Keywords
obstructive sleep apnea - mandibular advancement - mandibular condyle - cone-beam
computed tomography
Introduction
Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction
events during sleep, and it is associated with clinical signs and symptoms. Obstruction
can manifest as a respiratory effort-related or arousal-related awakening and as a
limitation or reduction in airflow (hypopnea), or complete cessation of airflow (apnea),
upon persistent breathing movements.[1]
[2] The etiology of OSA is multifactorial, with the possible involvement of anatomical,
functional, and neuromuscular characteristics, and its diagnosis is based on polysomnography
(PSG).[3]
The apnea-hypopnea index (AHI) is a PSG parameter that classifies OSA as mild (AHI = 5
to 15 events/hour), moderate (AHI = 15 to 30 events/hour), or severe (AHI ≥ 30 events/hour).[4]
[5] Moderate OSA may be associated with cardiac arrhythmias, while severe OSA may be
associated with heart or coronary insufficiency. To prevent cardiovascular risks and
other OSA symptoms, such as snoring, nonrestorative sleep, excessive daytime sleepiness,
neurocognitive alterations, depression, and anxiety, the treatment of this disorder
is essential.[3]
[6]
[7]
[8]
Continuous positive airway pressure (CPAP) is the gold-standard treatment for OSA;
however, orthognathic surgery for mandibular advancement[9] and the use of a mandibular advancement device (MAD) are efficient therapies for
patients who are not eligible for the CPAP treatment.[3]
[6]
[7]
[8] The mechanism of action of an MAD is based on the extension and distension of the
upper airway; this distension prevents the collapse of the oropharynx and the base
of the tongue, which, in turn, prevents the closure of the upper airway.[3]
[10] Although the mechanism of action of MADs is well understood, their effects on the
condylar position during OSA treatment remain unclear.[1]
[11]
[12]
Cone-beam computed tomography (CBCT) enables a reliable evaluation of the morphological
and positional changes of the mandibular condyles. The three-dimensional (3D) evaluation
of images from CBCT scans may significantly help in the identification and quantification
of mandibular condyle changes during MAD use for OSA treatment.[13] Accordingly, the present study aimed to evaluate and quantify the positional changes
of the mandibular condyle using CBCT images during treatment with MADs, and assess
whether these changes in condylar influence OSA PSG parameters.
Materials and Methods
Study Design
In the present before-and-after pilot study, 10 volunteers with mild to moderate OSA
were referred for MAD treatment. Initially, 83 patients were selected from the Sleep
and Breathing Disorders Center of the Universidade Federal do Ceará, state of Ceará,
Brazil. Following the inclusion criteria, 33 patients diagnosed with mild or moderate
OSA were referred for treatment with an MAD; of these 18 were excluded; subsequently,
based on the exclusion criteria, another 5 subjects were excluded, resulting in a
final sample of 10 patients ([Fig. 1]), who underwent a sequence of evaluations: initial, sequential, and final. Cone-beam
computed tomography and PSG assessments were performed before the MAD treatment (T0)
and after 8 months (T1) of MAD placement ([Fig. 2]).
Fig. 1 Study sample.
Fig. 2 Study design.
Eligibility Criteria
The present study included individuals of both genders aged between 18 and 65 years,
with a body mass index (BMI) ≤ 35 kg/m2, an AHI > 5 and < 30 (mild to moderate OSA), with a varied spectrum of severity levels
according to the criteria of the American Academy of Sleep Medicine (AASM),[4] and negative diagnosis of temporomandibular disorders (TMD) according to the Research
Diagnostic Criteria for Temporomandibular Disorders (RDC/TMD).
The exclusion criteria were as follows: loss of posterior dental support that compromised
the retention of an MAD; active periodontal disease; dental crown/dental root ratio
≤ 1; need for primary dental treatment (for caries, endodontic treatments, or retreatments
and dental prostheses, for example); anterior open-bite; mandibular protrusion movement < 5 mm;
limited mouth opening; history of alcoholism; use of sleep inducers; patients with
habits or professions that led to the deprivation of sleep or alterations in the sleep-wake
cycle; sleep disorders other than OSA; history of OSA treatment (for example, MAD,
surgeries or CPAP, or diagnosis of TMD according to the RDC/TMD); and patients with
tomographic images that did not enable adequate evaluations due to movements during
acquisition. Of the 33 patients initially selected, 23 were excluded; therefore, the
total sample comprised 10 OSA patients.
Mandibular Advancement Device
The MAD used in the present study was an individualized acrylic appliance with a vertical
dimension of 5 mm called Brazilian Dental Appliance (BRD; NeoSleep, Curitiba, PR,
Brazil). The BRD has two independent (right and left) expanding mechanisms (screws
positioned with their long axes in the anteroposterior direction) positioned in the
posterior palatine region of the upper acrylic base. From these expander mechanisms,
two independent palatine stems (one right and one left) are inserted into two small
tubes located in the anterior portion (distal to the lower canines) of the lower support
acrylic base[15] ([Fig. 3]). To make this individualized appliance, dental impressions were obtained, and the
mandibular positions of centric relation and maximum protrusion were registered with
the George Gauge device (Great Lakes Dental Tech, Tonawanda, NY, United States) and
condensation silicone (dense). The MAD was initially placed at 50% of the maximum
advancement, and all patients were instructed to advance the device by 0.5 mm each
week until 85% of therapeutic protrusion was achieved, considering the improvement
in signs/symptoms in the medical record.[16]
[17] To assess adherence to the treatment Weekly follow-up was performed until the therapeutic
protrusion position was achieved to.
Fig. 3 (A) Frontal view of the Brazilian Dental Appliance (BRD). (B) Lateral view with the appliance placed in an OSA patient.
Tomographic Assessment
The tomographic images were obtained using the iCAT (Imaging Sciences International,
Hatfield, PA, United States) set at 120 Kvp, 30 mA, and 0.4 mm voxels. To perform
the CBCT examination, all patients were positioned with the Frankfurt plane parallel
to the floor and were instructed not to swallow and to keep the maximum intercuspation
position (T0). At T1, CBCT was performed with placement of the MAD. Reconstruction
and interpretation of the 3D images and tomographic measurements of the structures
were performed with the Dental Slice software (BioParts, Brasília, DF, Brazil). The
images had the 3D reconstructions oriented with the axial plane passing through the
orbitale (Or) and porion (Po) points (parallel to the Frankfurt plane), with the sagittal
plane through the nasion (N) point, and with the coronal plane perpendicular to the
axial plane, through the left and right Po points.
To determine the measurements related to the position of the right and left mandibular
condyles, reference lines and measurements were performed on the CBCT images obtained
at T0 and T1 ([Fig. 4]).
Fig. 4 (A) Sagittal view perpendicular to the long axis of the condyle to determine all lines
and measurements. (B) Line B, reference line tangent to the uppermost portion of the mandibular condyle,
used to determine its highest point. (C) Line C, vertical measurement from the deepest point of the joint fossa up to line
B, used to determine the extrusion of the mandibular condyle in relation to the joint
fossa. (D) Line D, horizontal measurement from the highest point of the mandibular condyle
up to line C, used to determine the advancement of the mandibular condyle.
Polysomnography
The 10 patients underwent PSG for the diagnosis of OSA (T0) and again with the MAD
in a mandibular position at 85% of maximum protrusion (T1). The PSGs were performed
at night by an experienced technician in a specialized center. The mean time between
the first and second PSG assessments was of eight months, and the basal movements
were calibrated before performing the examination. A computerized PSG apparatus (Embla
N7000, Embla Systems, Inc., Broomfield, CO, United States) was used to record the
following sleep parameters: electroencephalography (EEG: C3-A2, C4-A1, O2-A1, and
O1-A2), submentonian and tibial electromyography, and bilateral electrooculography,
and chest and abdominal movements were recorded using noncalibrated breathing electrocardiography
(ECG; modified V1 derivation). Breathing was monitored using a nasal cannula that
gauged the airflow by pressure transduction. A thermal sensor was used to measure
oral flow plethysmography. For oxyhemoglobin saturation, an infrared pulse oximetry
reader was placed on the fingertip of the patient. A sensor placed over the region
of the sternum recorded the body position, and a tracheal microphone measured snoring.
The following parameters were evaluated according to the previous criteria: sleep
staging, respiratory events, arousals, and leg movements. The OSA diagnosis was established
by a physician specialized in sleep medicine and the severity classification of each
patient was based on the AASM criteria: mil OSA – AHI = 5 to 15 events/hour; moderate
OSA – AHI = 15 to 30 events/hour; and severe OSA – AHI ≥ 30 events/hour.[4]
[5]
Study Error
To avoid study bias, the measurements were performed by an experienced examiner and
an assessment of intraexaminer reliability was performed by repeating the 3D measurements
3 times with an interval of 7 days, without statistical differences among the measurements
in the 3 time points. The reliability data were subjected to the Kolmogorov-Smirnov
normality test, as well as to the Friedman test and Spearman correlation analysis
(nonparametric data), to evaluate the calibration of the operator in three moments
(the data were expressed as mean ± standard deviation [SD] and median [minimum–maximum]
values).
Statistical Analysis
After tabulation and analysis of the sample distribution pattern through the Shapiro-Wilk
normality test, all variables were analyzed through the paired t-test (parametric data) and subjected to Pearson correlation analysis. The analyses
were performed using the SPSS Statistics for Windows software,version 17.0 (SPSS Inc.,
Chicago, IL, United States), with confidence set at 95%.
Results
Study Error
There were no statistically significant differences regarding the first (4.0 ± 3.2;
3.9 [-2.3–10.3]), second (4.3 ± 3.7; 4.8 [-2.1–12.1]), and third (4.4 ± 3.6; 4.9 [-2.7–11.8])
condylar measurements (p = 0.880; Friedman test). There was a statistically significant correlation between
the first and the second (p < 0.001; r = 0.791), the first and the third (p < 0.001; r = 0.817), and the second and the third (p < 0.001; r = 0.973) measurements (Spearman correlation).
Tomographic Assessment
We observed an increase in the advancement and extrusion values of the right and left
mandibular condyles in all patients with the use of the MAD ([Table 1] and [Fig. 5]); the extents of the advancement and extrusion were statistically significant (p < 0.001) ([Table 2]).
Table 2
Advancement and extrusion values of the right and left mandibular condyles and polysomnographic
parameters.
|
T0: mean ± SD
|
T1: mean ± SD
|
p-value
|
Right TMJ extrusion
|
3.25 ± 1.26
|
7.14 ± 2.05
|
< 0.001
|
Right TMJ advancement
|
-0.76 ± 1.00
|
6.42 ± 1.88
|
< 0.001
|
Left TMJ extrusion
|
3.38 ± 1.39
|
6.87 ± 1.52
|
< 0.001
|
Left TMJ advancement
|
-0.66 ± 0.89
|
5.93 ± 2.10
|
< 0.001
|
AHI
|
17.71 ± 5.63
|
4.50 ± 3.44
|
< 0.001
|
Mean SpO2
|
80.40 ± 9.80
|
94.90 ± 1.91
|
0.001
|
Minimum SpO2
|
90.20 ± 2.90
|
96.50 ± 0.97
|
< 0.001
|
Abbreviations: AHI, apnea-hypopnea Index; SpO2, oxyhemoglobin saturation; SD, standard deviation; T0, before the treatment with
a mandibular advancement device (MAD); T1, eight months after MAD placement; TMJ,
temporomandibular joint.
Note: *p < 0.05; paired t-test (mean ± SD).
Fig. 5 Tomographic images of the temporomandibular joint (TMJ) of the 10 patients before
the treatment with a mandibular advancement device (MAD; T0) and 8 months after (T1)
MAD placement.
Table 1
Tomographic measurements of the position of the right and left mandibular condyles
before (T0) and after (T1) the placement of a mandibular advancement device.
Patient
|
Temporomandibular joint
|
T0
|
T1
|
1
|
Right extrusion
|
+1.12
|
+2.65
|
|
Right advancement
|
0
|
+7.87
|
|
Left extrusion
|
+0.89
|
+3.71
|
|
Left advancement
|
0
|
+7.03
|
2
|
Right extrusion
|
+2.64
|
+6.09
|
|
Right advancement
|
-2.13
|
+2.4
|
|
Left extrusion
|
+3.26
|
+6.33
|
|
Left advancement
|
-1.91
|
+2.16
|
3
|
Right extrusion
|
+4.42
|
+9.02
|
|
Right advancement
|
-1.57
|
+6.60
|
|
Left extrusion
|
+4.04
|
+5.51
|
|
Left advancement
|
0
|
+6.43
|
4
|
Right extrusion
|
+3.76
|
+5.28
|
|
Right advancement
|
0
|
+5.01
|
|
Left extrusion
|
+3.66
|
+6.2
|
|
Left advancement
|
0
|
+5.67
|
5
|
Right extrusion
|
+4.8
|
+9.63
|
|
Right advancement
|
0
|
+7.64
|
|
Left extrusion
|
+5.76
|
+8.53
|
|
Left advancement
|
0
|
+4.65
|
6
|
Right extrusion
|
+2.55
|
+8.01
|
|
Right advancement
|
-2.2
|
+4.95
|
|
Left extrusion
|
+3.01
|
+8.81
|
|
Left advancement
|
-1.51
|
4.85
|
7
|
Right extrusion
|
+3.75
|
+7.62
|
|
Right advancement
|
0
|
+7.49
|
|
Left extrusion
|
+4.59
|
+7.38
|
|
Left advancement
|
0
|
+6.76
|
8
|
Right extrusion
|
+4.54
|
+7.85
|
|
Right advancement
|
-1.7
|
+7.49
|
|
Left extrusion
|
+4.12
|
+7.85
|
|
Left advancement
|
0
|
+10.41
|
9
|
Right extrusion
|
+1.52
|
+6.82
|
|
Right advancement
|
0
|
+6.02
|
|
Left extrusion
|
+2.02
|
+6.82
|
|
Left advancement
|
-2.13
|
+5.41
|
10
|
Right extrusion
|
+3.43
|
+8.41
|
|
Right advancement
|
0
|
+8.76
|
|
Left extrusion
|
+2.4
|
+7.53
|
|
Left advancement
|
-1.03
|
+5.95
|
Polysomnography
Comparing the T0 and T1 PSG results, with the use of the MAD, all patients presented
a decrease in AHI during sleep and an increase in the values of minimum oxyhemoglobin
saturation. Seven patients presented an increase in the mean percentage of oxyhemoglobin
saturation, while three maintained their initial values ([Table 3]). The changes in AHI (p < 0.001) and in mean (p = 0.001) and minimum (p < 0.001) oxyhemoglobin saturation were statistically significant ([Table 2]).
Table 3
Polysomnographic values in T0 and T1.
Patient
|
T0:
AHI
|
T1:
AHI
|
T0:
mean SpO2
|
T1:
mean SpO2
|
T0:
minimum SpO2
|
T1:
minimum SpO2
|
1
|
15.4
|
0.9
|
97
|
97
|
69
|
89
|
2
|
19.3
|
12.2
|
94
|
97
|
88
|
92
|
3
|
27.6
|
5.8
|
93
|
96
|
84
|
90
|
4
|
6.9
|
0.3
|
96
|
97
|
87
|
93
|
5
|
16.8
|
5.9
|
94
|
97
|
86
|
90
|
6
|
16.3
|
4.3
|
95
|
97
|
84
|
95
|
7
|
15.4
|
1.2
|
96
|
96
|
81
|
84
|
8
|
25
|
3.9
|
91
|
94
|
57
|
90
|
9
|
16.5
|
4.9
|
97
|
97
|
85
|
89
|
10
|
17.9
|
5.6
|
96
|
97
|
83
|
90
|
Abbreviations: AHI, apnea-hypopnea index; SpO2, oxyhemoglobin saturation; T0, before the treatment with a mandibular advancement
device (MAD); T1, eight months after MAD placement; TMJ, temporomandibular joint.
Influence of Condylar Position in Polysomnography
A correlation between condylar advancement and AHI values was observed: the greater
the anterior displacement of the right (p = 0.003; r = -0.792) and left (p = 0.015; r = -0.685) condyles, the better the AHI and the lower the number of respiratory
pauses per hour of sleep. The mean percentage of oxyhemoglobin saturation decreased
with the anterior position of the condyles. There was no correlation between condylar
advancement and the increase in minimum oxyhemoglobin saturation ([Table 4]).
Table 4
Correlation between extrusion/advancement values and polysomnographic results.
|
|
Δ right extrusion
|
Δ right advancement
|
Δ left extrusion
|
Δ left advanced
|
Δ AHI
|
Δ mean SpO2
|
Δ mininum
SpO2
|
Δ right extrusion
|
r
|
−
|
0.234
|
0.515
|
-0.022
|
-0.144
|
0.395
|
-0.002
|
|
p-value
|
−
|
0.258
|
0.064
|
0.476
|
0.346
|
0.130
|
0.498
|
Δ right advancement
|
r
|
−
|
−
|
0.088
|
0.633*
|
-0.792*
|
-0.592*
|
-0.156
|
|
p-value
|
−
|
−
|
0.405
|
0.025
|
0.003
|
0.036
|
0.334
|
Δ left extrusion
|
r
|
−
|
−
|
−
|
0.262
|
0.21
|
- 0.054
|
0.277
|
|
p-value
|
−
|
−
|
−
|
0.232
|
0.280
|
0.441
|
0.219
|
Δ left advancement
|
r
|
−
|
−
|
−
|
−
|
- 0.685*
|
- 0.828*
|
0.003
|
|
p-value
|
−
|
−
|
−
|
−
|
0.015
|
0.002
|
0.497
|
Δ AHI
|
r
|
−
|
−
|
−
|
−
|
−
|
0.569
|
0.082
|
|
p-value
|
−
|
−
|
−
|
−
|
−
|
0.054
|
0.411
|
Δ mean SpO2
|
r
|
−
|
−
|
−
|
−
|
−
|
−
|
0.050
|
|
p-value
|
−
|
−
|
−
|
−
|
−
|
−
|
0.446
|
Δ minimum SpO2
|
r
|
−
|
−
|
−
|
−
|
−
|
−
|
−
|
|
p-value
|
−
|
−
|
−
|
−
|
−
|
−
|
−
|
Abbreviations: AHI, apnea-hypopnea index; SpO2, oxyhemoglobin saturation; TMJ, temporomandibular joint.
Note: *p < 0.05; Pearson correlation analysis.
Discussion
The present study assessed the effects of an MAD in the condylar position, as well
as the influence of condylar displacement on PSG parameters in OSA patients. Several
studies[18]
[19]
[20]
[21] have evaluated the effectiveness of MADs, which have been reported to ensure an
increase in airflow in the upper airway, reduce the AHI, and minimize the clinical
signs and symptoms of OSA. However, the literature still fails to explain condylar
positioning after OSA treatment with an MAD.
The present study showed that the use of an oral appliance resulted in extrusion and
advancement of the right and left mandibular condyles in all cases. In addition, we
observed that, when 85% of maximum mandibular protrusion was achieved, there was a
greater anterior displacement of the mandibular condyles and a significant reduction
in the AHI of the patients, as well as an increase in the mean and minimum oxyhemoglobin
saturation. There was a significant association between condylar anteriorization and
improvements in the AHI. In agreement with the present study, de Almeida et al.[12] after analyzing six OSA patients treated with an MAD, reported that this device
may decrease the AHI. In contrast to the present findings, the authors[12] reported no important condyle anterior displacement with MAD therapy, the minimum
oxyhemoglobin saturation significantly only increased in one patient, and no correlation
was observed regarding the condylar positions and the PSG findings.[12] Chen et al.[22] evaluated changes in the temporomandibular joint (TMJ) after bilateral sagittal
split ramus osteotomy for mandibular advancement and noted different outcomes: three
months after the mandibular advancement surgery, the condyles were placed in a concentric
position in relation to the glenoid fossa, not showing an anterior alignment after
the procedure.
There are several types of oral appliances for OSA therapy, of different shapes and
materials, which fit into two main categories: tongue retention devices and MADs,
or mandibular advancement devices; the latter are the ones most commonly used in the
treatment of sleep disorders. These devices may vary according to the manufacturer
(noncustomized or personalized devices), and in terms of retention, titration of the
mandibular position, anterior vertical opening, freedom of mandibular movement, and
clothing material, among other factors.[7] It should be emphasized that nonadjustable repositioning devices present difficulties
regarding patient adaptation and efficiency. The MAD used in the present study was
the BRD, which is an appliance made in a specialized laboratory and individualized
for the shape of the dental arch of each patient. Use of the BRD may result in stable
vertical (opening) and anteroposterior (mandibular protrusion) mandibular positions,
and the device is extremely versatile due to its ability to yield progressive and
measurable mandibular advancements.[7] To reduce obstructive events during sleep, the maximum mandibular protrusion should
preferably be higher than 70%. In the present study, the percentage of mandibular
advancement was initially of 50%, which was increased considering the OSA improvement.
Patients with 70% of advancement who did not respond had their percentages increased
as tolerated.[16]
[17] The patients in the present study showed improvement in the signs/symptoms of OSA
with mandibular advancement of 85%, which is an extensive protrusive position that
should be carefully determined, taking into account the results observed in each patient.
The treatments should aim for lower levels of advancement with better results.
Based on the responses obtained with the RDC/TMD questionnaire and with the examination
of the muscular and articular structures according to the RDC/TMD criteria, none of
the patients presented with adverse effects with MAD use, leading to a high adherence
to the treatment and, consequently, to the study. In the present study, the second
evaluation was performed at 8 months, when the duration of MAD use had not been long
enough to cause adverse effects in the articular disc, occlusion, and masticatory
muscle activities that are important anatomic stomatognathic structures for TMD development.
These outcomes are in agreement with those of a study[6] on changes in the TMJ of OSA patients before and after the MAD treatment, which
demonstrated that, in a short period, the effect of an MAD on the stomatognathic system
is minimal.
A limitation of the present study is the small sample size; however, it is a pilot
study, and further investigation involving a greater number of volunteers is planned
in the future. The absence of a control group is also a limitation; nonetheless, this
may be justified by ethical reasoning, as CBTC exposure may be unnecessary for patients
without OSA diagnosis. We have found no previous studies on the correlation of mandibular
condyle positional changes and the AHI or oxyhemoglobin saturation. This highlights
the originality of the present paper, pointing to a lack of redundancy between the
present study and other studies.
The present study provides clinicians with important knowledge on OSA treatment with
an MAD. At 85% of maximum protrusion, it may be expected that patients with greater
condylar advancement will present better AHI. This information is essential for adequate
planning and prognosis of OSA patients to be treated with oral advancement appliances.
Moreover, according to Gurgel et al.,[16] tomographic anatomic measurements may influence OSA severity and MAD outcomes in
OSA treatment, as well as the amount of protrusion for successful therapy with intraoral
advancement devices. Therefore, more studies on the anatomical positions of the condyles
with an MAD and PSG parameters are still necessary.
Conclusion
-
The use of an MAD for the treatment of OSA significantly changed the condylar position;
the positional changes were advancement and extrusion. The amount of condylar advancement
obtained with 85% of maximum protrusion showed a direct correlation with the improvement
in obstructive events during sleep: the greater the advancement of the mandibular
condyles, the lower the AHI.