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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
118
Class III
S.-J. Kim and K. B. Kim
Class I
Class II
9
. Fig. 9.13 The minimum cross-sectional area (Min-CSA) in patients with different skeletal patterns. Class II showed the smallest Min-
CSA in both anteroposterior and transverse dimensions, but Class III showed the largest Min-CSA. (Zheng etal. [64])
causes of pediatric OSA [69]. Pierre Robin sequence
includes mandibular hypoplasia, allowing the tongue to
be posteriorly located and thereby impairing closure of
the palatal shelves that must grow over the tongue to
meet in the midline, resulting in U-shaped palatal cleft.
The tongue’s posterior displacement may impair the
action of the genioglossus muscle, an important parapharyngeal dilator known to contribute to airway
obstruction.
Studies have compared the pharyngeal airway form
in addition to the volume among different skeletal patterns in relation to the craniocervical angle. Grauer etal.
[70] assessed the pharyngeal airway form and volume in
62 Caucasian postadolescent subjects (aged between 17
and 46years) with different craniofacial pattern. They
elucidated that skeletal Class II patients had more forward inclination of the pharyngeal airway with smaller
volume, whereas Class III patients had a more vertically
oriented pharyngeal airway with larger volume
(. Fig.9.15). Consistent with these data, Oh etal. [71]
reported that the larger the craniocervical angle is, the
larger the pharyngeal angle, and the more backward
orientation of the oropharyngeal angle is evident
(. Fig.9.16) based on the correlation analysis between
craniofacial form and pharyngeal airway form in 60
healthy Korean children (mean age 11.79years, range 10
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
. Fig. 9.14 Examples of
three airway-shape types with
tongue position against the
palate and oropharyngeal
airway: a the wide type has a
at shape and a lower position
of the tongue, resulting in
reduced oropharyngeal
airway; b the long type has
hypertrophic palatine tonsils.
The tongue is positioned more
anteriorly to maintain the
oropharyngeal airway.
(Iwasaki etal. [65])
Wide Long
ab
Palate
Square
Palate
119
9
OA
Tongue
Tongue
OA
. Fig. 9.15 Different airway shapes of skeletal Class II and Class
III subjects, depicting a more vertical orientation of the airway in
Class III subjects. a, c This nding was statistically signicant.
b, d Differences between subjects in the vertical groups are less
apparent; differences not statistically signicant. (Grauer etal. [70])
120
ab
cd
ef
S.-J. Kim and K. B. Kim
9
. Fig. 9.16 Types of pharyngeal airway form according to anteropos-
terior facial patterns. a, c More backward orientation of the oropharyngeal airway to the FH plane in skeletal Class II group. b, d More vertical
orientation of the oropharyngeal airway in skeletal Class III group. The
anterior border of the nasopharyngeal airway, which is the coronal
plane passing through the posterior nasal spine (PNS) and superior tip
of the nasopharyngeal airway: (1) ang- PA, (2) ang-oropharyngeal airway, (3) Vol-NA, and (4) Vol- oropharyngeal airway. (Oh etal. [71])
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
121
9
and 13years). The inclination of oropharyngeal airway
to the FH plane in the sagittal plane (ang-oropharyngeal airway) was greater in Class II with more backward
pharyngeal form than in Class III.The ang-oropharyngeal airway had signicant correlation with the ANB
angle and Pog-N perpendicular at around the puberty
of growth.
Currently, however, upper airway dimensions differ
in various sagittal skeletal patterns and remain controversial. Some studies found a weak relationship between
growth pattern, craniofacial morphology, and pharyngeal airway [59, 72–74]. Allhaija etal. [46] reported that
sagittal skeletal patterns were weakly correlated with
glosso- and hypo-pharyngeal dimensions, but still statistically signicant. De Freitas etal. [75] reported that the
sagittal skeletal pattern does not inuence retropalatal
airway width; furthermore, both sagittal and the vertical
growth patterns also do not inuence retroglossal airway width.
A recent systematic review on the upper airway
dimensions in different sagittal craniofacial patterns
included only 11 of 758 identied studies in their nal
review [76]. Roughly 75% of studies did not report differences in the nasopharyngeal dimensions among craniofacial patterns. Because 5 of the 11 studies found
these to be smaller in Class II subjects, and 6 of 11 studies concluded that oropharynx size is larger in Class III
pattern, the oropharyngeal dimension ndings are controversial. Furthermore, the vertical growth type of the
subjects was not considered in ve of the investigations,
and 45% of the included studies used lateral cephalometry as their only tool for assessing airway dimensions.
The clinical signicance and reliability of the SNB
angle and the ANB angle have been debated in the literature [77].
Although these are still widely used parameters to
describe anteroposterior dentofacial discrepancies, it
should be recognized that they have limitations inuenced by many variables, such as morphology of the
nasion area, the vertical dimensions of the face, and the
inclination of the anterior cranial base. Therefore, threedimensional evaluation incorporating the inuence of
sagittal, vertical, and transverse skeletal patterns simultaneously is recommended when interpreting the inuence of developing skeletal discrepancy on the upper
airway volume and shape.
9.2.3 Pharyngeal Airway inDierent
Vertical Craniofacial Discrepancy
Vertical craniofacial discrepancy might develop during
pubertal growth because of several etiologic factors,
which may include abnormal growth of the maxilla and
mandible, dentoalveolar development, and function of
the tongue [78]. According to Schudy [79] and Isaacson
etal. [80], backward mandibular rotation and bite opening occur when vertical growth of condyles is less than
that of the craniofacial sutures and alveolar process. It
has been suggested that Class I subjects with vertical
growth patterns may exhibit narrower airway passages
than subjects with horizontal growth patterns.
Ucar et al. [81] conducted a lateral cephalometric
analysis and identied signicant differences between
vertical skeletal patterns and airway dimensions in
ClassI subjects. When 31 low-angle subjects (mean age,
14.0years), 40 high-angle subjects (mean age, 12.7years),
and 33 normal-angle subjects (mean age, 13.9 years)
with Class I malocclusion were examined, signicant
differences were found between the low-angle and highangle groups at the level of the nasopharyngeal airway
space, the palatal tongue space, the upper posterior airway space (PAS), and tongue gap. Furthermore, the
authors reported that the nasopharyngeal airway space
and upper PAS decreased from low angle to normal to
high angle, and the tongue gap distance was greater in
high-angle subjects vs. normal- and low-angle subjects.
These ndings were conrmed by CBCT study comparing the pharyngeal airway volume among different vertical skeletal patterns of 100 healthy Turkish young adult
patients (aged 18–30years) with normal sagittal skeletal
pattern [82]. Accordingly, total airway volume, as well as
individual nasopharyngeal and oropharyngeal volumes,
was lowest in the high-angle group (mean age 23.9years)
and highest in the low-angle group (mean age 24.3years).
Park et al. [83] investigated morphometric growth
changes of the nasopharyngeal space in association with
the development of the adenoids in different vertical craniofacial features. The authors assessed a longitudinal
sample of Caucasian children (4–13years of age) using
lateral cephalometric radiography (.
reported that the hyperdivergent types started with greater
nasopharyngeal airway areas than did the hypodivergent
types, but this relationship reversed with time. Even
though the distance from the most superior point of adenoid tissue to the posterior nasal spine (PNS) was consistently greater for the hyperdivergent types across all age
groups (supposedly due to the forward and downward
movement of the PNS), the nasopharyngeal airway area
became smaller than that in the hypodivergent group
after 8years of age. It was posited that this was attributable to more pronounced adenoid enlargement that lasted
longer in the hyperdivergent types. However, one limitation of this study was that conclusive evidence was lacking to establish a causal relationship.
On the contrary, Grauer etal. [70] showed in their
study that there was no signicant difference in pharyngeal airway volumes among long, normal, and short
facial height groups. One limitation was the fact that
vertical grouping was performed simply by dividing the
sample by face height although each subject belonged to
both a sagittal group and a vertical group. Many sub-
Fig. 9.17). They
122
CombinedHyper divergent
4 yrs 5 yrs 6 yrs 7 yrs 8 yrs 9 yrs10 yrs 11 yrs 12 yrs 13 yrs
S.-J. Kim and K. B. Kim
4 yrs 5 yrs 6 yrs 7 yrs 8 yrs 9 yrs10 yrs 11 yrs 12 yrs 13 yrs
4 yrs 5 yrs 6 yrs 7 yrs 8 yrs 9 yrs10 yrs 11 yrs 12 yrs 13 yrs
Hypo divergent
. Fig. 9.17 Mean shapes of the adenoids according to chronologic age for the hyperdivergent and hypodivergent subjects are shown
together and separately. (Park etal. [83])
9
jects with longer faces also were classied as skeletal
Class II or Class III, whereas those with shorter faces
tended to be classied as skeletal Class I.Bias from this
source may be responsible for false differences in airway
volumes between the vertical groups or to conceal the
real differences.
9.2.4 Upper Airway inTransverse
Craniofacial Discrepancy
Underdevelopment of the nasomaxillary complex in a
transverse dimension (especially underdevelopment of
that nasal cavity, maxilla, and hard palate) has not been
clearly described as an etiologic factor of airow reduction and OSA.Guilleminault etal. [84] studied the relationship between maxillary constriction and the etiology
of OSA, suggesting a familial tendency of narrow high
palates in the relatives of OSA patients. Cistulli and
Sullivan [85] showed a high prevalence of OSA with elevated nasal airway resistance in patients with Marfan syndrome who have characteristic constricted maxilla and
high-arched palate. Zhao et al. [86] reported that their
CBCT analysis of oropharyngeal airway volume showed
that it was signicantly smaller in growing patients with
maxillary constriction than in those without constriction.
On the other hand, Johal etal. [87] investigated the role of
maxilla in the etiology of OSA and found no signicant
maxillary morphological differences between OSA groups
and normal subjects, except for the signicant difference
of the palatal angle (ANS-PNS-uvula).
It is not possible to determine from the literature
whether transverse skeletal discrepancies are etiologic
factors for airway constriction and pediatric sleep-
disordered breathing. It remains questionable as to
whether maxillary constriction can be a primary etiological factor or a resultant factor in OSA and, more
importantly, whether or not treatment directed at maxillary expansion is supported by sufcient evidence.
In summary, the effect of anteroposterior or transverse skeletal relationships on the upper airway dimension is not completely understood. Not all children with a
retruded mandible or constricted maxilla will have airway
problems; however, the upper airway of the children with
retruded jaws with a hyperdivergent growth pattern may
need special attention and, potentially, early intervention.
9.3 Craniofacial Alteration by Abnormal
Respiratory Function
While some researchers have found no association
between airway function and dentofacial morphology
[88–92], there seems to be consensus that healthy nasal
breathing with adequate pharyngeal patency plays a role
in the favorable development of the dentofacial complex.
Any obstruction in nasal breathing will affect various
fundamental orofacial functions during early development causing SDB and can be a risk factor of craniofacial deformation beyond the inherited skeletal pattern.
9.3.1 Prevalence ofCraniofacial
Deformation inSDB Children
Ameli etal. [93] orthodontically evaluated a cohort of
118 suspected pediatric OSA patients prior to prearranged adenotonsillectomy and found that 65% of them
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
123
9
. Fig. 9.18 Inuence of
sleep-disordered breathing
on orofacial growth.
(Guilleminault etal. [101])
Frequent respiratory
dysfunction
Swollen nasal
mucosa
Enlarged adenoids
and tonsils
Lowered tongue
position
Constricted
Maxillary arch
had malocclusion. According to Kim and Guilleminault
[94], 93.3% of 400 nonobese children (between 2 and
17years of age) with diagnosed SDB had craniofacial
features considered to be risk factors for SDB, including
small retruded mandible and high and narrow hard palate associated with narrow nasomaxillary complex.
Craniofacial dysmorphosis in the nonobese or slightly
obese patients with OSA is commonly recognized, which
may be associated with a genetic or epigenetic predisposition or a growth disorder during childhood [95]. On
the other hand, severely obese children with OSA (mean
body mass index of 48kg/m2) were observed to have no
signicant craniofacial abnormalities [96]. Instead, dysfunction seemed to be related to the changes around the
upper airway soft tissues, head posture, and hyoid bone
position induced by obesity [97, 98]. The prevalence of
craniofacial deformation in OSA patients may therefore
vary depending on the obesity, severity of OSA, age,
gender, and race of the study sample.
9.3.2 Craniofacial Alteration by Physical
Upper Airway Obstruction inChildren
It was previously assumed that enlarged adenoids and
palatine tonsils were the major cause of SDB in early
childhood. Long-standing inuence of nasopharyngeal
obstruction by adenotonsillar hypertrophy on the facial
morphology is described as “adenoid face” or “longface syndrome” [99]. Physical upper airway obstruction
gives rise to mouth breathing and environmental impair-
Nasal septal
deviation
Reduced
Nasal breathing
Mouth breathing
Craniofacial
deformation
Constricted
maxillary arch
Decreased nasal
cavity width
Extended head
posture
Lowered
mandibular posture
ment of orofacial muscle activity, particularly in the
geniohyoid, the genioglossal muscles of the tongue, the
suprahyoid dorsal tongue bers, the upper lip elevators,
and the digastric muscles. Impaired nasal breathing had
an impact on the development of nasomaxillary complex in related to the extended head posture, and secondarily on the mandibular position. The position of
the condyle in the articulation changes transferring cartilaginous production more posteriorly [100]. This will
alter the incline at which bone grows, causing a posterior
mandibular rotation narrowing the upper airway conversely. This leads to craniofacial deformation such as
vertical maxillary excess, constricted maxilla, high palatal vault, retrognathic mandible, long face with hyperdivergent vertical pattern, and excessive lower facial
height, which deteriorates the airway dimension and
mouth breathing, particularly during sleep (. Fig.9.18)
[101]. McNamara [102] insisted that there was a potential interaction between the respiratory obstruction and
vertical growth patterns based on the comparison of
clinical cases between patients with untreated nasopharyngeal obstruction and patients who chose adenotonsillectomy (. Fig. 9.19). Even with a normal sagittal
skeletal relationship, the mouth breather exhibited the
increase in anterior facial height and relative posterior
displacement of the maxillary complex, causing the face
to become more retrognathic (. Fig.9.20).
In terms of hyoid bone position, it was found that
the children with enlarged tonsils impinging on the
oropharynx had a more inferiorly positioned hyoid
bone in reference to the mandibular plane (hyoid to
124
S.-J. Kim and K. B. Kim
a
c
IDEAL
9 - 0 11 - 0
8 - 9 12 - 3
42 months
b
7 - 28 - 4
14 months
d
12 - 0
16 - 9
57 months
9
. Fig. 9.19 A, Ideal face growth from 9 to 11years of age: The
maxilla descended vertically with nasion and point A retaining the
same anteroposterior relationship. The mandible was displaced forward with condylar growth, and the mandibular plane angle was
slightly decreased. B, Growth in children who underwent adenotonsillectomy from 7years 2months to 8years 4months of age: Dramatic closure of the mandibular plane angle and reduction of vertical
growth pattern occurred without any orthodontic intervention. C,
Growth in children with untreated nasopharyngeal obstruction from
mandibular plane, H-MP) [103]. However, there were
no signicant differences observed between the
enlarged tonsils groups and the normal children when
the sagittal position of the hyoid bone was compared
in relation to either the cervical spine or the gnathion
(the most anterior and inferior point of the symphysis). Nelson etal. [104] reported that snorers showed a
lower position of the hyoid bone with respect to the
mandibular plane (greater H-MP distance) during the
prepubertal and pubertal period. Even in adults, snorers displayed lower position of the hyoid compared to
nonsnorers.
Regarding the mechanism of craniofacial alteration,
adenoids and tonsils inuence function due to their relative size compared to the available space in the pharynx
and not because of their absolute size [105]. Because of
their entrapment in a relatively small space due to adenotonsillar hypertrophy, pharyngeal soft tissues will also
become functionally impaired. If this impairment is
counteracted by an increase in tongue and facial muscle
8years 9months to 12years 3months of age: Vertical facial growth
pattern with increased anterior facial height was noted and posterior
maxillomandibular rotational displacement caused the face more retrognathic. D, Growth in children with complete pharyngeal airway
obstruction by surgical intervention of submucous cleft of soft palate
from 12years to 16years 9months of age: Severe distortion of facial
pattern was progressed presumably due to pharyngeal ap surgery
which might cause the alterations in neuromuscular function and the
subsequent adaptation necessary for maintaining oral respiration
activity, there may be no soft-tissue functional decits.
However, patients with inadequate tongue and facial
muscle strengthening to counteract soft-tissue impairment will not return to normal breathing even after
treatment like adenotonsillectomy or nasal allergy.
Harvold [106] speculated that the nature of the structural alterations produced by nasal obstruction in experimental monkeys depended on their unique, individual
ability to achieve neuromuscular adaptation. If there is
a direct form-and-function relationship between nasal
obstruction and the course of craniofacial alteration, it
can be assumed that removal of the causative obstruction would initiate a reversal of functional changes,
leading to a gradual corrective change in the previously
altered craniofacial conguration. However, this does
not always happen. The understanding of these relationships between function and growth of the craniofacial structures gave rise to the necessity of myofunctional
therapy to correct the decits caused by abnormal
growth patterns.
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
125
9
. Fig. 9.20 A patient who showed craniofacial alteration of
increased vertical dimension and retruded chin at 3.5years after
tonsillectomy. Persistent mouth breathing with low tongue posture
Macari etal. [107] performed a study whose results
have great clinical signicance to help determine the
optimal timing of early adenoidectomy in consideration
of the critical age of irreversible dysmorphologic growth
change. They evaluated the relationship between adenoid hypertrophy and facial morphology in children
(mean age: 6years) dividing groups younger than 6years
and older than 6 years. Facial dysmorphology developed, starting with the maxilla, tilted posteroinferiorly
as measured by reverse inclination of palatal plane
(around −8°), at mean age of 4.37years in the younger
group (<6years) with the smallest distance between the
adenoid and soft palate. This study implies that early
clearance of the nasal passage is required to arrest or
reverse facial alteration in the most severely affected
children.
Again, however, this is not always the case. Studies
of various clinical populations have indicated that
mouth breathing by respiratory obstruction existed in
patients with a variety of sagittal and vertical skeletal
types [94, 106, 108]. Feres etal. [109] insisted that there
was no difference between obstructive and nonobstructive patients concerning all cephalometric skeletal vari-
probably in relation to narrow retroglossal airway with residual
lingual tonsils might aggravate Class II hyperdivergent skeletal
pattern
ables. Furthermore, correlations between skeletal
parameters and the percentage of adenoid obstruction
were reported to be low or insignicant (. Fig.9.21).
9.3.3 Craniofacial Characteristics
ofPediatric SDB Patients
Previous studies in nonsyndromic children with SDB
symptoms have shown a positive association with craniofacial disharmony [110–112]. The evidence from case
series and some excluded trials have suggested that
mouth-breathing children with OSA largely present with
a retrognathic mandible, micrognathia, excessive lower
anterior face height with increased mandibular plane
angle, and narrow maxilla with a high palate [113–116].
On the other hand, Huynh etal. [110] demonstrated
that SDB symptoms in the pediatric cohort were primarily associated with the long face with increased vertical dimension and the narrow face with transverse
deciency, whereas the anteroposterior skeletal deciency like retrognathism was not signicantly related to
the SDB symptoms. These ndings were obtained from
126
S.-J. Kim and K. B. Kim
9
. Fig. 9.21 Different facial growth patterns of young children with adenotonsillar hypertrophy. The patient at left showed a Class II hyper-
divergent pattern with extended head posture, whereas the patient at right showed a Class III hypodivergent pattern. (Feres etal. [109])
604 Canadian orthodontic population (mean age
13.01years; range 7–17years).
Kim etal. [117] discovered that some Korean chil-
dren aged 9–11 years who had impaired respiration
exhibited protrusive growth of the maxilla and mandible in puberty. The authors explained that the active
compensational changes of facial growth for the narrow
airway might result in a Class III skeletal relationship.
Anderson etal. [118] categorized the craniofacial patterns of 236 Korean children with chronic snoring into
three characteristic clusters according to different age
groups (. Fig. 9.22): cluster 1 included younger children 5–8 years of age with increased vertical discrepancy and without denite sagittal skeletal discrepancy;
cluster 2 included older children 9–12years of age with
progressed sagittal and vertical discrepancy representing
a skeletal Class II, hyperdivergent pattern; and cluster 3
included children aged 7–8years of age with a skeletal
Class III, hyperdivergent pattern. The authors agreed
that adenotonsillar hypertrophy-related snoring might
cause earlier inuence on vertical growth pattern, showing no typical sagittal pattern of craniofacial alteration,
a nding supported by a more recent study of 30
Caucasian children with nasal obstruction-related primary snoring [119].
Other contradictory studies did not report such associations [120, 121]. A recent systematic review by Katyal
et al. [122] concluded that evidence of a direct causal
effect between craniofacial structure and pediatric SDB
was lacking, even though there was strong support for
reduced upper airway dimension in children with OSA
(between 0 and 18years of age). Children with SDB had
an increased ANB angle but by less than 2 degrees compared to controls, which could be regarded as having
marginal clinical signicance. The mandibular plane
angle showed a trend toward hyperdivergence, but with
signicant heterogeneity across the studies. This nding
is in contrast to prior studies, showing increased lower
anterior face height and mandibular plane hyperdivergence in adults with OSA [123, 124].
Cluster 1
Cluster 2Cluster 3
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
127
9
In summary, inherent craniofacial growth might be
altered by functional problems of respiratory obstruction and SDB despite present controversies arising
from limitations of methodologic inconsistency across
studies (. Table9.1). This suggests that early inter-
. Fig. 9.22 Simplied
three-dimensional scatter plots
describing the result of a cluster
analysis. a A scatter plot
constructed using the factors
ANB (X-axis), age (Y-axis), and
FMA (Z-axis). b A scatter plot
constructed using the factors age
(X-axis), ANB (Y-axis), and
FMA (Z-axis). Three clusters
can be identied in the three
dimensions, and clusters 1, 2,
and 3 are indicated by blue, red,
and green dots, respectively.
(Anderson etal. [118])
45
40
35
30
25
20
15
ANB (°)
5
678910 11 12
FMA (°)
FMA (°)
vention to treat pediatric SDB improving nasal breathing, such as adenotonsillectomy and nasal allergic
treatment, should be considered to prevent irreversible craniofacial alteration, especially in the vertical
direction.
Age (yr)
10
5
0
–5
–10
Cluster 1
Cluster 2Cluster 3
45
40
35
30
25
20
15
15 10 50
Age (yr)
–5 –10
ANB (°)
12
11
10
9
8
7
6
5