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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
X
- •Contents
- •Contributors
- •1.6 Mixed Disorders
- •1.7 Isolated Symptoms
- •1.7.1 Snoring
- •1.7.2 Catathrenia
- •1.8 Summary
- •References
- •1.1 Introduction
- •1.2 Obstructive Sleep Apnea
- •1.2.1 Obstructive Sleep Apnea, Adult
- •1.2.2 Obstructive Sleep Apnea, Pediatric
- •1.3 Central Sleep Apnea
- •1.3.5 Primary Central Sleep Apnea
- •1.5 Sleep-Related Hypoxemia Disorder
- •2.7 Summary
- •References
- •3: Health Consequences of Obstructive Sleep Apnea
- •3.1 Cardiovascular Consequences
- •3.1.1 Chronic Heart Failure
- •3.1.2 Systemic Hypertension
- •3.1.3 Coronary Heart Disease
- •3.1.4 Arrhythmias
- •3.1.5 Cerebrovascular Disease
- •3.2 Respiratory Consequences
- •3.2.1 Asthma
- •3.2.3 Pulmonary Embolism
- •3.2.4 Pulmonary Hypertension
- •3.3.1 Diabetes Mellitus
- •3.3.2 Metabolic Syndrome
- •3.3.3 Sexual Dysfunction
- •3.4 Gastrointestinal Consequences
- •3.4.2 Nonalcoholic Fatty Liver Disease
- •3.5 Obstetric Outcomes
- •3.5.2 Gestational Diabetes
- •3.5.4 Maternal Surgical Complications
- •3.6 Perinatal Outcomes
- •3.6.1 Impaired Fetal Growth
- •3.6.2 Preterm Birth
- •3.6.4 Stillbirth
- •3.6.5 NICU Admission
- •3.7 Perioperative Outcomes
- •3.8 Accident-Related Consequences
- •3.9 Cancer-Related Outcomes
- •3.10 Survival Outcomes
- •3.10.1 Overall Mortality
- •3.10.2 Cardiovascular Death
- •3.10.4 Perioperative Mortality
- •References
- •4.1 Patient Case
- •4.2 Introduction
- •4.3 History
- •4.4.1 Oxygen
- •4.4.2 Vascular
- •4.4.3 Endocrine
- •4.6.1 Attention & Executive Function
- •4.6.4 Visual-Spatial
- •4.7 Summary
- •References
- •5.1 Introduction
- •5.2 Obesity
- •5.3 Hypertension
- •5.4 Diabetes Mellitus
- •5.5 Fatty Liver Disease
- •5.6 Conclusions
- •References
- •6.1 Background
- •6.2 History Taking
- •6.3 Physical Examination
- •6.4 Conclusion
- •References
- •Further Reading
- •7.1 Background
- •7.2.2 Screening Tools
- •7.2.3 Diagnostic Tests
- •7.2.7 Clinical Guidelines
- •7.3 Home Sleep Apnea Test (HSAT)
- •7.3.1 Advantages
- •7.3.2 Disadvantages
- •7.3.3 Patient Selection
- •7.3.4 Data Obtained
- •7.3.8 Recommended Follow-Up
- •7.3.9 Clinical Outcomes
- •7.4 Polysomnography (PSG)
- •7.4.1 Patient Selection
- •7.4.4 Follow-Up
- •7.5 Conclusions
- •Further Reading
- •8.1 Introduction
- •8.4 CBCT and OSA
- •8.5.1 CPAP
- •8.5.2 Oral Appliances
- •8.5.3 Maxillomandibular Advancement
- •8.6 Upper Airway Stimulation
- •8.7 Summary
- •References
- •9.1.1.1 Cranial Base Lengthening
- •9.1.1.2 Cranial Base Flexion
- •9.1.5.3 Tongue Growth
- •References
- •10.2.1.1 Cranial Base
- •10.2.1.2 Facial Height
- •10.2.1.4 Pharyngeal Airway Space
- •10.2.1.6 Hyoid Bone Position
- •10.3.1 Maxillary Expansion
- •10.3.1.4 RME for OSA
- •References
- •11.2 Pathophysiology
- •11.3 Clinical Exam
- •11.5 Treatment
- •11.6 Summary
- •References
- •12.1 Introduction
- •12.5 Mask Options
- •12.6.1 Dry Mouth
- •12.6.2 Tangled Tubing
- •12.6.3 Condensation
- •12.6.4 Headgear Problems
- •12.6.6 Ramp
- •12.6.7 Cleaning Equipment
- •12.6.8 Skin Irritation
- •12.6.9 Nasal Congestion
- •12.6.10 Aerophagia
- •12.7 Cleaning Equipment
- •12.7.1 Travel Options
- •References
- •13: Oral Appliance Therapy
- •13.1 Introduction
- •13.2 Terminology
- •13.3.2 Device Designs
- •13.4 Methodology
- •13.7.2 Device Design
- •13.7.5 Non-anatomical Traits
- •13.7.6 Disease Severity
- •13.7.7 Supine Dependency
- •13.12.3 Adherence
- •13.12.4 Mean Disease Alleviation
- •13.13 Long-Term Outcomes
- •13.16 Guidelines
- •References
- •14.1 Introduction
- •14.2 Positional Therapy
- •14.2.1 Weight Loss
- •14.2.2 Nasal EPAP Therapy
- •14.2.3 Oral Pressure Therapy
- •14.2.4 Hypoglossal Nerve Stimulation
- •References
- •15.1 Introduction: Background Information
- •15.4 Preoperative Assessment
- •15.4.1 Physical Examination
- •15.4.2 Polysomnography
- •15.4.3 Clinical History
- •15.5 Preoperative Consent
- •15.6 Preoperative Assessment
- •15.6.1 Surgical Setting
- •15.8 Instrumentation
- •15.8.1 Tonsillectomy
- •15.8.2 Adenoidectomy
- •15.9 Postoperative Management
- •15.9.1 Pain
- •15.9.2 Diet
- •15.9.3 Follow-Up
- •15.10 Expected Outcomes by Population
- •15.10.1 General Population
- •15.10.2 Complex Children
- •15.10.2.1 Obese Children
- •15.10.2.2 Down Syndrome
- •15.10.2.3 Craniofacial Syndromes
- •15.10.2.4 Synchronous Airway Lesion
- •15.11.3 Cardiovascular Parameters
- •15.13 Conclusion
- •References
- •Further Reading
- •16.1 Introduction
- •16.3.1 Anatomic Factors
- •16.8 Summary
- •References
- •17: Palatal Surgery for OSA Patients
- •17.1 Introduction
- •17.2.2 Nasopharyngeal Endoscopy
- •17.2.3 Cephalometrics
- •17.3.1.1 Success Rate of UPPP
- •17.3.1.2 Limitations of UPPP
- •17.3.1.3 Impact of UPPP
- •17.3.1.4 Complications of UPPP
- •17.3.2.2 Z-Palatopharyngoplasty
- •17.3.2.3 Expansion Sphincter Pharyngoplasty
- •References
- •18: Hypopharyngeal Surgery for OSA Patients
- •18.1 Introduction
- •18.2 Historical Perspective
- •18.3 Patient Selection
- •18.4 Physical Exam
- •18.5 Imaging I
- •18.5.1 Imaging
- •18.6 Drug-Induced Sedated Endoscopy
- •18.7 Treatment Algorithm
- •18.8 Procedures
- •18.8.1 Transoral Robotic Surgery
- •18.8.2 Radiofrequency Ablation (RFA)
- •18.8.3 Genioglossus Advancement
- •18.8.4 Tongue Base Suspension
- •18.8.5 Hyoid Suspension
- •18.8.7 Hypoglossal Nerve Stimulators
- •18.9 Future Directions
- •References
- •Suggested Reading
- •19.1.1 Imaging
- •19.2.1.1 Pierre Robin Sequence
- •19.2.1.2 Craniofacial Microsomia
- •19.2.2.1 Crouzon’s Syndrome
- •19.2.2.2 Apert Syndrome
- •19.2.3.1 Treacher Collins Syndrome
- •19.2.3.2 Goldenhar Syndrome
- •19.3 Surgical Correction
- •Bibliography
- •20.1 Introduction
- •20.4.2 Surgical Technique (DOME)
- •20.4.4 Consolidation Phase
- •20.6 Discussion
- •References
- •21.3.3 Maxillomandibular Setback
- •References
- •22.1 Introduction
- •22.3 Results
- •22.3.1 Success Rate
- •22.4 Cases
- •22.5 Discussion
- •22.6 Conclusion
- •References
- •23.1 Patient Evaluation
- •23.1.1 Patient Concerns
- •23.1.4 Facial Evaluation
- •23.1.5 Lateral View
- •23.1.6 Oral Examination
- •23.1.7 Periodontal Evaluation
- •23.1.8 Tongue Assessment
- •23.1.9 Temporomandibular Joint
- •23.1.10 The Nose
- •23.1.11 Oropharyngeal Airway Assessment
- •23.2 Radiographic Evaluation
- •23.2.2 Lateral Cephalometric Radiograph
- •23.2.5 Cephalometric Analysis
- •23.3 Dental Model Analysis
- •23.3.1 Arch Length Measurements
- •23.3.2 Tooth Size Analysis
- •23.3.3 Tooth Position
- •23.3.4 Arch Width Analysis
- •23.3.6 Cuspid-Molar Position
- •23.3.7 Tooth Arch Symmetry
- •23.3.10 Ankylosed Teeth
- •23.4 Summary
- •References
- •24.1 TMJ Articular Disc Displacement
- •24.3 Reactive Arthritis (ReA)
- •24.5 Trauma
- •24.6 TMJ Ankylosis
- •24.7 Other End-Stage TMJ Conditions
- •24.8 Summary
- •References
- •25.1 Background
- •25.2 Treatment Planning Maxillary Surgery
- •25.2.1 Bone Anatomy
- •25.2.2 Vascular Anatomy
- •25.5 Adjunct Procedures
- •25.6 Complications
- •References
- •26: Mandibular Surgical Procedures
- •26.1 Genioplasty Procedures
- •26.2 Osseous Genioplasty
- •26.2.1 Anteroposterior Augmentation
- •26.2.2 Surgical Procedure
- •26.2.3 Anteroposterior Reduction
- •26.2.4 Vertical Augmentation (Downgraft)
- •26.2.5 Vertical Reduction
- •26.3 Alloplastic Augmentations
- •26.3.1 Surgical Procedure
- •26.4 Genioplasty Complications
- •26.5 Mandibular Subapical Procedures
- •26.5.3 Possible Complications
- •26.6 Mandibular Body Surgery
- •26.7.1 Nonunion or Malunion
- •26.7.3 Infections
- •26.7.4 Periodontal Defects
- •26.7.5 Nerve Damage
- •26.8 Mandibular Ramus Surgery
- •26.9 Vertical Ramus Osteotomy
- •26.11.1 Early Relapse
- •26.11.2 Condylar Sag
- •26.11.4 Unfavorable Splits or Fractures
- •26.11.6 Periodontal Defects
- •26.11.8 Nerve Injury
- •26.11.9 Infections
- •26.11.10 Nonunion
- •26.11.11 Bleeding Problems
- •References
- •27.1 Occlusal Plane Alteration
- •27.1.1 History
- •27.2 Corrected Frankfort Horizontal Plane
- •27.3 High Occlusal Plane (HOP) Facial Type
- •27.3.6 MRI Evaluation
- •27.3.7 TMJ Disc Displacement
- •27.3.9 Reactive Arthritis
- •27.3.11 Other End-Stage TMJ Pathologies
- •27.6 Summary
- •References
- •28: Maxillomandibular Advancement
- •28.1.1 Symptoms
- •28.1.3.1 Noninvasive Treatments
- •28.1.3.2 Surgical Interventions
- •28.4.1 Preoperative Medical Assessment
- •28.5 Procedure
- •28.5.1.2 Plates Vs. Screws
- •28.7 Post-MMA Follow-Up Care
- •28.8 Conclusion
- •References
- •29.2.1 CASS Adoption Widespread
- •29.2.2 Overall CASS Accuracy
- •29.2.2.1 Soft-Tissue Prediction Simulators
- •29.2.3 Cost
- •29.4.1 Overall CASS Process
- •29.4.1.1 Step 1: Patient Referral
- •29.4.1.7 Step 7: Procedure
- •29.4.4 Case 3
- •29.5 Conclusion
- •References
- •30.1 Introduction
- •30.2 Preoperative Considerations
- •30.2.1 Surgical Facility
- •30.2.2 Medical Clearance
- •30.2.3 Anesthesia Considerations
- •30.3 Inpatient Postoperative Management
- •30.3.1 Immediate Postoperative Course
- •30.3.2 Acute Pain Management
- •30.3.5 DVT Prophylaxis
- •30.3.6 Nutrition
- •30.3.7 Antibiotics
- •30.4.1 Follow-Up Regimen
- •30.4.2 Postoperative Occlusal Guidance
- •30.5 Conclusion
- •References
- •31.1 Paradigm
- •31.2 Preoperative
- •31.3 Acute Post-surgical
- •31.4 Long-Term Post-surgical
- •References

108
S.-J. Kim and K. B. Kim
strong tendency to Class II relationships, which is in
agreement with Bjork [5] and Enlow and McNamara [6].
In this population, large cranial base angles might be
caused by a clockwise rotation of sphenoid bone and a
much greater clockwise rotation of occipital bone. In
contrast, none of the children with the smallest cranial
base angles had Class III occlusions and most were
Class I, even though their condyles were located more
forward and downward (inconsistent with the ndings
of Enlow [7] and Lavelle [8]). A likely explanation to
explain this is that their small cranial base angles might
be formed mostly by greater counterclockwise rotation
of occipital bone with less clockwise rotation of sphenoid bone.
Likewise, it should be noted that the individual bony
units of the cranial base can be remodeled or rotated
independently of each other, resulting in different mechanisms of cranial base exion and different types of craniofacial morphology. This morphometric diversity is
controlled primarily by genetics, but also affected by
9
environmental factors, such as head posture and respiratory function, before 6years of age.
essential for the forward and downward displacement of
the nasomaxillary complex determining maxillary depth
and height, additionally contributing to the development of maxillary width. Volumetric increment of nasomaxillary complex with forward and downward
displacement will increase the dimension of upper airway, at least maintaining the relative airway space and
passage in spite of the growth changes of parapharyngeal soft tissues, as will proper positioning of the mandible (mostly determined by the early growth of cranial
base).
According to the aponeurotic tension model of
craniofacial growth, brain growth and cranial rotation create cephalad tension within the interrelated
craniofacial musculoaponeurotic system (CFMAS)
of head and face, adding clarity to the mechanism of
maxillomandibular rotation, temporomandibular joint
development and positioning, and airway development
(. Fig.9.3) [9]. Rotation of the cranium at the occipital
condyles and asymmetric growth at the Sphenooccipital
synchondrosis (SOS) are proposed to cause the face to
rotate counterclockwise, opening the airway with normal jaw rotation and extension of tissues, such as lin-
9.1.1.3 Growth ofCranial Base Aecting
theUpper Airway
Under the genetic inuence, the growth of brain, skull,
and cranial base may impact the size of upper airway by
dening the relationship between the maxilla and the
mandible. Both cranial base lengthening and exion are
gual tonsils and velum. Transverse development of the
maxilla and nasal cavity, with greater posterior relative
to anterior increase, is believed to be a result of muscle mass increases leading to greater CFMAS tension,
thereby increasing the transverse airway dimension and
providing room for the tongue.
. Fig. 9.3 Algorithmic adaptation of the proposed CFG model.
Displayed is brain growth modulation of cranial rotation and
CFMAS tension. Brain growth can display temporal regional
growth and mylenization with normal development and as a result
of trauma (e.g., concussion, drug use). Cranial rotation modulates
CFMAS tension and itself is inuenced by brain development and
Brain
growth
(+/−) Trauma
Growth modularity
Cranial
rotation
(+/−) Airway /
posture
CFMAS
Strong
CFMAS
phenotype
tension
CCW
Maxillo-
mandibular
rotation
postural control. CFMAS tension manifests as a strong or weak
phenotype. A strong CFMAS phenotype will be expected to
develop a counterclockwise/forward maxillomandibular rotation,
while a weak CFMAS phenotype will be expected to develop a
clockwise/backward maxillomandibular rotation pattern. (Standerwick and Roberts [9])
Maxillo-
mandibular
rotation
Weak
CFMAS
phenotype
CW

Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
109
9
9.1.2 Postnatal Growth ofNasomaxillary
Complex
9.1.2.1 Growth Mechanisms ofNasomaxillary
Complex
The nasomaxillary complex (NMC), or midface, includes
the circummaxillary suture system connecting it to the
neurocranium and intermaxillary suture system, which
are comprised of the midpalatal, transpalatal, intermaxillary, and internasal sutures. Postnatal development of
NMC occurs principally by intramembranous ossication on the circummaxillary and intermaxillary sutures,
although the nasal septum contributes to forward and
downward displacement of the midface by cartilaginous
bone growth, especially during the rst 3–4years [10].
The compensatory sutural growth in response to midface displacement by the growth of surrounding soft
tissues leads to the majority of vertical, sagittal, and
transverse changes of midface during both childhood
and adolescence by lengthening of the anterior cranial
base during the rst 6years of age. In addition, extensive surface modeling takes place over the entire NMC
along its posterior and superior aspects.
of maxilla. Bony resorption is associated with inferior
drifts of the anterior nasal spine and the inferior–posterior drift of A-point. Resorption occurs along the oor
of nasal cavity with apposition on the roof of palate,
which increases vertical displacement of NMC and
increases nasal cavity volume. Although vertical maxillary growth rates peak during adolescence at the same
time as stature, anteroposterior maxillary growth remains
more or less constant with no distinct adolescent spurt.
9.1.2.3 Growth oftheNasomaxillary Complex
Aecting theUpper Airway
Three-dimensional changes of the nasomaxillary complex show increases in nasal cavity volume and the forward and downward displacement of the posterior nasal
spine on the hard palate. This increases the size of the
bony nasopharynx and contributes to the developing
nasopharyngeal and velopharyngeal airway, compensating the growth of adenoids and soft palate tissues and
the nasopharyngeal walls (.
9.1.3 Postnatal Growth ofMandible
Fig.9.5).
9.1.2.2 Dierential Growth ofthe
Nasomaxillary Complex
The midface undergoes differential growth in its width,
length, and height. The midface increases the most in
height, followed by increases in depth, and the least in
width. Inversely, the growth of midface ends earliest in
width, next in depth, and the latest in height.
The growth in width, which is mostly associated with
the expansion of brain and eyes separating the intermaxillary sutures between the two halves of nasal bones,
maxillae, and palatine bones, essentially diminishes at
about 7years of age when the central nervous system
completes growth. Thereafter, maxillary basal width
slowly increases from 7 to 16years of age by growth of
the midpalatal suture, as well as the buccal surface bone
apposition and expanding growth of the maxillary alveolar process. The growth activity on the midpalatal and
transpalatal sutures drops down at around 15–16years
of age [11], although the biological fusion age of those
sutures varies among studies [12–14].
In the meantime, the midface increases more dramatically in depth and height since the typical forward and
downward growth of the midface relative to the anterior
cranial base continues to be signicant, with substantially
greater vertical growth potential compared to the anteroposterior cranial base (.
placed forward and downward, compensatory bony
deposition occurs along the posterior surface of the maxillary tuberosity increasing the maxillary length despite
resorptive surface bone modeling on the anterior surface
Fig.9.4). As the midface is dis-
9.1.3.1 Growth Mechanisms ofMandible
The mandible has the greatest postnatal growth potential of any craniofacial complex structure. In contrast to
the nasomaxillary complex, both endochondral and
periosteal activities are signicantly inuential in mandibular growth, whereas displacement created by growth
of the cranial base (moving the mandibular condyle)
plays a negligible role. The overall growth pattern of the
mandible can be represented as forward and downward
translation of the chin in reference to the cranium
(. Fig.9.6), while the body and the corpus of the mandible grow longer and wider. The actual growth occurs
at the secondary cartilage on the mandibular condyle by
endochondral bone formation and along the entire surface of the mandible by differential formation and
resorption. At the same time, the mandible undergoes
substantial true vertical rotation but limited transverse
rotation. The typical pattern is forward rotation due to
greater inferior displacement of the posterior rather
than anterior aspects of the mandible, ultimately leading to a decreased mandibular plane angle.
9.1.3.2 Dierential Growth ofMandible
The greatest changes in mandibular growth occur during
the rst few years to secure the pharyngeal airway in
infancy and make room for the rapidly developing dentition. Corpus length is the most consistently mature region
(closely approximating maturity of midfacial height), followed by overall length, and ramus height is least mature
[16]. The greatest increases in mandibular length (from

110
S.-J. Kim and K. B. Kim
9
. Fig. 9.4 Result of differential growth of nasomaxillary complex in width, length, and height from neonate to adult
condyle head to chin) occur between 4 and 17years of
life, followed by corpus length and ramus height. By the
age of 5years, ramus height grows to approximately 70%
its adult size in males and 74% in females.
Like the maxilla, growth in mandibular width is typically complete prior to the spurt in adolescent growth.
Increases in length and height continue throughout
puberty. The condyle demonstrates the most growth
superiorly compared to posteriorly during later childhood and adolescence. The juvenile growth spurt prior
to the adolescent spurt is a key reason why careful evaluation of physiologic age is required to determine the
timing of orthodontic intervention, particularly in
females. Treatment planning should also consider differences between rapid-maturing girls and slow-maturing
boys because of their differences in mandibular growth,

4 years
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
particularly as they become most pronounced during
adolescence.
There is more true mandibular rotation that occurs
during childhood than adolescence compared to any time
thereafter, particularly in the transition period to early
mixed dentition at 6–7 years of age. Furthermore, the
mandible rotates transversely because of its greater posterior expansion compared to the anterior aspects of the
two corpii. Transverse rotation is also related to age. The
mandible’s posterior aspect expands between 65% and
70% as much as the posterior maxilla expands at the midpalatal suture. The growth of the mandible, therefore,
closely follows the growth of the midface. As the midface
is translated forward and downward with counterclockwise rotation, the mandible keeps pace in the normally
growing face based on that the relative rate and amount
of growth of maxilla and mandible differ over time.
9.1.3.3 Growth ofMandible Aecting
. Fig. 9.5 The aponeurotic tension model explains the effects of
angular invariance between the back of the face (behind the PM
plane) and the top of the face, which is also the bottom of the anterior cranial base (S-FC). Changes in cranial base angle cause the face
to rotate together around an imaginary axis through the PM point.
Counterclockwise rotation of the midface increases the bony nasopharynx affecting the nasopharyngeal airway length. (Standerwick
and Roberts [9])
The most critical craniofacial bony structures affecting
the upper airway size are mandible and hyoid bone
where the related muscles and soft tissues are attached.
Along with forward and downward translation of the
mandible, normal mandibular rotation is expected to
direct the tongue forward through muscle attachment at
theUpper Airway
the genial tubercles (internal surface of the mandibular
symphysis) balancing the position of hyoid bone and its
10 years
20 years
related muscle groups, to open the oropharyngeal and
hypopharyngeal airway spaces.
111
9
. Fig. 9.6 Superimposition of implants for an individual with a
normal pattern of growth, showing surface changes in the mandible
from ages 4 to 20years. As a variation between individuals, approximately a negative 10 to negative 15 degrees of internal rotation is
compensated and concealed by external rotation with surface remodeling, as is expressed by 2 to negative 4 degrees change in the mandibular plane angle. (Bjork and Skieller [15])
9.1.4 Postnatal Growth andPositional
Changes ofHyoid Bone
The hyoid bone is located between the mandibular symphysis and the larynx in the front of the neck, joining
together the cranial base, tongue, mandible, sternum, scapula, thyroid cartilage, and pharynx [17]. The hyoid bone is
suspended in the soft tissues without bony articulation
[18]. Hyoid bone position is determined by the combined
activity of suprahyoid, infrahyoid, and pharyngeal dilator
muscles, as well as changes of head posture, body position,
and oral functions. The hyoid maintains the positional
balance of the upper airway patency and upright head
position in association with tongue activity [18].
9.1.4.1 Growth ofHyoid Bone
The hyoid bone begins to ossify at the end of the third
trimester and may never fully fuse until late in life [19].
The growth trend of the different components of the
hyoid bone was similar during the rst few years of life,
while other bony structures seem to have a second phase

112
Greater cornu length left (mm)
50
50
Age (years)
Age (years)
ab
cd
S.-J. Kim and K. B. Kim
45
40
35
30
25
20
15
10
5
2468101214161820
Age (years)
9
50
45
40
35
Female
Male
45
40
35
30
25
Total length left (mm)
20
15
10
5
246810 12 14 16 18 20
Age (years)
50
45
40
35
Female
Male
30
25
20
Greater cornu width (mm)
15
10
5
2468101214161820
. Fig. 9.7 Developmental growth pilot data from ages 2 to 20 from
invivo CT scans. Despite variability in the growth trend of the different measurements, all variables show a rapid period of growth
Female
Male
of rapid growth during puberty. Cotter etal. [20] showed
a rapid period of growth during the rst few years of
life, with discrete differences in growth of different portions of the hyoid bone after about age 6–8years showing gender-specic differences as well (. Fig.9.7).
30
25
Total hyoid length (mm)
20
15
10
5
246810 12 14 16 18 20
during the rst few years of life with discrete differences in growth
after 6–8 years of age, along with the known growth differences
between sexes. (Cotter etal. [20])
Female
Male
growth periods. Under normal conditions, forward
translation of the hyoid is likely associated with the forward displacement of mandible, while the descent of the
hyoid is reported to occur mostly by vertical growth of
the cervical vertebrae [22]. According to Cotter etal.’s
longitudinal study [20], the hyoid bone descended at a
9.1.4.2 Positional Changes ofHyoid Bone
inRelation toMandible, Tongue,
andUpper Airway
The hyoid bone descends and moves slightly forward up
to age 18years [21], although the relative position of
hyoid bone is constant within the individual through
faster rate than the lowest point of mandibular symphysis, which closely parallels the behavior of the fourth
cervical vertebra in growth increment between ages 2
and 7, and thereby, the relative position of the hyoid was
maintained between the third and the fourth cervical
vertebrae afterward despite its size increase (. Fig.9.8).

Growth of adenoid tissue - infancy to adolescence
Age 13 1/2Age 9
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
113
9
PNS
Tongue
C4
MN
C4
. Fig. 9.8 Vertical growth of fourth cervical vertebra in various
age groups was compared with descent of hyoid bone, mandibular
border, tongue, and posterior nasal spine. Hyoid bone remained relatively stable to fourth cervical vertebra but moved away from border
of mandible. However, all areas displayed consistent vertical increase.
(Bench etal. [25])
Hyoid
In other aspects, Sheng etal. [23] found that the vertical position of the hyoid bone had a strong relationship
with ramus length. They deduced that the suprahyoid
muscles play a vital role in relationships between the
hyoid bone position and mandibular morphology or
position. In addition, growth increment of tongue size
relative to the oral cavity may cause downward movement of the tongue, leading to the downward and forward movement of the hyoid bone [24]. Accordingly, the
hyoid bone controls the tongue functions when its position is normally related with the cervical column, and
stable hyo-cervical relation is important to preserve the
upper airway patency, especially the retroglossal airway.
Adenoid
Tubal tonsil
Palatine tonsil
(˝tonsil˝)
Lingual tonsil
. Fig. 9.9 Intraoral view of Waldeyer’s ring comprising adenoids,
lateral pharyngeal bands, palatine tonsils, and lingual tonsils
Age 6 nos Age 2
Age 7
9.1.5 Postnatal Growth ofPharyngeal
Soft Tissues
The complex of lymphoid tissues encircling the pharynx
is referred to as Waldeyer’s ring, which includes (1) pharyngeal tonsils (adenoids), (2) lateral pharyngeal bands,
(3) palatine tonsils, and (4) lingual tonsils (. Fig.9.9).
The growth of adenoids and tonsils shows considerable
variation in size among all age groups, suggesting that
these tissues are more responsive to environmental stress
than to the classical lymphoid growth curve published
by Scammon etal. [26], which did not include measurements of the adenoids and tonsils [25].
9.1.5.1 Growth ofPharyngeal Tonsils
(Adenoids)
In a 1954 cephalometric study, Subtelny [27] found
that adenoid tissues follow a denite growth pattern
without signicant gender difference (. Fig. 9.10).
J.G.
. Fig. 9.10 Serial tracings of cephalometric head plates revealing
changes in the adenoid tissue mass with age. The stippled area represents adenoid tissue as well as the soft tissue underlying the roof
of the bony nasopharynx. (Subtelny [27])
Adenoids are not radiographically evident until
6months to 1year of postnatal life. The sloping nasopharyngeal roof looks straight or concave in conguration as it faces the superior surface of the soft palate.
The contour is replaced by convex prominence by
rapid growth of adenoids by 2–3years of age, occupying one-half of the nasopharyngeal cavity. At this
stage, the growth of adenoids occurs predominantly
downward and forward possibly affected by the growth
of upper face. Thereafter, the adenoids continue to
grow dominantly in a downward direction, but at a
retarded rate until their greatest bulk are attained as

114
S.-J. Kim and K. B. Kim
early as 10–11years or as late as 14–15years of age.
After the peak of adenoids growth, reverse growth
occurs with progressive decrease in size, and usually,
they are atrophied completely in adults.
9.1.5.2 Growth Changes ofPalatine
andLingual Tonsils
Arens etal. reported that tonsil size increases linearly in
the rst decade of life and achieved the maximum size
between 7 and 10years of age [28]. The palatine tonsils
may continue growth until 15years of age, then tend to
involute [29]. Currently, however, Oztürk [30] assessed
the palatine tonsil size using transcervical ultrasonography in 680 healthy children ranging from 1 to 17years of
age, and proposed a positive correlation between tonsil
size and age in the pediatric population. There is consensus that objective tonsil size shows wide variation that is
inuenced by both body mass index (degree of obesity)
and age [31].
9
The lingual tonsils, located in the dorsal surface at
the base of the tongue behind the foramen cecum and
the terminal sulcus, develop later than other lymphoid
tissues in the pharynx and persist into adulthood.
Enlarged lingual tonsils have been identied as a signicant cause of persistent obstructive sleep apnea (OSA),
based on the report suggesting that obese children exhibit
a higher prevalence of enlarged lingual tonsils [32].
9.1.5.3 Tongue Growth
The tongue in newborns is large relative to its small
oral cavity. At birth, the entire tongue is positioned forward and lies in the oral cavity. As the oral cavity
enlarges in concert with mandibular growth and the
larynx descends over the rst 5years of life, the base of
the tongue eventually moves backward to sit in the oropharynx. After this descent, the base of the tongue
becomes the anterior wall of oropharynx. The tongue
continues to increase in size during deciduous and
mixed dentition, keeping pace with the dropping of the
hyoid. The tongue’s overall size doubles from birth to
adolescence in thickness, length, and width. Its position is maintained or slightly dropped during 3–12years
of age [25].
The volume of the tongue and the suprahyoid muscle
groups inuence the anterior growth of the symphysis.
During the rst 2years of life, the tongue changes to a
rounder shape which may modify the position of the
suprahyoid muscle insertions at the lingual side of the
mental region by pushing them downward. Thus, the
mandibular symphysis inclines posteriorly, which
increases the prominence of the chin, and the hyoid
bone is relocated forward and downward relative to the
inferior border of the symphysis [33].
9.1.6 Postnatal Development
ofPharyngeal Airway
A newborn’s pharynx is approximately one-third the size
of an adult [34] and continuously enlarges to adult
dimensions at 6years of age [35]. Compared to adults,
the nasopharynx and oropharynx in children include
more lymphoid tissues extending into the airway [36].
9.1.6.1 Developmental Change
ofNasopharynx
The size of the soft-tissue nasopharyngeal wall and the
adenoids relative to the size of the bony nasopharynx
determines the dimension of the nasopharyngeal airway. Jeans etal. [36] evaluated the longitudinal changes
in growth of the nasopharyngeal soft tissue, the area of
the nasopharynx, and the nasopharyngeal airway from
3 to 19years of age in 41 normal children using lateral
cephalometry. The area of the nasopharyngeal bony
framework steadily increased during this period, but the
nasopharyngeal soft tissue (adenoids) grew from 3 to
5 years of age, but then remained unchanged until
19years of age. Accordingly, the nasopharyngeal airway
dimensions decrease following this same pattern.
However, the current consensus is that overall change of
nasopharyngeal airway dimension during growth is not
signicant since the growth change of the bony nasopharynx affected by craniofacial growth may cancel out
the age-dependent difference of the soft tissues. The forward and downward displacement of the posterior nasal
spine (PNS) of the hard palate with the descent of nasal
cavity oor will move the soft palate forward (decrease
of angle of soft palate inclination to the palatal plane)
to compensate the pharyngeal airway dimension.
Moreover, the age-dependent growth changes cannot
exceed the overwhelming interindividual variation [37].
9.1.6.2 Developmental Change
ofOropharynx
During the development of upright body posture in the
rst few years after birth, the oropharynx and the hypopharynx are at the crossroads between the forward positioning of the cervical vertebrae alongside the foramen
magnum under the inuence of the cranial base exion.
Hence, during early postnatal growth, the oropharyngeal airway may not increase substantially because the
mandible, the tongue, and the suprahyoid muscles are
tightly packed superiorly by the ethmomaxillary complex and posteriorly by the cervical column.
The Bolton-Brush Growth Study [38] examined 32
healthy children to investigate the pattern of skeletal
and soft-tissue growth of the oropharynx. Lateral ceph-

Distance ˝p˝
Age (y)
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
20
18
16
14
12
10
8
6
4
2
0
5678910 11
26
24
22
20
18
16
14
12
10
8
Distance ˝t˝ (mm) Distance ˝p˝ (mm)
6
4
2
0
5678910 11
Po
N
S
Ar
Or
Spa
p
Go
t
Me
Spa
A
B
Pg
Gn
12 13 14 15 16 17
Age (y)
Distance ˝t˝
12 13 14 15 16 17
115
9
. Fig. 9.11 Graphical distribution of airway distance (p) and (t)
corresponding to the age of the subjects (n=880) and Loess interpolation line. The small yet statistically signicant age-related increase
alometric analysis of untreated normal subjects at 6, 9,
12, 15, and 18years of age showed that pharyngeal soft
tissues exhibited two periods of accelerated growth periods (ages 6–9years and 12–15years) and two periods of
quiescence (ages 9–12 years and 15–18 years). The
increase in oropharyngeal width is thought to occur due
to the continued growth of the pharyngeal region and
natural involution of palatine tonsils. On the other
hand, Arens etal. [28] used MRI to assess linear dimensions of the upper airway structures in 92 normal children from 1 to 11years of age and found that the soft
tissues in the oropharyngeal airway (i.e., the tongue, soft
palate, and tonsils) maintained growth proportional to
the craniofacial skeleton growth. Any deviations in the
linearity of these relationships represent critical risk factors for Obstructive sleep apnea (OSA) in childhood.
was found, but a large interindividual distribution was apparent.
(Mislik etal. [39])
Mislik etal. [39] reported on a large sample size of 880
healthy Caucasian children (.
Fig.9.11), nding that the
dimensions of the pharyngeal airway are established in
early childhood and remain stable from 6 to 17years of
age. Mean retropalatal width (p) increased continuously
from age 6 (8.12mm) to age 17 (9.15mm), which is probably related to the size decline of the adenoids during this
growth period [40]. Mean retroglossal width (t) decreased
from age 6 (10.61mm) to age 10 (9.31mm), but increased
thereafter up to age 17 (11.19mm), a nding similar to
that of prior research [41–43]. The initial decrease of “t”
might be attributed to the distinct growth of the tongue
resembling a neural growth pattern. Thus, during the juvenile phase, tongue growth will be more intense compared
to the growth of all its surrounding structures following
visceral growth pattern.

116
S.-J. Kim and K. B. Kim
Caution should be applied when interpreting the
small yet statistically signicant age-related increases,
9.2.1 Extended Head andCervical Posture
Aecting Craniofacial Deformation
since a large interindividual distribution was apparent.
No difference was found between the genders and no
correlations of distances “p” and “t” with Point
A-Nasion-Point B angle indicating the maxillomandibular relationship (ANB) in a population of individuals
with normal growth.
It is fundamentally important to understand the contribution of postural mechanisms to normal or abnormal
craniofacial development for the diagnosis and treatment of morphological and functional disorders of the
stomatognathic system. Solow and Siersbaek-Nielsen’s
“soft-tissue stretching” hypothesis [53] links posturalinduced stretching of the soft-tissue facial layer, cranio-
9.2 Upper Airway Impairment with
Abnormal Craniofacial Growth
facial morphology, and airway adequacy into a cycle of
factors related to craniofacial morphogenesis. Softtissue layer of facial skin and muscles passively stretches
Although still somewhat controversial, it makes sense
that abnormal position of the jaws would inuence
the airway space. Craniofacial discrepancies developed
during the growth period, such as a short cranial base,
mandibular and/or maxillary retrognathism, a short
mandibular body, backward and downward rotation
9
of the mandible, and constricted maxillary width, may
all result in the reduction of pharyngeal airway dimension and passage alone or combined [44]. Decreased
space between the mandibular corpus and the cervical
column may lead to changes in posterior posture of the
tongue and soft palate, leading to not only respiratory
dysfunction during the day but also nocturnal problems,
such as snoring, upper airway resistance syndrome, and
OSA [45].
Likewise, abnormal development of the upper airway is closely related to abnormal craniofacial growth as
well as abnormal respiratory function. Considering that
genetic and environmental factors have similar impact
on craniofacial growth and dimension of the upper airway; however, it is not easy to discern if the impaired
development of the upper airway, even when abnormal
craniofacial development occurs, might be caused by
heredity or by environmental functions resulting in
abnormalities. When assessing craniofacial and pharyngeal development, differences in ethnicity and gender
should be considered. Despite the controversies, it has
been predominantly reported that there were no signicant gender differences in pharyngeal dimensions inuenced by abnormal craniofacial growth and development
in children [46–49]. Besides, a subject’s height [50] and
body weight [51, 52] are other factors positively correlated with pharyngeal airway volume.
Moreover, it is impossible to clarify a causal relationship between craniofacial deformation and abnormal
upper airway development. Nonetheless, it is important
to know that further abnormal development of craniofacial structures by delayed growth modication treatment or myofunctional therapy would be a key factor to
induce upper airway constriction and secondary development of sleep-disordered breathing (SDB).
when the head is extended in relation to the cervical column, which increases the forces on skeletal structures,
restricting forward growth of the maxilla and mandible
and redirecting them caudally.
Two longitudinal studies found a clear pattern of
associations between head and cervical posture with
craniofacial growth determined by the structural superimposition method [54, 55]. Subjects with greater cervicohorizontal and smaller craniocervical angles have
been associated with a horizontal facial growth pattern
characterized by reduced backward displacement of
the mandibular condyle, increased growth in length of
the maxilla, increased maxillary and mandibular prognathism, and larger-than-average forward true rotation
of the mandible. In contrast, subjects with lower cervicohorizontal and large craniocervical angles were associated with a vertical facial development and are likely
to exhibit large backward displacement of the mandibular condyle, reduced growth in length of the maxilla,
increased maxillary and mandibular retrognathism,
and backward true rotation of the mandible, impinging
the upper airway dimension. A recent systematic review
by Gomes etal. [56] found that greater craniocervical
and craniovertical angles were signicantly associated
with shorter maxillary and mandibular lengths and
greater maxillary and mandibular retrognathism, and a
skeletal Class II pattern (.
Fig.9.12) [57]. In vertical
aspects, greater craniocervical and craniovertical angles
were associated with a large anterior face height and a
small posterior face height, thereby presenting with a
reduced face-to-height ratio. Greater craniocervical
and craniovertical angles were also associated with a
high mandibular plane angle and a high occlusal plane
angle, as well as a hyperdivergent vertical pattern, portending increased risks of pharyngeal constriction and
breathing problems. However, because correlation
coefcients ranged from low to moderate, the authors
cautioned careful interpretation of such associations
[56]. Although posture appears to inuence facial
development, many other factors must also affect this
mechanism.

Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
with mandibular deciency had less airway volume,
less minimum axial area, and narrower retropalatal airway width than the Class I children. Zheng et al. [64]
suggested the signicance of the site of minimal crosssectional area (Min-CSA) in the upper airway among
different sagittal discrepancies (.
lyzed three-dimensional volume and the Min-CSA of
the pharyngeal airway of 60 Japanese patients (between
14 and 18years of age) with different sagittal skeletal
patterns. Class II showed the smallest mean Min-CSA,
which was usually in the upper oropharyngeal region,
whereas Class III had the largest mean Min-CSA, which
was generally found in the lower hypopharyngeal region.
Normally, Class I subjects tend to have the Min-CSA in
the lower oropharynx or upper hypopharynx.
Focusing on the oropharyngeal airway of Class III
. Fig. 9.12 Cephalometric postural variables. The convention
employed for angles related to the true vertical was that downward opening angles formed behind the true vertical (VER) were taken as negative,
whereas angles formed in front were positive. (Gomes etal. [56])
malocclusion, Iwasaki etal. [65] obtained three oropharyngeal airway shapes by cluster analysis from 45
ClasssI (mean age of 8.8years) and Class III (mean age
of 8.4years) Japanese children. They found that 84% of
children with Class I had a square oropharyngeal air-
9.2.2 Pharyngeal Airway inDierent
Sagittal Craniofacial Discrepancy
way, but 70% of the children with Class III had a relatively at shape, either left–right (55% wide type) or
anteroposterior (15% long type) (.
Class II subjects with retrognathic mandible have been
reported to have signicantly smaller airway volume
than Class I subjects [58, 59]. Relatively short and/or
posteriorly placed mandibles with respect to the cranial
base might force the tongue and soft palate back into
the pharyngeal space, causing a reduction in oropharyngeal airway volume [60]. More specically, oropharyngeal airway space has been reported to be more
vulnerable to the sagittal skeletal pattern than nasopharyngeal airway space [47, 61, 62].
Zhong etal. [61] supported the notion that skeletal
discrepancy may predispose to upper airway obstruction. They analyzed 370 healthy Chinese children (ages
11–16years) and found that widths of both the oropharyngeal and hypopharyngeal airway were greater in
Class III vs. Class I and Class II patients, though no difference was found at nasopharyngeal level. Uslu-Akcam
[63] assessed the pharyngeal airway dimension of 124
children with skeletal Class II division 1 and division 2
patterns during the prepeak, peak, and postpeak growth
periods for comparison with a skeletal Class I group.
They reported that the nasopharyngeal and oropharyngeal airway spaces showed a signicant difference among
the groups throughout the growth periods, with the
smallest dimensions in the skeletal Class II division 2
during the prepubertal period.
Alves et al. evaluated pharyngeal airway dimensions of the 50 healthy Caucasian children (mean age
9.16 years, range 8–10 years) with Class I or Class II
skeletal patterns using Cone-beam computed tomography (CBCT).They reported that the Class II children
smallest cross-sectional area was observed in the square
type. This result suggests that both volume and shape of
oropharyngeal airway are affected by tongue posture,
soft palate conguration, size of palatine tonsils, and
anteroposterior position of the mandible.
A correlation analysis between craniofacial and pharyngeal measurements showed signicant positive correlations of the Sella-Nasion-Point B (SNB; indicating
anteroposterior position of mandible) angle, indicating
anteroposterior position of mandible to the cranial base
and the pharyngeal airway space [41]. Ceylan and Oktay
[47] reported that oropharyngeal airway area decreases
with the increase of the ANB angle from lateral cephalometric analysis. El and Palomo [62] observed that oropharyngeal airway volume measured on CBCT was
signicantly negatively correlated with ANB angle and
positively correlated with the SNB angle. Hwang etal. [66]
reported that a constricted nasopharyngeal airway is correlated with detruded mandible and maxilla. Furthermore,
Trenouth and Timms [67] found that oropharyngeal airway width was positively correlated with the length of the
mandible (between gonion and menton). This was conrmed by a three-dimensional CBCT analysis on the preadolescent Korean children by Kim etal. [68], who showed
that mandibular body length had a signicant positive
correlation with total airway volume.
Cases of mandibulofacial dysostosis are characterized by bilateral and symmetrical underdevelopment of
the midface and the mandible along with a hypoplastic,
retro-positioned tongue, such as Treacher Collins syndrome and Pierre Robins sequence, which are all known
117
Fig.9.13). They ana-
Fig. 9.14). The
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