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Mouth breathing, “nasal disuse,” and pediatric sleep-disordered breathing

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Adenotonsillectomy (T&A) may not completely eliminate sleep-disordered breathing (SDB), and residual SDB can result in progressive worsening of abnormal breathing during sleep. Persistence of mouth breathing post-T&As plays a role in progressive worsening through an increase of upper airway resistance during sleep with secondary impact on orofacial growth. Retrospective study on non-overweight and non-syndromic prepubertal children with SDB treated by T&A with pre- and post-surgery clinical and polysomnographic (PSG) evaluations including systematic monitoring of mouth breathing (initial cohort). All children with mouth breathing were then referred for myofunctional treatment (MFT), with clinical follow-up 6 months later and PSG 1 year post-surgery. Only a limited subgroup followed the recommendations to undergo MFT with subsequent PSG (follow-up subgroup). Sixty-four prepubertal children meeting inclusion criteria for the initial cohort were investigated. There was significant symptomatic improvement in all children post-T&A, but 26 children had residual SDB with an AHI > 1.5 events/hour and 35 children (including the previous 26) had evidence of "mouth breathing" during sleep as defined [minimum of 44 % and a maximum of 100 % of total sleep time, mean 69 ± 11 % "mouth breather" subgroup and mean 4 ± 3.9 %, range 0 and 10.3 % "non-mouth breathers"]. Eighteen children (follow-up cohort), all in the "mouth breathing" group, were investigated at 1 year follow-up with only nine having undergone 6 months of MFT. The non- MFT subjects were significantly worse than the MFT-treated cohort. MFT led to normalization of clinical and PSG findings. Assessment of mouth breathing during sleep should be systematically performed post-T&A and the persistence of mouth breathing should be treated with MFT.
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ORIGINAL ARTICLE
Mouth breathing, nasal disuse,and pediatric
sleep-disordered breathing
Seo-Young Lee &Christian Guilleminault &
Hsiao-Yean Chiu &Shannon S. Sullivan
Received: 9 December 2014 /Revised: 6 February 2015 /Accepted: 25 February 2015
#Springer-Verlag Berlin Heidelberg 2015
Abstract
Background Adenotonsillectomy (T&A) may not completely
eliminate sleep-disordered breathing (SDB), and residual
SDB can result in progressive worsening of abnormal breath-
ing during sleep. Persistence of mouth breathing post-T&As
plays a role in progressive worsening through an increase of
upper airway resistance during sleep with secondary impact
on orofacial growth.
Methods Retrospective study on non-overweight and non-
syndromic prepubertal children with SDB treated by T&A
with pre- and post-surgery clinical and polysomnographic
(PSG) evaluations including systematic monitoring of mouth
breathing (initial cohort). All children with mouth breathing
were then referred for myofunctional treatment (MFT), with
clinical follow-up 6 months later and PSG 1 year post-surgery.
Only a limited subgroup followed the recommendations to
undergo MFT with subsequent PSG (follow-up subgroup).
Results Sixty-four prepubertal children meeting inclusion
criteria for the initial cohort were investigated. There was sig-
nificant symptomatic improvement in all children post-T&A,
but 26 children had residual SDB with an AHI> 1.5 events/
hour and 35 children (including the previous 26) had evidence
of mouth breathingduring sleep as defined [minimum of
44 % and a maximum of 100 % of total sleep time, mean 69 ±
11 % mouth breathersubgroup and mean 4± 3.9 %, range 0
and 10.3 % non-mouth breathers]. Eighteen children (fol-
low-up cohort), all in the mouth breathinggroup, were in-
vestigated at 1 year follow-up with only nine having under-
gone 6 months of MFT. The non- MFT subjects were signif-
icantly worse than the MFT-treated cohort. MFT led to nor-
malization of clinical and PSG findings.
Conclusion Assessment of mouth breathing during sleep
should be systematically performed post-T&A and the persis-
tence of mouth breathing should be treated with MFT.
Keyword Sleep-disordered breathing .Adenotonsillectomy .
Mouth breathing .Myofunctional treatment .
Apnea-hypopnea index worsening
Introduction
Adenotonsillectomy (T&A) improves but often does not
completely eliminate pediatric obstructive sleep apnea
(OSA) at systematic post-surgical follow-up [16]. A long-
term study showed that persistence and recurrence of the syn-
drome with slow worsening of the apnea-hypopnea index
(AHI) may frequently occur within 3 years even in the setting
of shorter-term postoperative benefit [7]. Recent work has
indicated that a substantial portion of those with pediatric
SDB will have persistence of SDB up to 4 years later [8].
Based on short-term follow-up periods, children with atopy
(allergies, asthma) are thought to have increased risk of having
persistence of sleep-disordered breathing (SDB) with snoring,
flow limitation, and/or low amounts of apnea-hypopnea
during sleep post-T&A, but this finding was not confirmed
in the 3-year follow-up study [7].
S.<Y. Le e :C. Guilleminault (*):H.<Y. C h i u :S. S. Sullivan
Stanford Outpatient Medical Center, Stanford University Sleep
Medicine Division, 450 Broadway Street, Pavilion B 2nd floor, MC
5730, Redwood City, CA 94063-5730, USA
e-mail: cguil@STANFORD.EDU
Present Address:
S.-Y. Lee
Kangwon National University College of Medicine,
Kanwon-do, Republic of Korea
Present Address:
H.-Y. Chiu
Graduate Institute of Nursing College of Nursing, Taipei Medical
University, Taipei, Taiwan
Sleep Breath
DOI 10.1007/s11325-015-1154-6
Data from Rhesus monkey investigations [9,10] and from
human orthodontic studies demonstrated that mouth breathing
leads to abnormal orofacial growth that can be readily ob-
served [1114]. Similarly, there are data showing that abnor-
mal orofacial growth is associated with sleep-disordered
breathing [15,16]. Finally, it has been previously shown that
mouth breathing leads to a significant increase in upper airway
resistance [17]. Chronic mouth breathing is detrimental in
developing individuals, and it has been shown that nasal
breathing is the primary route of airflow responsible for about
92 and 96 % of inhaled ventilation during wakefulness and
sleep, respectively [18]. We previously found that mouth
breathing was a commonly seen finding in children who were
later found to have symptomatic abnormal breathing during
sleep [19]. Despite this knowledge, no systematic attention is
paid to restoration of nasal breathing when treating sleep-
disordered breathing with surgical approaches such as T&A
and nasal surgery when assessing response to treatment, in-
cluding with polysomnography (PSG).
We questioned as a first step how frequent mouth breathing
during sleep was before T&A surgery in SDB children and
how much improvement of this abnormal behavior was noted
at post-surgical evaluation. Also, as a second goal, we search
for a possible approach in treating the persistent mouth breath-
ing noted during sleep in the studied children.
As mentioned above, there are data demonstrating that oral
breathing impact on oral-facial growth. Also, orofacial muscle
training and reeducation of normal oral-nasal functions along-
side orthodontic treatment has been implemented for many
years because of the successful results of treating open bites
and crossbites when combining both approaches [16,2024].
In teenagers with low to moderate AHI, daily orofacial muscle
training (termed myofunctional therapy[18,19]) has been
reported to help eliminate abnormal breathing during sleep,
including detrimental mouth breathing, at follow-up [20,
2427]. Similarly, in young school-aged children, oropharyn-
geal exercises performed after T&A improved residual symp-
toms of OSA. Indeed, similar findings have been seen in
adults, with specific orofacial muscle training that significant-
ly reduced AHI [28,29]. We questioned, as a preliminary
investigation, if such approach can be a helpful addition to
treatment particularly when mouth breathing was present
post-surgery, collaborating with myofunctional therapists that
are well aware of sleep-disordered breathing in our region.
One of the goals of myofunctional therapy in an orthodon-
tic setting is to modify the swallowing pattern, mastication,
and suction and eliminate mouth breathing that may interfere
with or reduce the results of orthodontic treatment [20]. Long-
term follow-up of children treated with T&A shows that even
with systematic administration of montelukast and nasal aller-
gy treatment, recurrence or worsening of abnormal breathing
during sleep is possible. As there exists some component of
SDB that can remain after T&A and anti-inflammatory
therapy, we have also recommended regular clinical and
PSG follow-up to evaluate long-term evolution; this recom-
mendation has not been systematically followed by pediatri-
cians in the community and parents, but some results are how-
ever available.
This study reports the results of a retrospective analysis of
children with SDB who underwent post-T&A
polysomnography (PSG) with quantifiable data on mouth
breathing. We investigated whether myofunctional reeduca-
tion was effective to alter the mouth breathing pattern in chil-
dren and whether this had an impact on nighttime respiratory
parameters in SDB children. This retrospective investigation
performed on data rendered anonymous was approved by the
IRB.
Methods
Protocol
Inclusion criteria. To be in the study, children had to be pre-
pubertal at entry. They must have had complete clinical charts
indicating the clinical presentation at entry, with demonstra-
tion by examination of the absence of nasal allergies and the
absence of orthodontic crossbites or significant dental
crowding. All subjects had an in-laboratory polysomnogram
(PSG) and those children referred to otolaryngology and who
had adenotonsillectomy performed, with a post-T&A PSG
taken, were included.
Exclusion criteria. Overweight/obese children, children with
syndromic craniofacial malformations, and children with oth-
er medical problems including asthma and desensitization for
upper airway allergies were excluded from the review.
Taking into account inclusion and exclusion criteria, we
created a retrospective cohort. All children with complete data
and successively seen during the 24-month period ending in
December 2012 were included in the review. We then collect-
ed follow-up data available for this cohort, evaluating clinical
data, the presence or absence of myofunctional therapy rec-
ommendations, whether the recommendation was implement-
ed, and PSG if it was performed about 12 months later. We
ended with an initial cohortand a follow-up subgroup.
The goal of the follow-up subgroup was to obtain a prelimi-
nary investigation on possible means of restoring nasal breath-
ing if this normal function was lacking post-surgery.
Data collection
All children responding to inclusion and exclusion criteria are
included in the study. At entry, all children completed the
Pediatric Sleep Questionnaire [30] and underwent a systemat-
ic sleep-medicine evaluation guided by a standardized form.
Sleep Breath
Anatomic scales evaluating the upper airway (Mallampati-
Friedman scale, Friedman tonsils scale inferior nasal
turbinates, dental crowding, presence of overjet, overbite,
and facial harmony) were used [31]. Systematic evaluation
for presence of nasal allergies and rhinitis and presence of
orthodontic problems was also performed with referrals to
specialists if needed. An in-laboratory PSG was performed
with a test lasting a minimum of 7 nocturnal hours with
light-out at regular home sleep time and one parent sleeping
on a fold-out bed in the same room as the child.
PSG recording
The following variables were collected: EEG (four leads), eye
movement chin and leg EMG, ECG (one lead), and body
position. Respiration was monitored using nasal pressure
transducer, mouth breathing was monitored using an oral
scoop (Braebon Medical, ON, Canada) which was modified
to accurately detect oral flow and separate it from any nasal
flow alteration [32](Fig.1), chest and abdominal movements
using inductive plethysmography bands, diaphragmatic-inter-
costal, and rectus-oblique muscle EMGs, pulse oximetry
(Massimo
TM
) from which both oxygen saturation (SaO
2
)
and finger plethysmography were derived, and continuous
video monitoring was done (see Fig. 2). All children, per
study design, were referred to ENT, and all had T&Awithout
indication of significant post-surgery complications. In all, six
different ENT surgeons performed surgery, and all children
were considered healed from surgery when seen again in the
sleep clinic for post-surgery evaluation and PSG. Per clinic
policy, the pre- and post-surgical PSGs were usually scored by
same individuals.
Based on the findings at post-T&A PSG recordings, par-
ents were referred to myofunctional therapy (three different
therapists were used) and/or were recommended to have a 6-
month follow-up clinical visit and a yearly reevaluation at the
sleep clinic with PSG if needed.
Child and parents go to the specialist for training sessions a
mean of three times/week initially. Parents and child are
instructed how to perform daily exercises, and a log of each
daily session and types of exercise is filled on a daily basis;
based on the progresses and collaboration of child, the fre-
quency of weekly session with the specialist decrease with
time, but daily logging with evaluation of the log at each
session by the specialist is carried till end of training. There
is a regular interaction between the reeducator-specialist and
the sleep-physician, and regular written reports outlying num-
ber of sessions, findings from the log, and difficulties with
training are sent evaluating compliance with treatment. At
regular interval, the reeducator-specialist performs a system-
atic evaluation of oral-facial muscle activity that is kept in the
child file. Only a subset of children came back for the sleep
follow-up 6 months and 12-month reevaluation. The evalua-
tion included the same questionnaire, same clinical evaluation,
and same PSG protocol as at entry and post-surgery time
points. Thus, after the initial evaluation, there were three other
appointments for sleep follow-up. The children were seen
post-T&A and again at 6 and 12 months post-T&A.
Analysis
As mentioned, anatomical scales were used to analyze oral-
facial anatomy following published scoring criteria [28].
Sleep and respiratory scoring of PSGs followed the recom-
mended pediatric scoring, according to the American
Academy of Sleep Medicine (AASM) [33]. The presence of
nasal flow limitation was determined using criteria published
by Palombini et al. [34] and Guilleminault et al. [35]. Mouth
breathing during sleep was calculated based on the recording
obtained from a modified cannula with oral scoop [31]. Each
30-s epoch of sleep recording was scored for presence/
absence of mouth breathing. To be scored as a mouth breath-
ing epoch,more than 50 % of the epoch must have shown
recording of air flow with the oral scoop thermocouple. We
defined mouth breathing during sleepto occur when a sub-
ject spent a minimum of 35 % of total sleep time (TST) with
mouth breathing. [This cutoff was based on analysis of 10
pediatric PSG children not included in the present study and
part of a preliminary investigation: there was absence of clin-
ical complaint when mouth breathing was below 20 % and
presence of some complaints if mouth breathing was present
for more than 40 % of sleep monitored with PSG. The deci-
sion to select 35 % was thus a preliminarydecision, and all
records in the study were scored assessing mouth breath-
ing]. The compliance to treatment with myofunctional ther-
apy came from the data collected by the reeducator-specialist
and were derived from parental report and daily logs.
Fig. 1 Equipment to record mouth breathing (Courtesy of Oscar
Carrillo). Legend Oral breathing is determined by a thermocouple
fixed on a scoop that allows collecting flow coming from mouth
breathing. The system allows to monitor nasal pressure and end tidal
CO
2
. The system was validated using measurement of endtidal CO
2
collected directly at the mouth and comparing the mouth end tidal CO
2
signal to the thermocouple signal [31]
Sleep Breath
Statistical evaluation
Data were de-identified and placed in an Excel file for analy-
sis. Chi-squared (percentage) and ttests for repeated measures
were used. In cases where datum was not normally distributed,
the Wilcoxon signed-rank test was used. To compare data
from three successive time points (baseline, post-surgery,
and 12 months post-surgery), a repeated measures analysis
using general linear modeling for AHI, flow limitation, and
SaO
2
was performed. SPSS version 12 was used for statistical
analysis.
Results
There were 92 children for potential inclusion between the
ages of 3 and 9 years identified during the selected time peri-
od. Of these, 64 individuals met the inclusion criteria for the
initial cohort. They represented the study group. The clinical
symptoms and results of PSG before T&A surgery are pre-
sented in Table 1.
Overall, this group of normal weight children without al-
lergy or orthodontic problems had positive surgical results,
and parents reported symptomatic improvement in all cases.
As shown in Table 1, following surgery, there was significant
improvement of an increase of SaO
2
nadir and a decrease in
mean AHI (8.58 before, 1.71 after, p<0.001). However, there
was still residual SDB in 26 children (40.6 %), as they had an
AHI equal or higher than 1.5 events/hour, and 35 children had
the presence of mouth breathing for at least 35 % of total sleep
time (see Fig. 2).
Tab le 1shows that the 26 children with residual post-op
OSA had some symptoms (particularly reports of fatigue,
n=25) despite overall improvement. Comparison of children
with and without mouth breathing is presented in Table 2.
Overall, the mouth breathers had a significantly higher resid-
ual AHI compared to the nasal breathing children.
Interestingly, nine children with no symptoms, as reported
by parents, had an AHI below 1.5 event/hour and mouth
breathing for more than 35 % of total sleep time on post-
T&A PSG.
Prior to surgery, 63 of the 64 children in the initial cohort
showed mouth breathing during sleepper our definition,
and post-surgery there was 35/64 children with mouth
breathing during sleep.In this mouth breathingsubgroup,
mouth breathing was present during sleep for a minimum of
44 % and a maximum of 100 % of total sleep time, with a
mean percentage PSG with mouth breathing during sleep of
Fig. 2 PSG recording indicating mouth breathing in a 5-year-old child.
Legend top segment: 30-s recording during NREM sleep with from top to
bottom. EEG (four leads 14), chin EMG (one lead5),
electrooculogram (two leads6, 7), electrocardiogram (one lead8),
pulse-oxymetry (9) with write-up of oxygen saturation (10), finger
plethysmography (11), nasal cannula-pressure transducer (12), mouth
breathing recording (13), chest and abdomen inductive
plethysmography recording (14, 15), leg EMG (16), transcutaneous
CO
2
(17), and intercostal diaphragmatic EMGs (18, 19). Bottom
segment: All-night recording of pulse oximetry (20) and of mouth
breathing (21)bottom signal. As can be seen looking at top segment:
there is continuous mouth breathing during the 30-s segment; it is
associated with a flatteningof the inspiratory wave contour of the
nasal cannula-pressure transducer and a lengthening of inspiration (per
convention, inspirationis upin the recording). The bottom segment
shows that there is very limited change in oxygen saturation during the
entire night, but (bottom recording) mouth breathing is observed during a
large amount of total sleep time. The segments without mouth breathing
do not correlate with specific sleep states or specific body position. One
hypothesis that could not be verified was related to the question of the role
of the cyclical alternating physiological turbinate turgescence during
sleep
Sleep Breath
69±11 %. The nasal breathing subgroup had a mean total
mouth breathing sleep time of 4±3.9 %, ranging from be-
tween 0 and 10.3 % of total sleep time.
Myofunctional therapy
All subjects with persistence of mouth breathing >35 % of
total sleep time on postoperative PSG were educated at the
follow-up visit on the negative impact of mouth breathing on
orofacial growth. Parents were provided with an introduction
to myofunctional exercises through web pages (www.
myofunctionaltherapy.blogspot.com and www.sleep-apnea-
guide.com/oropharyngeal-exercises.html) and demonstration
of types of possible exercises to perform for at least
6 months. Parents were also systematically given referrals to
myofunctional therapists in contact with the sleep clinic.
Yearly follow-up recall at the sleep clinic was recommended
to assess status. Myofunctional therapy was administered by
three different specialists.
Follow-up at +6 and +12 months post-surgery
After the post-T&A evaluation and PSG, subjects, identified
with persistent mouth breathing with our definition, were ad-
vised to have follow-up clinical appointment 6 months after
the post-surgery sleep clinic visit and repeat PSG investigation
1 year after the initial post-surgery sleep clinic visit. Twenty-
nine of the 35 children with mouth breathing (91 %) came for
a 6-month clinical follow-up, but only 7 of these 29 reported
participating in a myofunctional therapy program. At this vis-
it, repeat recommendations for myofunctional therapy and
referral for therapy were again made. At 12 months post-
T&A, 18 children in the persistent mouth breathing post-
T&A group (i.e., 51.4 % of the initial subgroup) were seen
again and underwent PSG. In this subgroup, nine children
reported having received myofunctional therapy (see
Tab les 3and 4). As a total group (n=18), AHI, O
2
saturation
nadir, and nasal flow limitation were not significantly different
12 months after T&A, compared to immediately after T&A.
However, there were significant differences between those
who reported undergoing myofunctional therapy compared
to those who did not, with all three measures of AHI, O
2
saturation nadir, and nasal flow limitation showing improve-
ment in the myofunctional therapy group (see Table 4). Two
of the children without symptoms but with mouth breathing at
post-T&A study are in the group of the nine untreated chil-
drenat the +12 months post-T&A PSG. These children pres-
ent worse PSG findings than just post-T&A and have now
abnormal findings.
Discussion
In this study, mouth breathing was noted before any treatment,
for a minimum of 1/3 of TSTon PSG in 63 out of 64 children
who met the inclusion criteria. Post-T&A, there were still 35
children (55.5 %) with persistent mouth breathing (as defined)
Tabl e 1 Disease characteristics before and 6 months after T&A
Before T&A After T&A p
n(%) n(%)
Disease characteristics
Overall symptoms 64 (100) 26 (40.6)
Fatigue 53 (82.8) 24 (37.5) <0.001
EDS 38 (59.4) 1 (1.6) <0.001
Poor sleep 43 (67.2) 8 (12.5) <0.001
Snoring 51 (79.7) 0 (0) <0.001
Inattention 8 (12.5) 4 (6.3) 0.344
Hyperactivity 13 (20.3) 1 (1.5) <0.001
Parasomnia 15 (23.4) 1 (1.6) 0.001
<0.001
Tonsil scale
2.5 2 (3.1) 0 (0)
3 40 (62.5) 0 (0)
4 22 (34.4) 0 (0)
Mouth breathing (35 % of TST) 63 (98.4) 35 (54.7) <0.001
PSG findings
AHI, mean±SD 8.58±3.15 1.71±1.21 <0.001
AHI 1.5 64 (100) 29 (45.3) <0.001
SaO
2
nadir, mean ±SD 89.97±1.75 96.30±1.44 <0.001
Flow limitation, mean± SD) 76.88±8.61 7.81±10.91 <0.001
Statistics were performed by paired ttest and McNemar test
SD standard deviation, AT tonsillectomy and adenoidectomy, EDS exces-
sive daytime sleepiness, TST total sleep time, PSG polysomnography
Table 2 Breathing parameters depending on presence of mouthing
breathing, based on PSG performed 6 months after T&A (n=64)
Mouth
breathing
(n=35)
Without mouth
breathing
(n=29)
p
Time s pent mouth
breathing (%)
44100 % 010.3 %
Age, mean±SD 5.16±1.31 4.77±1.38 0.58
Male/female 20:15 14:15 0.161
Overall symptoms 26 (74.3) 0 (0.0 %) <0.0001
AHI, mean±SD 2.34±1.19 0.96±0.71 <0.0001
AHI 1.5 24 (68.6 %) 3 (10.3 %) <0.0001
Flow limitation, mean± SD 13.85±11.64 0.57± 1.55 <0.0001
SaO
2
nadir, mean ±SD 95.71± 1.48 97.00± 1.04 <0.0001
Mouth breathing means presence of mouth breathing during 35 % or
more of total sleep time. Statistics was performed by paired ttest for
repeated measures
SD standard deviation, AHI apnea-hypopnea index, TST total sleep time
Sleep Breath
during sleep. These children tended to have persistence of
OSA and the presence of flow limitation despite overall sig-
nificant improvement of clinical and PSG variables. As spec-
ified for inclusion, these children had no evidence of nasal
allergies, and there was no indication for orthodontic treat-
ment, which are factors that may play a role in persistent
mouth breathing. Findings suggest the presence of nasal dis-
useduring sleep in these children who previously had en-
larged adenoids and/or tonsils for some time before the deci-
sion to perform treatment. The large percentage of residual
mouth breathing children post-T&A supports clearly the no-
tion that removal of obstructive upper airway tissues does not
systematically mean return to normal nasal breathing during
sleep. This is the first study that documents this finding of
residual mouth breathing after T&A, even in absence of snor-
ing. Our finding that the normal nasal breathing children
had on average about 4 % of total sleep time [range 0 to
10 %] is in agreement with an earlier study that showed that
normal subjects spend an average of 96 % of their sleep time
with nasal breathing [18]. We had selected a cutoff point of
35 % of mouth breathing during sleep based on a small pre-
liminary study. This largest study shows that this cutoff point
is most probably incorrect, with our maximum range of 10 %
mouth breathing asleep in our asymptomatic children with
normal PSGs. To date, we would change our cutoff point to
15 % of total sleep time.
Of interest is the finding that nine children without residual
symptoms and an AHI considered as within the normal range
presented an abnormal percentage of time with mouth breath-
ing during sleep. Only two of these nine had 1-year follow-up
recordings, but both presented mild symptoms and abnormal
AHI at this follow-up indicating the need for further
investigation.
Myofunctional therapy, prescribed with an aim to
eliminate mouth breathing and reestablish nasal breath-
ing, was associated with clinical and PSG improvement
in all children who followed the recommendations. No
other therapeutic approach was recommended between a
second and a third time point except for myofunctional
therapy, though it is possible that stochastic factors such
as time of year, intercurrent illness, etc., influenced the-
se results.
Our follow-up data are limited. Out of the initial 64, or out
of the 35 recognized with mouth breathing during sleep post-
T&A, we only had 18 children that came back at 12 months
for in-laboratory PSG. Those 18 may represent a bias group;
in the children group who had undergone myofunctional ther-
apy, parents were clearly encouraged by reeducators to check
results of intervention, and in the 9 children who came back
without having had intervention, we cannot eliminate the fact
that parents may have observed presence of low-grade symp-
toms that may have led to obtain a new PSG. This is not a
double-blind randomized study. But overall, our investigation
even with limited numbers supports our hypothesis:
myofunctional therapy may help in eliminating mouth breath-
ing during sleep. There are strong data indicating that chronic
mouth breathing leads to change in orofacial growth with
impairment of maxillomandibular development relatively ear-
ly in life.
In the Rhesus monkey model [9,10], impairment of nasal
breathing leads quickly to oral-facial changes through changes
in muscle recruitment. From an orthodontic perspective, the
negative role of mouth breathing on orofacial anatomy in chil-
dren has been documented by many authors [1116], and
maxillomandibular compromised associated with nasal
Tabl e 3 Repeated measures analysis of general linear modeling for AHI, flow limitation and SaO
2
before T&A, after T&A, and at 12 months after
T&A (n= 18) in children with persistent mouth breathing post-T&A
Before T&A After T&A 12 months Wilks
lambda
pLSD
Mean (SD) Mean (SD) Mean (SD)
AHI SD 9.17 2.72 2.69 0.68 1.91 1.36 .112 <0.001 Before>after, 12 months before>after
SaO
2
SD 89.21 2.39 95.4 1.28 95.43 1.74 .142 <0.001 Before >after, 12 months
FL SD 79.43 7.30 11.4 (8.19) 7.50 12.97 .20 <0.001 Before >after, 12 months after>12 months
Legend: There is a significant change in the respiratory variables obtained with PSG between pre- and post-T&A, but there is no significant differencefor
the 18 subjects group between post-T&A PSD results and +12 months post-T&A results with a trend toward improvement overtime
Tabl e 4 Distribution of AHI, flow limitation, and SaO
2
between the
myofunctional therapy group and the non-myofunctional therapy group
at 12 months after T&A (n=18)
Myofunctional
therapy (n=9)
Non-myofunctional
therapy (n=9)
p
Mean (SD) Mean (SD)
AHI 1.1 (1.19) 2.94 (1.37) 0.015
Flow limitation 0.56 (1.67) 19.44 (14.24) 0.003
SaO
2
96.11 (1.05) 94.56 (1.67) 0.037
Statistics was performed by Mann-Whitney test
Legend: two of the asymptomatic and with normal PSG after T&A chil-
dren are in the nine untreated childrensubgroup and now present ab-
normal findings at +12-month PSG with persistence of mouth breathing
during sleep
Sleep Breath
breathing alteration has also been reported despite T&A [16].
With mouth breathing, there is a disuseof nasal breathing
with changes in proprioception, posture, and loss of usage of
the nose [26]. Such observations were made long ago by or-
thodontists treating narrow palates, crossbites, and other
maxillomandibular problems, as absence of normal nasal
breathing and persistence of mouth breathing was found to
be a handicap for positive long-term results of some orthodon-
tic treatment approaches [20]. Recently, Souki et al. [36]have
looked at the impact of mouth breathing versus nose breathing
on cephalometric measurements in children in variable stages
of dental development (mean age 4 years and 8 months versus
7 years and 9 months). These authors concluded that a signif-
icant difference is noted in the dentofacial patterns of mouth
breathing children with some differences dependent on age
[36]. But none of these studies has considered sleep and SDB.
Myofunctional treatments were developed to encourage and
establish normal orofacial muscle tone associated with normal
nasal breathing through daily exercise involving orofacial mus-
cles and stimulation of sensory pathways. In children, these
exercises are done under parental supervision and with regular
sessions with trained therapists. The training given by the ther-
apist typically involves frequent interaction in the early stages
of muscle reeducation, with longer intervals between sessions
as therapy continues. Affirming compliance with treatment is
always difficult, usage of log books kept by child and parents
and regular interaction with the trained therapist are two tools
that have been used to maintain compliance.
In conclusion, children are thought of as obligatory nose
breathersat birth, and nasal breathing is of critical develop-
mental importance for normal oropharyngeal development.
The case against mouth breathing is growing, and given its
negative consequences, we feel that restoration of the nasal
breathing route as early as possible is critical. In fact, restora-
tion of nasal breathing during wake and sleep may be the only
valid completecorrection of pediatric sleep-disordered
breathing, although the importance of establishing daytime
nasal respiration in affecting night time upper airway proper-
ties is not known. Whats more, it appears that we cannot
assume that T&A alone can be relied upon to sufficiently
restore normal breathing during sleep. Nasal breathing during
wake and sleep is the demonstration of normal respiratory
functioning in a child, and persistence of mouth breathing is
an indicator for the need for further treatment of sleep-
disordered breathing. Finally, our findings emphasize the im-
portance of post-T&A PSG investigation with monitoring all
important variables including mouth breathing.
Acknowledgments Dr. Seo-Young Lee was a visiting associate profes-
sor at the Stanford University Sleep Medicine Division and was finan-
cially supported by the Kangwon National University College of Medi-
cine during her sabbatical year. We greatly appreciated advices, com-
ments, and corrections from Dr. Stacey Quo DDS, University of Califor-
nia San Francisco Dental School.
Ethical considerations This retrospective study on data rendered anon-
ymous was approved by the IRB.
Conflict of interest None of the authors has conflict of interest.
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... Compensation is seen in the forward posture of the head. Other features may include an elongated soft palate, a high arched palate, or a longer or larger tongue [21,22]. Enlarged tongue muscles (and obstructive) may be seen resulting from tongue tie or from compensatory work demanded of it in response to the posturing of the jaw (aberrant tongue posture). ...
... The presence of mouth breathing may also negatively affect the development of craniofacial features. As Ngiam et al. and Lee et al. have demonstrated, features that develop from mouth breathing include a long face, lower frontal facial height, and a reduced inter-maxillary space [21,22]. A reduced inter-maxillary space will reduce space for the tongue in which the tongue will be displaced posteriorly into the retroglossal airway space. ...
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