Treatment of obstructive sleep apneawith the Karwetzky oral appliance

Rose E, Staats R, Schulte-Monting J, Jonas IE. Treatment of obstructivesleep apnea with the Karwetzky oral appliance. Eur J Oral Sci 2002; 110: 99–105# Eur J Oral Sci, 2002

The aims of this retrospective study were to assess the effect of a Karwetzkymandibular protrusion appliance for treating patients with mild, moderate, andsevere obstructive sleep apnea. Eighty-one of 116 patients (69.8%) suffering fromobstructive sleep apnea were treated with an activator model according toKarwetzky. After 4 months (SD 4.0 months) treatment outcome was controlled bypolysomnography. Therapeutic outcome depended on the severity of obstructivesleep apnea. The median apnea-hypopnea index decreased from 10.6 events/h(range 2.0–14.9) to 5.8 events/h (range 0.2–17.3, P<0.01) in the mild group, from21.7 events/h (range 17.3–28.4) to 7.7 events/h (range 1.0–30.1, P<0.001) in themoderate group, and from 42.1 events/h (range 33.2–64.9) to 18.1 events/h (range2.4–48.8, P<0.001) in the severe group. Sleep variables did not show consistentimprovement except for a trend towards more REM sleep and slow-wave sleep.The numbers of retentive teeth did not statistically influence treatment efficacy.Comparing the pre- and post-treatment polysomnographic variables, it was foundthat the respiratory events rather than sleep stages were significantly reduced bythe Karwetzky appliance investigated.

Edmund Rose1, Richard Staats2,Jurgen Schulte-Monting3,Irmtrud E. Jonas1

1Department of Orthodontics, 2Department ofPulmonary Diseases, 3Department ofBiometrics and Medical Informatics, Universityof Freiburg, Freiburg i. Br., Germany

Edmund Rose, Department of Orthodontics,University of Freiburg, Hugstetter Strasse 55,79106 Freiburg i. Br., Germany

Telefax: +49–761–2704809E-mail: rose@zmk2.ukl.uni-freiburg.de

Key words: obstructive sleep apneasyndrome; oral appliance; activator; treatment

Accepted for publication December 2001

Of all the intrinsic dyssomnias, obstructive sleep apnea(OSA) is the most common of the primary sleepdisorders. Its degrees of severity cover a broad spec-trum: loud obstructive snoring, upper airway resistancesyndrome, and obstructive sleep apnea syndrome.

Nasal continuous positive airway pressure (nCPAP) isregarded as the gold standard in the treatment of OSA.It is effective, easy to administer, and can be tailored tothe degree of severity by changing the nCPAP pres-sure. Side-effects, often leading to the discontinuationof therapy, are problems with nasal patency, intoleranceof high pressures, and mask leaks that might lead tokeratoconjunctivitis (1). In addition, the mask can causeskin lesions, especially around the glabella, and patientsmay be claustrophobic, and in particular youngerpatients suffering from mild OSA may consider nCPAPas ‘overkill’ (2). Alternative options to nCPAP, especiallyfor milder forms, are improvement in sleep hygiene,weight reduction, avoiding alcohol in the evening, andpositional training. Medications have not been found toplay a consistent role in the treatment of OSA. Surgicaloptions are tonsillectomy, adenoidectomy, uvulopalato-pharyngoplasty, somnoplasty, and, limited to selectpatients, maxillomandibular advancement (3). Oralappliances are being used clinically; practical guidelinesregarding the indications, efficacy, and limitations of thistherapeutic option were developed in 1995 (4–7).

Numerous types of oral appliances have beendescribed, each of which differs in design and efficacy(8). In general, three basic designs exist: tongue retainers,

soft palate lifters, and mandibular advancement appli-ances (MAA) (9–12). The clinical application of tongueretainers and soft palate lifters is narrow, however MAAhave enjoyed wide acceptance. They act by advancing themandible and opening the bite vertically; this increasesthe oropharyngeal volume and provides more space forthe tongue by stretching the soft tissue (13, 14). Thevelopharnygeal and suprahyoid muscles are therebystabilized, and there is less chance of a collapse of theoropharyngeal structures (15).

In terms of oral appliance retention, one can dis-tinguish between two types: tooth-borne appliances,requiring firm retention on the teeth, fixing the mandiblein a permanent forward and downward position, asopposed to appliances which are passively tooth- andtissue-borne and fit loosely. Whereas there have beenpolysomnographic (PSG) studies done with tooth-borneappliances, the therapeutic efficacy of passive tooth- andtissue-borne devices has not been reported yet. Westudied the initial nocturnal respiratory and somno-graphic efficacy of a Karwetzky activator (16) as a meansof treatment for mild, moderate, and severe OSA.

Material and methods

Subjects

A total of 116 consecutive patients using a Karwetzkyactivator were studied between July 1995 and October 1999at Freiburg University, Germany. The patients’ (15 females

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Copyright# Eur J Oral Sci 2002

European Journal ofOral Sciences

ISSN 0909-8836

(13.7%) and 101 males (86.3%)) mean age was 55 yr (SD 9.9;range 24–75) and the mean body mass index was27.8 kg mx2 (SD 3.6; range 22.7–38.7). The patients,diagnosed with mild-to-severe OSA, were recruited fromthe Sleep Center, Department of Pulmonary Diseases atFreiburg University Hospital. Patients with moderate tosevere OSA were fitted with an oral appliance after refusingto use nCPAP, which had been provided as a first-linestandard treatment, on a life-long basis and they weretherefore offered oral appliance treatment instead. Patientswith mild OSA were offered oral appliance treatmentprimarily.

They all had to agree to regular use of the oral appliancesand to medical and dental follow-up examinations accordingto the protocol. Patients suffering from EDS and severeOSA were not allowed to drive until the first controlpolysomnography with the appliance had been carried out,and patients had reported a relief in symptoms. Exclusioncriteria included Cheyne-Stokes respiration, a body massindex of over 40 kg mx2, acute peridontitis, arthralgias,temporomandibular joint dysfunction, or psychosomaticcomplaints.

The patients had undergone a thorough dental examina-tion by a dentist before the appliance was inserted. Anyacute dental or perioral infections were treated beforetherapy began. The number of teeth in the upper and lowerjaw was recorded. Possible dental changes which mighthave been caused by the activator, and the exact fit of theappliance, were examined prior to the second PSG by thesame dentist.

The patients were asked to present for follow-up PSGin order to assess the efficacy of the device; in 81 cases(69.8%), a follow-up sleep study was carried out withina mean period of 4 months (SD 4.0; range 2.5–8.2). Thepatients belonged to the following severity groups: 17patients were classified as having severe OSA, 31/51 patientsas having moderate OSA, and 33/48 patients as having mildOSA. In 12 patients, therapeutic efficacy was not assessedas optimal according to the results of a control polysomno-graphy and the comfort perceived by the patients, in whichcase the oral appliances were adjusted by 2–5 mm to obtaina larger degree of protrusion, and patients underwent repeatPSG. In those cases, the last PSG was analyzed statistically.Thirty-five patients (30.2%) were not present for follow-upPSG; 30 of those had discontinued therapy, 5 patients werecontent with the device but did not come for follow-up PSG.Reasons for discontinuing therapy were: 13 patients (37%)did not experience subjective improvement, 11 patients(25.7%) could not get used to the foreign body sensation intheir mouths, 5 patients (14.2%) complained of an increasedgag reflex, 2 patients (5.7%) complained of tenderness ofthe temporomandibular joint, and 6 patients (17.4%) gaveno reason.

Subjective assessment

Excessive daytime sleepiness (EDS) was assessed beforeinitiation of treatment in three degrees of severity: ‘notpresent’, ‘present’, and ‘severely present’. At the end of thestudy, the changes in EDS were assessed subjectivelyaccording to these categories: ‘reduced’, ‘unchanged’, and‘not present’.

Polysomnographic sleep recording

Standard 12-channel PSG was carried out: 2 electro-encephalograms (EEG’s), one occipital, one central; two

electro-oculograms (EOG), submental surface electro-myogram, oro-nasal air flow, abdominal and thoracalrespiratory effort, oxymetry, body position, and electro-cardiogram (ECG). The recording devices used were Sleeplab 1000P (Jaeger, Wuerzburg, Germany) and Sidas GS(Heinen and Loewenstein, Bad Ems, Germany). The studieswere scored by physicians specializing in sleep medicineunder blind conditions. Scoring of sleep stages and arousalswas done according to standard criteria (17, 18) using 30-sepochs. Sleep efficiency was total recording time dividedby total sleep time. The analysis of respiratory variables,and the classifying of disease as mild, moderate andsevere were done following the guidelines of the AmericanAcademy of Sleep Medicine Task Forces (19): OSAwas classified as mild in patients with an apnea/hypopneaindex (AHI) of 5–15 events per h, moderate with anAHI of 15–30 events per h, and severe with an AHI above30 events per h.

Treatment response was divided into three groups:optimal therapeutic efficacy was defined when patientshad a resulting AHI of under 5 events per h. Patients notresponding optimally based on those criteria, but whoshowed improvement in the AHI of at least 50%, weredefined as treatment responders. Treatment failures wereconsidered those as showing a decrease in the AHI of under50% of baseline, or a worsening of AHI (20, 21).

Mandibular advancement appliance

We used an appliance by KARWETZKY (16); the typical designof the device is shown in Fig. 1A–C. The appliance consistsof two dental splints, one in the upper and one in lowerjaw, which are connected by two U-claps (Scheu-Dental,Iserlohn, Germany). The U-claps are fixed in the lingual areaof the first molars, permitting lateral and vertical jawmovement during sleep. Compressing both U-claps togetherallows an adjustment of the protrusion of 8 mm. All thedevices were manufactured in the orthodontic laboratoryat the Department of Orthodontics using a hard acrylic(Orthocryl1; Dentaurum, Pforzheim, Germany). Therewere no retentive elements attached to the teeth; themaxillary as well as the mandibular segment contained apassive labial bow to stabilize the incisors, and non-retentiveleading-hocks were inserted in front of the first molars toprovide a loose fit. The protrusion and the opening of thebite were individually adjusted for each patient accordingto a construction bite (22); in the sagittal plane the pro-trusion was about 4–6 mm and in the vertical plane about5–10 mm. The degree of adjustment of the appliance wascontrolled in the vertical plane between the first centralincisors, and in the sagittal plane at the position of the firstmolar, using the patient’s dental models.

Statistical analysis

Patient data were analyzed in the Center of Biometrics andMedical Informatics at the University of Freiburg using thestatistical program SAS 6.12 (Statistic Analysis SystemInstitute, Cary, NC). We used the Wilcoxon signed rank testfor intraindividual changes in determining the appliance’stherapeutic efficacy. A logistic procedure was applied toanalyze the influence of the numbers of teeth, age, genderand body mass index on treatment efficiency. The zero-hypothesis was controlled at a level of significance ofP<0.05 or P<0.01.

100 Rose et al.

Results

The three severity groups did not differ in terms of age,total sleep time, sleep latency and sleep efficiency. Therewas no significant difference in average body mass indexin mild and moderate sleep apnea patients; the bodymass indices were 27.4 kg mx2 (SD 4.2) and 27.6 kg mx2

(SD 2.8), respectively. Patients with severe OSA hada significantly higher body mass index of 29.4 kg mx2

(SD 3.8). There was no significant change in averagebody mass index, total sleep time, sleep latency, sleepefficiency, and medication between the two registrations.

Respiratory variables

The respiratory variables AHI and AI improved in allthree severity groups. Mean oxygen saturation improvedstatistically significantly only in patients with severeOSA (P<0.05). In patients with moderate and mildOSA, there was no difference. However, the events ofoxygen desaturations per hour sleep which are importantfor assessing therapeutic efficacy, as well as the averageoxygen desaturation, were improved significantly byabout 50% in the moderately- to severely-affectedpatients and by about 25% in the mild cases; at thesame time, the minimal oxygen desaturation rose(Tables 1–3).

Out of the 17 patients with severe OSA, 7 patients(41%) were optimally treated, and 5 patients (29.4%) wereclassified as responders. In five cases, there was notherapeutic efficacy established; in fact in one case weobserved a deterioration. Among the moderately severepatients (n=33), 24 patients (72.7%) were treatedoptimally, and in 5 cases (15.2%) an improvement ofmore than 50% was achieved; four patients (12.1%)were treatment failures. In the patients with mild OSA(n=31), 27 patients (87.1%) were treated optimally; therewas a deterioration observed in four patients (12.9%)(Table 4). Body mass index influenced treatment out-come significantly (P>chi square: 0.008); neither age norgender affected treatment outcome.

Sleep variables

The arousal index significant decreased to about 50% ofbaseline. An increase in REM sleep was statisticallysignificant only with patients having moderate to severeOSA (P<0.05), patients with mild OSA showed nochange in the percentage of REM sleep. Significantly,more slow-wave sleep was noted only in patients withmoderate OSA; both in patients with mild and severeOSA, slow-wave sleep did not increase. Sleep efficiencyremained practically unchanged in all three groups(Tables 1–3).

Treatment success

With therapy, EDS was reduced in 40 (58%) of 69patients who had experienced symptoms before treat-ment. Eighteen (26%) of the 69 patients had completeresolution of EDS and 11 (16%) of the 69 patients con-tinued to have EDS; 9 of those patients were designatedas therapeutic failures based on the respiratory data.

Dental situation and side-effects

There were 11.2 (SD 2.7; range 0–14) teeth in the upperjaw and 12.0 (SD 2.4; range 2–14) in the lower jaw. Onaverage, 78 patients (67.2%) had more than 10 teeth inthe upper jaw, whereas this was the case for 89 patients

Fig. 1. (A) Modified activator, lateral view. (B) Modifiedactivator, oblique view. (C) Modified activator, backviewwith the adjustable U-claps. The U-claps allow an anteriordisplacement of about 6–8 mm.

Karwetzky device for OSA treatment 101

(76.7%) in the lower jaw. Statistically, the number ofteeth did not affect treatment efficiency, including AHI,AI and sleep variables. Dental side-effects were found inthree patients. One patient fractured an endodonticallytreated lower canine, one patient lost a periodontallypredamaged lower first molar, and one patient developeda posterior open bite. No one developed an anterior openbite. Only 5 patients complained of oral dryness and4 patients of hypersalivation. Fourteen patients (17.3%)reported on initial pain in the masseter muscle or/andtempomandibular joint, which had all but disappearedat the control investigation.

Discussion

There has been a growing interest in finding thera-peutic options with higher compliance than nCPAPfor patients with mild-to-moderate OSA. In our study,we retrospectively analyzed patients treated with aKarwetzky activator for OSA of all degrees. Whereasrespiratory variables had significantly improved with theKarwetzky appliance treatment, changes in sleep macro-structure were not as evident. However, the arousal indexwas significantly reduced in all three groups. Apart fromthe reduction in apneas and hypopneas, the significant

Table 1

Sleep variables – severe OSA patients

Baseline After treatment

PMedian Range Median Range

Respiratory variablesApnea hypopnea index (events/h) 42.1 33.2–64.9 18.1 2.4–48.8 <0.001Apnea index (events/h) 20.2 6.8–38.6 8.4 0–25.3 <0.001Mean oxygen saturation (%) 93.5 85.3–96.7 93.8 85.7–96.8 <0.05Minimal oxygen saturation (%) 82.7 55.7–94.4 84.2 72.8–93.5 <0.01Mean oxygen desaturation (%) 84.4 79.8–93.7 89.6 82.4–93.2 <0.01Desaturation index (events/h) 47.2 30.4–69.0 22.0 2.8–42.8 <0.001

Somnographic variablesSleep efficiency (%) 84.0 70.8–95.4 85.4 69.3–97.9 NSWakefulness (SW) (%) 10.5 0.9–18.2 6.7 0.5–20.0 <0.05N-REM S-1 (%) 14.0 6.9–27.2 15.8 2.9–32.3 NSN-REM S-2 (%) 53.3 37.1–67.2 40.4 29.7–65.2 NSN-REM S-3 & S-4 (%) 16.7 1.0–32.8 19.9 2.4–31.7 NSREM (%) 8.7 0.2–14.1 14.5 2.7–25.4 <0.01Arousal index (events/h) 32.2 2.0–52.7 11.7 2.4–21.4 <0.001

Patients with severe Obstructive Sleep Apnea (OSA) (n=17) at baseline and after treatment with an activator.Median, range, and significance P are given; NS=not significant.

Table 2

Sleep variables – moderate OSA patients

Baseline After treatment

PMedian Range Median Range

Respiratory variablesApnea hypopnea index (events/h) 21.7 17.3–28.4 7.7 1.0–30.1 <0.001Apnea index (events/h) 10.3 5.2–17.2 2.4 0.0–10.7 <0.001Mean oxygen saturation (%) 93.6 89.2–98.5 93.6 88.3–99.1 NSMinimal oxygen saturation (%) 78.7 67.1–90.2 84.0 70.5–92.8 <0.01Mean oxygen desaturation (%) 77.5 65.3–88.5 83.5 74.2–89.4 <0.01Desaturation index (events/h) 21.0 4.8–39.3 10.2 1.5–19.3 <0.01

Somnographic variablesSleep efficiency (%) 78.0 61.0–93.5 80.2 62.1–94.5 NSWakefulness (SW) (%) 12.3 1.3–26.3 10.5 2.5–23.2 NSN-REM S-1 (%) 12.8 3.8–28.2 11.7 1.0–28.3 NSN-REM S-2 (%) 38.2 17.2–60.3 33.6 15.3–59.2 NSN-REM S-3 & S-4 (%) 20.9 4.3–37.2 25.2 5.3–35.2 <0.05REM (%) 14.2 3.9–27.3 19.5 6.3–24.2 <0.05Arousal index (events/h) 25.2 5.2–36.2 10.4 0.0–22.7 <0.01

Patients with moderate obstructive sleep apnea (OSA) (n=33), at baseline and after treatment with an activator.Median, range, and significance P are given; NS=not significant.

102 Rose et al.

reduction in the number of desaturations, as well asreduction of subjective EDS, are additional signsdemonstrating therapeutic efficacy. When reviewing theliterature, a reduction in the AHI of about 50%, onaverage, can be achieved using oral appliances dependingon the appliances’ design and the particular study. Dataconcerning therapeutic efficacy of oral appliances inpatients with severe OSA is controversial; they rangefrom no therapeutic efficacy to some improvement(23–31). According to our cut-off criterion, optimaltreatment outcome was determined more frequently inthose with mild-to-moderate OSA, as compared topatients with severe OSA. However, in about one-thirdof patients with severe OSA, nocturnal respiratoryvariables were completely normal, another thirdimproved, and one-third was a therapeutic failure. Inpatients with moderate OSA, the Karwetzky activatorwas recommended in more than 70% as final treatment,but was contraindicated in 12% of patients.

The respiratory results in our patients with severe OASare in concordance with the findings of SCHOENHOFER

et al. (26), who found significant clinical improvement

in a third of the patients. This group used a retentiveprotrusion device. BARTHLEN et al. (32) found a reductionin mean AHI from 60 (SD 37) to 9 (SD 4.8) in five outof eight patients with severe OSA. At present, it is notexactly known why oral appliances have such a broadtherapeutic range; especially in patients with severeOSA, therapeutic efficacy can show extreme differences.Anatomical skeletal factors influencing the degree ofvertical and sagittal opening, possible displacement of themandible, the enlargement of the pharyngeal airway-space, and sleep position (13, 14, 22, 33) all play a roleas does the device’s design.

The significant reduction in the arousal index in allpatients and the increase in REM sleep in patients withmoderate-to-severe OSA underline the therapeutic effi-cacy of the Karwetzky activator. We have to state,however, that improvement in sleep macrostructure wasnot as pronounced as the improvement in respiratoryvariables. In patients with severe excessive daytimesleepiness and/or vigilance impairment, our activatorshould be considered with great care, particularly whenthere is a question of medical and/or occupational safety.When in doubt, the nCPAP treatment is more effectiveand medico-legally more prudent (10, 34, 35).

OSA becomes more frequent with increasing age.Elderly patients often present suboptimal conditions asthey may have missing teeth and mobility of teeth due toperiodontal damage (36), making it impossible to firmlyfix an appliance dentally. Most of the sleep studies onoral appliances have been carried out with devicesrequiring maximum dental retention to force the man-dible in a protrusive position (6, 8, 11, 19, 21, 23–32,33–35). A periodontally healthy and adequate dentitionis a prerequisite for this form of fixation. In general,10 teeth in each jaw are recommended to provide suf-ficient retention for a permanent mandibular protrusionduring treatment with an MAA (30, 34). The Karwetzky

Table 3

Sleep variables – mild OSA patients

Baseline After treatment

PMedian Range Median Range

Respiratory variablesApnea hypopnea index (events/h) 10.6 2.0–14.9 5.8 0.2–17.3 <0.01Apnea index (events/h) 4.2 0.0–10.2 2.2 0.0–3.9 <0.01Mean oxygen saturation (%) 94.7 90.3–99.2 95.1 89.5–99.1 NSMinimal oxygen saturation (%) 83.3 75.1–92.2 89.2 86.3–97.2 <0.01Mean oxygen desaturation (%) 90.2 88.3–90.5 90.5 87.2–91.4 NSDesaturation index (events/h) 9.1 0.0–18.3 6.5 0.0–15.1 <0.05

Somnographic variablesSleep efficiency (%) 82.5 63.2–98.8 84.1 65.1–97.5 NSWakefulness (SW) (%) 13.6 2.1–26.1 11.9 1.9–23.2 NSN-REM S-1 (%) 12.9 2.0–29.3 10.2 1.0–28.2 NSN-REM S-2 (%) 36.7 15.1–58.4 39.5 16.8–58.3 NSN-REM S-3 & S-4 (%) 23.1 5.3–43.5 24.8 8.2–38.1 NSREM (%) 13.2 2.1–21.7 14.9 2.5–23.8 NSArousal index (events/h) 12.3 1.0–25.2 7.1 2.0–16.8 <0.01

Patients with mild obstructive sleep apnea (OSA) (n=31) at baseline and after treatment with an activator.Median, range, and significance P are given; NS=not significant.

Table 4

Treatment outcome

n

Optimal Responder Non-responder

n % n % n %

Severe 17 7 41.2 5 29.4 5 29.4Moderate 33 24 72.7 5 15.2 4 12.1Mild 31 27 87.1 – – 4 12.9

Treatment outcome according to the severity degree of thedisease: optimal: AHI <5/h; responder: AHI >5/h and an AHIreduction of at least 50%; non-responder: a worsening of theAHI or a decrease in the AHI of under 50% of baseline.

Karwetzky device for OSA treatment 103

activator, being tooth- and tissue-borne, is not fixed tothe upper and lower teeth. Despite the differences inappliance retention, treatment efficacy of the Karwetzkyappliance studied herein is similar to the success rateobtained using other retentive protrusive appliances ofvarious designs (23, 25, 27, 28), whereas tongue-retainingdevices’ success rate tends to be lower (34). The currentstudy demonstrated that treatment outcome with thisparticular device was not influenced by the number ofteeth, and that the device can also be used by patientswith a reduced dentition.

At present, there are no diagnostic tools for predictingtreatment success and/or for monitoring patient com-pliance with oral appliances. Regardless of the subjectiveassessment by the patient, therapeutic efficacy must becontrolled polysomnographically in a sleep laboratory,as the device can lead to the condition’s deterioration.In the latter case, this raises the problem of associatedexpense, including the reimbursement for devices notleading to treatment success. Recent treatment options,such as those employing cheap thermoplastic appliancesfitted to test treatment effect in an overnight registration,might help in selecting appropriate patients for thisparticular treatment (37, 38).

The use of oral appliances and mechanical treatmentsuch as nCPAP call for lifelong therapy. Patient accept-ance and a healthy stomatognathic situation provide thebasis for effective treatment. The Karwetzky activator inthis study was tolerated by 86 of 116 patients (74.1%)during the 4-month study period. This concurs with theinitial tolerance found in the literature covering othertypes of appliances (31). The fact that the patients carryout the control registrations does not reflect patientcompliance. As opposed to nCPAP, patient complianceusing oral appliances cannot be verified. In the directcomparison with nCPAP, patients prefer oral appliancetreatment, even though the clinical usage complianceappears less satisfactory than expected. The main reasonsfor discontinuing therapy were lack of efficacy and ageneral non-specific discomfort. In two cases, temporo-mandibular joint pain led to discontinuing therapy. Itis speculative as to what variables influence treatmentcompliance, however a relief of clinical symptoms seemsto be a major one.

Long-term therapeutic efficacy was not assessed in thisretrospective study. Severity of OSA increases with ageand excess body mass index. As there is only a smallnumber of long-term studies (39, 40), this therapeuticoption can currently be recommended with precautionsand then only with routine follow-up studies.

The results from this study demonstrate that the use ofthe Karwetzky activator leads to a significant improve-ment in respiratory variables and a significant reduc-tion in the arousal index. The activator, as a non-dentallyfixed appliance, shows similarly therapeutic efficacy whencompared to retentive devices and might be used inpatients with reduced dentition. Therapeutic efficacy hasto be monitored at regular intervals by polysomnographyand dental examination, especially in patients withmoderate and severe OSA, as there are no long-termfollow-up studies with this therapeutic intervention.

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