep DisorderedBreathing. Currently Dr. Bennett is theDirector of the TMJ and Sleep Therapy Centreof San Diego and the Craniofacial PainCenter of Colorado. Dr. Bennett lectureslocally and nationally in the fields ofCraniofacial Pain and Dental Sleep Medicineand is involved in multiple research projects.He can be reached at (619) 466-2774 or viaemail at drbennett@tmjtherapycentre.com, oronline at tmjtherapycentre.com/sandiego.

Disclosure: Dr. Bennett reports no disclosures.

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Figure 14. Substantial increase in airflow.

Figure 15. Increase in size of airway afternasal therapy.

Figure 12. Patient with seated appliance.

Figures 10 and 11. Airway calculations in various views.

Figure 13. Baseline airway dimensions (left) and with bite registration (right).