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Cephalometric comparisons of craniofacial and upper airway structures in young children with obstructive sleep apnea syndrome.


We studied 15 children of preschool age who had obstructive sleep apnea syndrome to evaluate their dentofacial morphology in relation to the pharyngeal airway space. We found that (1) sleep apnea was often associated with mandibular retrognathia, (2) the lower incisors tended to exhibit a retrocline, (3) there were no significant differences in angular and linear measurements in the cranial base between patients with sleep apnea and a control group of 30 nonapneic children, and (4) the apneic children had a narrower epipharyngeal airway space than did the controls. These findings suggest that obstructive sleep apnea is probably caused by both adenoidal hypertrophy and abnormal development of the facial skeleton. We highly recommend cephalometric analysis as a valuable tool for conducting the presurgical evaluation of sleep apnea in children of preschool age.


Obstructive sleep apnea syndrome (OSAS) is characterized by the recurrent interruption of breathing during sleep. [1] Beginning at middle age, OSAS can cause episodes of "near miss" death from circulatory disturbances [2] in addition to traffic and other accidents as a result of hypersomnolence. [3] In children, OSAS can induce growth disorders. [4]

The primary cause of obstructive airway diseases in adults is obesity. In children who are in the primary dentition stage, the major cause of OSAS is hypertrophy of the adenoids and tonsils. Although OSAS in adults has long been the subject of study, in children it has only recently attracted attention. [5-10]

In this article, we describe our evaluation of the dentofacial morphology in relation to the pharyngeal airway space in OSAS patients of preschool age with primary dentition.

Subjects and methods

Patients and control groups. Our patient population was made up of 15 dentate Japanese preschool children--11 boys and 4 girls, aged 3 to 5 years (mean: 4.7)--who had documented OSAS. We used a standardized grading classification devised by Kawashima that is based on the relationship of the tonsils to the oropharynx in the medial to lateral plane as measured between the anterior pillars. [9] Their body mass index ranged from l4 to 19 (mean: 16.5).

All patients had a history of disturbed sleep that was characterized by heavy snoring, recurrent episodes of apnea, and sleeping with the mouth open. OSAS was confirmed by polysomnography in either the Department of Otorhinolaryngology at the Saitama Children's Medical Center in Saitama, Japan, or in the Department of Paediatric Dentistry at the Nihon University School of Dentistry in Tokyo. An apneic episode was defined as the cessation of airflow at the nose and mouth for more than 10 seconds. [1] The apnea index--that is, the mean number of apneic episodes per hour of sleep-- was calculated for each patient, and it ranged from 5 to 18 (mean: 12.5). None of the 15 patients was obese, and none had anatomic craniofacial abnormalities, neurologic disease, or cor pulmonale.

The control group consisted of 30 children who did not snore, who had no history of respiratory disorders, and who did not experience daytime somnolence. Evidence for the absence of snoring and apneic episodes was obtained from their parents. All the children in the control group had normal occlusion.

Cephalometric analysis. We obtained lateral cephalometric radiographs while each subject was standing in a natural position with his/her head inside the cephalometer. All cephalograms were obtained before any medical or surgical intervention was undertaken.

We used the definitions of landmarks, planes, and measurements proposed by Ricketts (figures 1-3). [11] We measured airway dimensions according to the cephalometric airway analysis methods described by McNamara [12] and Schulhof [13] (figure 4).


Craniofacial morphology. On skeletal analysis, we detected significant differences between the OSAS and control groups in the facial taper (p[less than]0.05), the mandibular plane angle (p[less than]0.01), the gonial angle (p[less than]0.001), and the lower facial height (p[less than]0.001) (table 1). We also found significant differences in the values of the interincisal angle (p[less than]0.001) and the L-1 to mandibular angle (p[less than]0.001 (table 2). At the cranial base, there were no significant differences with regard to any angular and linear measurements (table 3).

Pharyngeal airway structure. There were significant differences between the two groups in the size of the upper (p[less than]0.001) and lower (p[less than]0.05) pharynx (table 4).


The three types of sleep apnea are central, obstructive, and mixed. In OSAS, an obstruction of the upper respiratory tract prevents air from entering the lungs despite vigorous thoracic movement. Among the causes of the obstruction are redundant tissue in the upper airway, an increase in compliance of the pharyngeal wall, and a dorsally positioned tongue in the presence of a short posterior pharyngeal wall. Our study was designed to evaluate dentofacial morphology in children with OSAS. Accordingly, our subjects did not have any anatomic, neurologic, or secondary cardiopulmonary manifestations.

Regarding the mandible, we noted differences in both form and position. OSAS patients tended to have a posteriorly positioned and posteriorly rotated mandible with a higher gonial angle, a longer lower facial height, a greater mandibular plane angle, and a moderately retracted chin. We confirmed that preschool children with OSAS have mandibular retrognathia just as adults with OSAS do. [14,15]

In patients who are still growing, obstruction of the upper airway can lead to excessive vertical facial development. Lyberg et al reported that the mandibular plane inclination and the height of the anterior face were slightly greater in adults with OSAS--findings that are similar to ours in children. [15, 16] However, none of the children with OSAS in our study had mandibular micrognathia. We believe that preschool children with OSAS should be treated for skeletal problems by a pediatric dentist.

The lower incisors in the children with OSAS tended to exhibit a retrocline. Linder-Aronson reported that children with adenoid hypertrophy tend to have retroclined upper and lower incisors and a small overbite. [17]

In adults with OSAS, the entire structure of the cranial base has been reported to be rotated slightly counterclockwise in the sagittal plane, [15] but we did not observe a similar counterclockwise rotation in children.

In our study, the children with OSAS had a narrower epipharyngeal airway space than did the controls and a significantly larger value with regard to the height of the lower pharynx. Therefore, in the OSAS children, the root of the tongue was noted to be in an anterior position. The mandibular position clearly had an impact on the size of the posterior airway space.

Altogether, this study indicates that the retromandibular space, as measured by lateral cephalography, is smaller in most children with OSAS and appears to provide insufficient space for the tongue in the pharyngeal cavity. The primary cause of obstructive airway disease in children is hypertrophy of the adenoid and faucial tonsils, and we recommend a surgical approach for management. [6]

Although polysomnography is routinely performed to evaluate children with OSAS, normal polysomnographic values for children in the preschool-age group have not yet been established. Marcus et al found that polysom-nographic results in children differ from those in adults, and that the clinical significance of short apneic episodes in children has not yet been ascertained. [18] Therefore, we recommend a combination of morphologic and functional diagnosis. [10]


We thank Jack L. Pulec, MD, for his valuable advice regarding our study.

From the Department of Paediatric Dentistry, Nihon University School of Dentistry, Tokyo (Dr. Kawashima, Dr. Niikuni, Dr. Lo, Dr. Takahasi, Dr. Kohno, Dr. Nakajima, and Dr. Akasaka), and the Department of Otorhinolaryngology (Dr. Sakata) and the Department of Nephrology (Dr. Akashi), Saitama Children's Medical Center, Saitama, Japan.


(1.) Guilleminault C, Tilkian A, Dement WC. The sleep apnea syndromes. Annu Rev Med 1976;27:465-84.

(2.) Fletcher EC, Shah A, Qian W, Miller CC. "Near miss" death in obstructive sleep apnea: A critical care syndrome. Crit Care Med 1991;19:l158-64.

(3.) Findley LJ, Unverzagt ME, Suratt PM. Automobile accidents involving patients with obstructive sleep apnea. Am Rev Respir Dis 1988;138:337-40.

(4.) Goldstein SJ, Wu RH, Thorpy MJ, et al. Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea. Acta Endocrinol (Copenh) 1987;l16:95-101.

(5.) Leach J, Olson J, Hermann J, Manning S. Polysomnographic and clinical findings in children with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 1992;118:741-4.

(6.) Wiet GJ, Bower C, Seibert R, Griebel M. Surgical correction of obstructive sleep apnea in the complicated pediatric patient documented by polysomnography. Int J Pediatr Otorhinolaryngol 1997;41:133-43.

(7.) Preutthipan A, Suwanjutha S, Chantarojanasiri T. Obstructive sleep apnea syndrome in Thai children diagnosed by polysomnography. Southeast Asian J Trop Med Public Health 1997;28:62-8.

(8.) Nieminen P, Tolonen U, Lopponen H, et al. Snoring children: Factors predicting sleep apnea. Acta Otolaryngol Suppl (Stockh) 1997;529: 190-4.

(9.) Kawashima S, Niikuni N, Lo CH, et al. Clinical findings in Japanese children with obstructive sleep apnea syndrome: Focus on dental findings. J Oral Sci 1999;41:99-103.

(10.) Shintani T, Asakura K, Kataura A. The effect of adenotonsillectomy in children with OSA. Int J Pediatr Otorhinolaryngol 1998;44:51-8.

(11.) Ricketts RM. Orthodontic Diagnosis and Planning: Their Roles in Preventive and Rehabilitative Dentistry. Denver: Rocky Mountain/Orthodontics, 1982:127-36.

(12.) McNamara JA Jr. A method of cephalometric evaluation. Am J Orthod 1984;86:449-69.

(13.) Schulhof RJ. Consideration of airway in orthodontics. J Clin Orthod 1978;12:440-4.

(14.) Battagel JM. Obstructive sleep apnoea: Fact not fiction. Br J Orthod 1996;23:315-24.

(15.) Lyberg T, Krogstad O, Djupesland G. Cephalometric analysis in patients with obstructive sleep apnoea syndrome. I. Skeletal morphology. J Laryngol Otol 1989;103:287-92.

(16.) Tangugsorn V, Skatvedt O, Krogstad O, Lyberg T. Obstructive sleep apnoea: A cephalometric study. Part I. Cervicocraniofacial skeletal morphology. Eur J Orthod 1995;17:45-56.

(17.) Linder-Aronson S. Adenoids. Their effect on mode of breathing and nasal airflow and their relationship to characteristics of the facial skeleton and the dentition. A biometric, rhinomanometric and cephalometro-radiographic study on children with and without adenoids. Acta Otolaryngol Suppl (Stockh) 1970;265:l-132.

(18.) Marcus CL, Omlin KJ, Basinki DJ, et al. Normal polysomno-graphic values for children and adolescents. Am Rev Respir Dis 1992;146:1235-9.

Cephalometric landmarks and reference lines used in this study


A The deepest point on the concave outline of the upper labial alveolar process, extending from the anterior nasal spine to the prosthion (figure 1).

ANS The most anterior point at the sagittal plane on the bony hard palate (figure 1).

BA The most inferior posterior point of the occipital bone at the anterior margin of the occipital foramen (figures 1, 3, 4).

CC The intersection point of the BA-NA plane and the facial axis plane (figure 3).

CF The intersection point of the FH plane and the PTV plane (figure 1).

DC The midpoint of the condyle on the BA-NA plane (figure 1).

GN The intersection point of the mandibular plane and the facial plane (figure 1).

GO The intersection point of the mandibular plane and the ramus plane (figure 1).

NA The most anterior point of the frontonasal suture (figures 1, 3).

OR The most inferior point on the lower border of the bony orbit (figure 1).

PM The point where the curvature of the anterior border of the symphysis changes from concave to convex (figure 1).

PNS The most posterior point at the sagittal plane on the bony hard palate (figures 1, 4).

PO (porion) The most superior point on the radiolucency of the external and internal auditory meati. It is located posterior to the mandibular condyle and posterior clivus (figures 1, 3).

Pog (pogonion) The most prominent point of the chin (figure 1).

PT The intersection point of the inferior border of the foramen rotundum and the posterior wall of the pterygomaxillary fissure (figures 1, 3, 4).

S The center of the pituitary fossa of the sphenoid bone (figures 3, 4).

XI A point located at the center of the ramus (figure 1). The location of XI is keyed geometrically to the FH and PTV planes in four steps: (1) Planes are constructed perpendicular to the FH and PTV planes. (2) These constructed planes are tangent to points (R1, R2, R3, and R4) on the borders of the ramus. (3) The constructed planes form a rectangle enclosing the ramus. (4) XI is located in the center of the rectangle at the intersection of diagonals.


Facial axis plane A line connecting the PT and GN points (figures 1, 3).

Facial plane A line connecting the NA and Pog points (figures 1, 3).

FH Frankfort horizontal plane. A line connecting the PO and OR points (figures 1-3).

L-1 The mandibular incisor line (figure 2).

Mandibular plane A tangent line to the lower border of the mandible (figures 1, 2).

PTV Pterygoid vertical plane. A line perpendicular to the FH plane through the PT point (figures 1-4).

Ramus plane A tangent line on the posterior contour of the ramus ascendens (figure 1).

U-1 The maxillary incisor line (figure 2).
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Author:Akashi, Shunji
Publication:Ear, Nose and Throat Journal
Geographic Code:9JAPA
Date:Jul 1, 2000
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