Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
Cone-Beam CT Use forAirway Imaging
97
8
. Fig. 8.13 Three-dimensional rendering images of the upper air-
way with cone-beam computed tomography for one patient. a Resting breathing: Sagittal view during a cycle of resting breathing
showing the upper airway volume. b Application of positive pressure
(+10 cm H
+10cm H2O with an increase in the airway volume. c Frontal view in
resting breathing. d Frontal view in positive pressure of +10cm H2O
O) by facemask. Sagittal view during application of
2
98
J. M. Palomo et al.
8
. Fig. 8.14 Three-dimensional rendering images of the upper air-
way with cone-beam computed tomography for one patient. a Resting breathing: sagittal view during a cycle of resting breathing
showing the upper airway volume b Application of negative pressure
(−2 cmH
H2O with an increase in the airway volume. c Frontal view in resting
breathing d Frontal view in negative pressure of −2cm H2O
O) by facemask. Sagittal view during application of -2cm
2
Cone-Beam CT Use forAirway Imaging
99
8
. Fig. 8.15 Three-dimensional rendering images of the upper air-
way with cone-beam computed tomography for one patient. a Resting breathing: Sagittal view during a cycle of resting breathing
showing the upper airway volume. b Same patient with oral appliance showing an increase in the airway volume. c Frontal view in
resting breathing. d Frontal view with an oral appliance in place
100
J. M. Palomo et al.
8
. Fig. 8.16 Three-dimensional rendering images of the upper air-
way with cone-beam computed tomography for one patient. a Resting breathing: sagittal view during a cycle of resting breathing
showing the upper airway volume. b Same patient after MMA showing increase in the airway volume. b Frontal view in resting breathing. d Frontal view after MMA
Cone-Beam CT Use forAirway Imaging
101
8
. Fig. 8.17 Three-dimensional rendering images of the upper air-
way with cone-beam computed tomography for one patient. a Resting breathing: Sagittal view during a cycle of resting breathing
showing the upper airway volume. b Sagittal view during stimulation
AHI generally between 20 and 60/hour, (c) >75% of the
AHI being obstructive apneas and hypopneas, and (d)
closure during drug-induced sedation endoscopy showing a predominant anteroposterior collapse at the level
of the velopharynx. Subjects were evaluated by CBCT
scans and lateral cephalograms in regular breathing,
during UAS therapy. The rst scan was taken during a
cycle of resting breathing. The second scan was taken
during stimulation at voltage amplitude at or near that
used therapeutically during sleep in that patient. The
of the hypoglossal nerve with an increase in the upper airway volume. c Frontal view in resting breathing. d Frontal view during hypo-
glossal nerve stimulation
CBCT volumes taken under UAS of the hypoglossal
nerve showed a signicant increase along the upper airway (+48%). The hypopharynx increased 63%, followed
by the oropharynx with 54%, and the nasopharynx
with a 15% increase (. Fig.8.17). In six of seven subjects, the minimal cross-section area was found in the
retropalatal airway, while for the others, it was in the
nasopharynx. The average minimal cross-section area
2
before stimulation was 100.5mm
and after stimulation
it was 139.2mm2 [25].
102
J. M. Palomo et al.
8.7 Summary
This chapter outlines how CBCT can be used to assess
the airway for both diagnosis and treatment outcome
assessment. A CBCT alone cannot provide a diagnosis
for sleep apnea, but it has its uses, specially in monitoring and helping with treatment considerations. A lateral
cephalogram should not be used to assess the airway,
since it does not portray mediolateral information or
changes.
References
1. Strauss RA, Burgoyne CC.Diagnostic imaging and sleep medicine. Dent Clin N Am. 2008;52(4):891–915, viii.
2. Schwab RJ, Goldberg AN. Upper airway assessment: radiographic and other imaging techniques. Otolaryngol Clin N Am.
8
1998;31(6):931–68.
3. El H, Palomo JM. Measuring the airway in 3 dimensions: a
reliability and accuracy study. Am J Orthod Dentofac Orthop.
2010;137(4 Suppl):S50 e1–9; discussion S50–2.
4. Palomo JM, Rao PS, Hans MG. Inuence of CBCT exposure
conditions on radiation dose. Oral Surg Oral Med Oral Pathol
Oral Radiol Endod. 2008;105(6):773–82.
5. Osorio F, etal. Cone beam computed tomography: an innovative
tool for airway assessment. Anesth Analg. 2008;106(6):1803–7.
6. Ludlow JB, Walker C.Assessment of phantom dosimetry and
image quality of i-CAT FLX cone-beam computed tomography.
Am J Orthod Dentofac Orthop. 2013;144(6):802–17.
7. Ghoneima A, Kula K.Accuracy and reliability of cone-beam
computed tomography for airway volume analysis. Eur J Orthod.
2013;35(2):256–61.
8. Lagravere MO, etal. Three-dimensional accuracy of measurements made with software on cone-beam computed tomography
images. Am J Orthod Dentofac Orthop. 2008;134(1):112–6.
9. Schendel SA, Hatcher D.Automated 3-dimensional airway analysis from cone-beam computed tomography data. J Oral Maxillofac Surg. 2010;68(3):696–701.
10. Amirlak B, etal. Volumetric analysis of simulated alveolar cleft
defects and bone grafts using cone beam computed tomography.
Plast Reconstr Surg. 2013;131(4):854–9.
11. Tsolakis IA, et al. When static meets dynamic: comparing
cone- beam computed tomography and acoustic reection
for upper airway analysis. Am J Orthod Dentofac Orthop.
2016;150(4):643–50.
12. Smith T, etal. Three-dimensional computed tomography analysis of airway volume changes after rapid maxillary expansion.
Am J Orthod Dentofac Orthop. 2012;141(5):618–26.
13. RPJ W, Landers M, Hans MG.Anatomically based cranial landmarks for three dimensional superimposition. In: Orthodontic
department: Case Western Reserve University; 2011.
14. Strohl KP, Redline S.Nasal CPAP therapy, upper airway muscle
activation, and obstructive sleep apnea. Am Rev Respir Dis.
1986;134(3):555–8.
15. Ogawa T, etal. Evaluation of cross-section airway conguration
of obstructive sleep apnea. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod. 2007;103(1):102–8.
16. Enciso R, et al. Comparison of cone-beam CT parameters
and sleep questionnaires in sleep apnea patients and control
subjects. Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2010;109(2):285–93.
17. Buchanan A, et al. Cone-beam CT analysis of patients with
obstructive sleep apnea compared to normal controls. Imaging
Sci Dent. 2016;46(1):9–16.
18. Cohen AM, Vig PS.A serial growth study of the tongue and
intermaxillary space. Angle Orthod. 1976;46(4):332–7.
19. Nelson S, Cakirer B, Lai YY.Longitudinal changes in craniofacial factors among snoring and nonsnoring Bolton-Brush study
participants. Am J Orthod Dentofac Orthop. 2003;123(3):338–
44.
20. Sforza E, et al. Upper airway collapsibility and cephalometric
variables in patients with obstructive sleep apnea. Am J Respir
Crit Care Med. 2000;161(2 Pt 1):347–52.
21. Schendel SA, Broujerdi JA, Jacobson RL. Three-dimensional
upper-airway changes with maxillomandibular advancement
for obstructive sleep apnea treatment. Am J Orthod Dentofac
Orthop. 2014;146(3):385–93.
22. Verin E, etal. Comparison between anatomy and resistance of
upper airway in normal subjects, snorers and OSAS patients.
Respir Physiol. 2002;129(3):335–43.
23. Hevener B, Hevener W. Continuous positive airway pressure
therapy for obstructive sleep apnea: maximizing adherence
including using novel information technology-based systems.
Sleep Med Clin. 2016;11(3):323–9.
24. Patel SR, et al. Continuous positive airway pressure therapy
for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med.
2003;163(5):565–71.
25. ElShebiny T, et al. Hyoid arch displacement with hypoglossal
nerve stimulation. Am J Respir Crit Care Med. 2017;196(6):790–2.
26. Ng AT, etal. Effect of oral appliance therapy on upper airway
collapsibility in obstructive sleep apnea. Am J Respir Crit Care
Med. 2003;168(2):238–41.
27. Kushida CA, et al. Practice parameters for the indications for
polysomnography and related procedures: an update for 2005.
Sleep. 2005;28(4):499–521.
28. Doff MH, etal. Oral appliance versus continuous positive airway pressure in obstructive sleep apnea syndrome: a 2-year follow- up. Sleep. 2013;36(9):1289–96.
29. George PT. Selecting sleep-disordered-breathing appliances. Biomechanical considerations. J Am Dent Assoc. 2001;132(3):339–47.
30. Doff MH, et al. Long-term oral-appliance therapy in obstructive sleep apnea: a cephalometric study of craniofacial changes.
J Dent. 2010;38(12):1010–8.
31. Doff MH, etal. Long-term oral appliance therapy in obstructive
sleep apnea syndrome: a controlled study on dental side effects.
Clin Oral Investig. 2013;17(2):475–82.
32. Chan AS, et al. The effect of mandibular advancement on
upper airway structure in obstructive sleep apnoea. Thorax.
2010;65(8):726–32.
33. Almeida FR, etal. Long-term sequellae of oral appliance therapy in obstructive sleep apnea patients: part 2. Study-model
analysis. Am J Orthod Dentofac Orthop. 2006;129(2):205–13.
34. Hammond RJ, etal. A follow-up study of dental and skeletal
changes associated with mandibular advancement splint use
in obstructive sleep apnea. Am J Orthod Dentofac Orthop.
2007;132(6):806–14.
35. Robertson C, Herbison P, Harkness M. Dental and occlusal
changes during mandibular advancement splint therapy in sleep
disordered patients. Eur J Orthod. 2003;25(4):371–6.
36. Buttereld KJ, etal. Linear and volumetric airway changes after
maxillomandibular advancement for obstructive sleep apnea. J
Oral Maxillofac Surg. 2015;73(6):1133–42.
37. Fairburn SC, etal. Three-dimensional changes in upper airways
of patients with obstructive sleep apnea following maxillomandibular advancement. J Oral Maxillofac Surg. 2007;65(1):6–12.
Cone-Beam CT Use forAirway Imaging
103
8
38. Gale A, Kilpelainen PV, Laine-Alava MT. Hyoid bone position after surgical mandibular advancement. Eur J Orthod.
2001;23(6):695–701.
39. Pirklbauer K, etal. Maxillomandibular advancement for treatment of obstructive sleep apnea syndrome: a systematic review. J
Oral Maxillofac Surg. 2011;69(6):e165–76.
40. El AS, et al. A 3-dimensional airway analysis of an obstructive sleep apnea surgical correction with cone beam computed
tomography. J Oral Maxillofac Surg. 2011;69(9):2424–36.
41. Woodson BT, etal. Three-year outcomes of cranial nerve stimulation for obstructive sleep apnea: the STAR trial. Otolaryngol
Head Neck Surg. 2016;154(1):181–8.
42. Woodson BT, etal. Randomized controlled withdrawal study of
upper airway stimulation on OSA: short- and long-term effect.
Otolaryngol Head Neck Surg. 2014;151(5):880–7.
43. Strollo PJ Jr, et al. Upper-airway stimulation for obstructive
sleep apnea. N Engl J Med. 2014;370(2):139–49.
44. Soose RJ, etal. Upper airway stimulation for obstructive sleep
apnea: self-reported outcomes at 24 months. J Clin Sleep Med.
2016;12(1):43–8.
45. Eisele DW, Schwartz AR, Smith PL.Tongue neuromuscular and
direct hypoglossal nerve stimulation for obstructive sleep apnea.
Otolaryngol Clin N Am. 2003;36(3):501–10.
105
Craniofacial Morphology
Related toObstructive Sleep
Apnea: Growth ofCraniofacial
Bones andtheUpper Airway
Su-JungKim andKiBeomKim
Contents
9.1 Upper Airway Development withNormal
Craniofacial Growth – 106
9.1.1 Postnatal Growth oftheCranial Base – 106
9.1.2 Postnatal Growth ofNasomaxillary Complex – 109
9.1.3 Postnatal Growth ofMandible – 109
9.1.4 Postnatal Growth andPositional Changes ofHyoid Bone – 111
9.1.5 Postnatal Growth ofPharyngeal Soft Tissues – 113
9.1.6 Postnatal Development ofPharyngeal Airway – 114
9
9.2 Upper Airway Impairment withAbnormal
Craniofacial Growth – 116
9.2.1 Extended Head andCervical Posture Aecting Craniofacial
Deformation – 116
9.2.2 Pharyngeal Airway inDierent Sagittal Craniofacial Discrepancy – 117
9.2.3 Pharyngeal Airway inDierent Vertical Craniofacial Discrepancy – 121
9.2.4 Upper Airway inTransverse Craniofacial Discrepancy – 122
9.3 Craniofacial Alteration by Abnormal
Respiratory Function – 122
9.3.1 Prevalence ofCraniofacial Deformation inSDB Children – 122
9.3.2 Craniofacial Alteration by Physical Upper Airway
Obstruction inChildren – 123
9.3.3 Craniofacial Characteristics ofPediatric SDB Patients – 125
References – 129
© Springer Nature Switzerland AG 2021
K. B. Kim et al. (eds.), Management of Obstructive Sleep Apnea, https://doi.org/10.1007/978-3-030-54146-0_9
106
S.-J. Kim and K. B. Kim
9.1 Upper Airway Development
withNormal Craniofacial Growth
and its contents in healthy children, which varies from
year to year, to assess the signicant variations from the
normal.
Upper airway, which comprises the nasal cavity, pharynx, and larynx, is more relevant to craniofacial structural environment than the lower airway. The pharynx is
9.1.1 Postnatal Growth oftheCranial Base
a tube-shaped structure that extends from the cranial
base to the level of the inferior surface of the sixth cervical vertebra [1]. It lies dorsal to the nasal and mouth
cavity and is cranial to the esophagus, larynx, and trachea. The pharynx can be anatomically separated into
three parts: the nasopharynx, oropharynx, and hypopharynx. In a midsagittal image, the nasopharynx is
shown to extend from the nasal turbinates to the hard
palate. The oropharynx can be subdivided into the retropalatal pharynx (from the hard palate to the caudal
margin of the soft palate) and the retroglossal pharynx
(from the caudal margin of the soft palate to the base of
the epiglottis). The hypopharynx spans from the base of
9
the epiglottis to the larynx (.
As upper airway is located below the skull base and
Fig.9.1) [2].
behind the face, the growth and developmental changes
of craniofacial structures will affect the development of
the upper airway, and subsequently the dimension and
function of the upper airway. It is necessary to understand the normal growth pattern of the upper airway
It is important to understand the forces within the cranial base that drive facial growth and upper airway
development. The cranial base provides the platform
around which the nasomaxillary complex and mandible
develop, both of which inuence craniofacial morphology and function.
Although the sutural growth on the cranium and
cranial base accounts for multidirectional expansion of
the cranial base, overall postnatal growth of the cranial
base depends on endochondral growth on the synchondrosis, differential sutural growth of the calvaria wall,
and surface cortical drift on the endocranial oor in
response to the growth of cerebral lobes and sinuses.
Among these mechanisms, endochondral growth of two
principal synchondroses directly determines growth of
the cranial base after birth. The sphenoethmoidal synchondrosis is most active in relation to growth of the
anterior cranial base through approximately 7–8years
of age. The spheno-occipital synchondrosis, which fuses
shortly after puberty (16–17 years in females and
18–19years in males), is most prominent throughout the
period of active craniofacial growth. Once synostosis
occurs, growth of the cranial base length in the anteroposterior direction has mostly completed, and subsequent changes in the form of the cranial base may be
attributable to bone remodeling. The cranial base undergoes a dramatic shift in its growth pattern during the
rst 2–3 postnatal years, and growth changes, thereafter,
are smaller and steadier. Both cranial base lengthening
and cranial base exion are important growth mechanisms.
. Fig. 9.1 Upper airway on the lateral cephalogram comprising
nasal cavity, nasopharynx, oropharynx, and hypopharynx
9.1.1.1 Cranial Base Lengthening
Up to the end of the rst year of life, the intrasphenoidal
synchondrosis denes the junction of the anterior and
posterior cranial bases. The anterior cranial base grows
primarily due to the growth of sphenoethmoidal synchondrosis by 6years in concert with the frontal lobes of
the brain and continues to increase after its fusion at
7–8years of age. This is due to bony apposition on the
outer surface of the frontal bone associated with the
development of frontal sinus. The posterior cranial base
lengthens primarily due to growth at the spheno-occipital synchondrosis, and it represents differential maturation from the anterior cranial base. The anterior cranial
base grows more and is also more mature than the posterior cranial base throughout the postnatal growth
between birth and 17years of age. According to longitu-
Craniofacial Morphology Related to Obstructive Sleep Apnea: Growth of Craniofacial Bones…
107
9
dinal analyses, the anterior cranial base has attained
nearly 90% of its adult size by 4.5years of age, while the
posterior cranial base has attained only about 80% of its
adult size [3]. As a consequence, anteroposterior growth
of cranial base length is almost complete during the rst
6 years of life. Thereafter, any additional lengthening
occurs by bony apposition, affecting the forward displacement of nasomaxillary complex.
9.1.1.2 Cranial Base Flexion
In newborns and infants, the cranial base is quite at.
With growth into childhood, a more convex superior or
exed appearance emerges. The cranial base angulation
decreases more than twice as much during the rst
2years than between 2 and 17years of age, primarily
due to the differential growth of spheno-occipital synchondrosis. Between 2 and 6years of age, cranial base
exion occurs because of bone remodeling that results
in the clockwise rotation of the sphenoid bone and
counterclockwise rotation of the occipital bone, which is
accompanied by shortening and widening of the cranial
base. The degree of bony rotation and its direction tends
to be determined during the rst 6 years of life when
facial dynamics begin to compete with cranial dynamics.
Individuals with impaired cranial base exion tend
to keep their cranial bases narrow and long (a dolichocephalic pattern), and accordingly have narrow and long
faces (. Fig. 9.2). A combination of a counterclockwise sphenoidal and a clockwise occipital rotation may
develop maxillary protrusion with deep and narrow
maxillary arch and locate mandibular condyles backward, representing skeletal Class II. In contrast, individuals with large cranial base exion by combined
clockwise sphenoidal and counterclockwise occipital
rotation tend to exhibit wide and short cranial bases (a
brachycephalic pattern) with decient midface and anteriorly located mandibular condyles, representing skeletal Class III.
On the other hand, a longitudinal study from
Burlington Growth Centre with the annually examined
Caucasian sample [4] found no signicant differences in
cranial length, cranial width, cephalic index, and anterior cranial base length between the 10% of the children
with the most open cranial base angles and the 10% with
the most closed cranial base angles. Children with the
attest cranial bases had a slightly shorter posterior cranial base, mandibular condyles located further backward and upward, and retrognathic maxilla, showing
. Fig. 9.2 CBCT volume images of an individual with impaired cranial base exion, showing a dolichocephalic pattern and long face