Abstract
The aim of this study was to examine the effects of mandibular setback surgery on pharyngeal airway space and respiratory function during sleep. The subjects were 22 patients in whom mandibular prognathism was corrected by bilateral sagittal split ramus osteotomy; either one jaw or two jaw surgery. Polysomnography was performed before surgery and 6 months after surgery, and the apnea hypopnea index (AHI) and arterial oxygen saturation during sleep were measured to assess respiratory function during sleep. Morphological changes were studied using cephalograms taken immediately before, a few days after and 6 months after surgery. As a control, 10 subjects without sleep-disordered breathing underwent the same examinations. AHI was not changed significantly after surgery, although two patients were diagnosed with mild obstructive sleep apnea (OSA) syndrome after surgery. They were not obese, but the amounts of mandibular setback at surgery were large. In conclusion, a large amount of mandibular setback might inhibit biological adaption and cause sleep-disordered breathing, and it might be better to consider maxillary advance or another technique that does not reduce the airway for patients with skeletal class III malocclusions who have large anteroposterior discrepancy and/or maxillary hypoplasia.
Mandibular setback surgery is a common treatment for mandibular prognathism that results in functional and aesthetic improvements. The authors are interested in the effects of mandibular setback surgery on the pharyngeal airway space and respiratory function during sleep. Many studies on changes in craniofacial and pharyngeal morphology after mandibular setback surgery have been carried out . Most of them showed reduction in pharyngeal airway space and changes in surrounding hard and soft tissues mainly by using lateral cephalograms, and it has been suggested that mandibular setback surgery might induce sleep-disordered breathing, typified by obstructive sleep apnea (OSA) syndrome. Some cases have been reported in which OSA was caused by mandibular setback surgery. OSA is a potentially life-threatening disorder caused by repetitive narrowing and obstruction of the pharyngeal airway during sleep, and it has been associated with loud snoring and apnea. The criterion for diagnosing OSA is five or more episodes of apnea or hypopnea per hour of sleep. OSA is regarded as one of the risk factors of hypertension, ischemic myocardial diseases, and cerebral vascular diseases . It is also thought to be one of the causes of traffic accidents. The most accurate and comprehensive method for diagnosing OSA is overnight polysomnography (PSG), but there have been few studies using PSG to assess the effect of mandibular setback surgery on respiratory function during sleep.
The aim of this study was to investigate whether mandibular setback surgery causes OSA with morphological changes. The authors investigated changes in the apnea hypopnea index (AHI) and arterial oxygen saturation (SpO 2 ) measured overnight with PSG and craniofacial and pharyngeal morphology before and after mandibular setback surgery.
Materials and methods
The subjects were 22 patients (eight male; 14 female) in whom mandibular prognathism was surgically corrected in the authors’ clinic. They all agreed to take part in this clinical study and had no symptoms of OSA such as snoring or apnea. Bilateral sagittal split osteotomies were performed for mandibular set back in all patients, and Le Fort I osteotomies were combined with bilateral sagittal split osteotomy in 11 patients to improve mandibular prognathism with facial asymmetry, open bite and/or maxillary retrusion. No cases of cleft palate or craniofacial syndrome were included. The mean age at surgery was 22 years (range 16–38 years) and mean body mass index (BMI) values before surgery and 6 months after surgery were 21.3 kg/m 2 (range 17.2–33.7 kg/m 2 ) and 21.3 kg/m 2 (range 16.9–32.8 kg/m 2 ), respectively. All of the subjects received pre- and postoperative orthodontic treatment, and osteosynthesis was achieved using titanium miniplate and resorbable fixation devices (Neofix: Gunze Co., Osaka, Japan) made by poly- l -lactic acid. Maxillomandibular fixation was performed the day after surgery and maintained for a mean period of 14 days. PSG was performed before surgery and 6 months after surgery.
As a control group, 10 subjects (four male; six female) with normal occlusions and no sleep-disordered breathing underwent the same examinations as those performed on the patients. The mean age of the control subjects was 28 years (range 24–31 years) and their mean BMI was 20.8 kg/m 2 (range 18.2–24.8 kg/m 2 ).
Morphological changes were evaluated on lateral cephalograms taken with the Frankfort horizontal (FH) plane parallel to the floor and with the patient in a centric occlusion before surgery (T0), a few days after surgery (T1) and more than 6 months after surgery (T2). The cephalograms were traced to identify hard and soft tissue landmarks. The measuring points were registered on each cephalogram, and serial cephalograms were superimposed using the sella and nasion as fixed cephalometric landmarks ( Fig. 1 ). These points were digitized as two-dimensional coordinate values to calculate 10 angles and four distance measurements using the authors’ original computerized program ( Figs 2 and 3 ). The magnitudes of horizontal and vertical changes in the maxilla, the mandible and the hyoid bone were determined by measuring the parallel and perpendicular movements of points ANS, Pog and H to the FH plane. Positive values were assigned to anterior and inferior movements. Cephalometric tracing was performed by only one examiner to decrease the measurement error.
Overnight PSG using a Somnostar Alpha System (SensorMedics Corp., USA) was performed before surgery (T0) and more than 6 months after surgery (T2). SpO 2 was measured overnight at the same time with pulse oximetry (pulsox-300i or pulsox-3Si, Konica Minolta Sensing Inc., Japan). AHI was calculated as the sum of apneas and hypopneas per hour of sleep. An apnea was defined as a cessation of airflow for more than 10 s and a hypopnea was defined as 70% or less of a normal breath and/or a 4% or greater drop in SpO 2 during sleep. The data obtained from pulse oximetry were analysed using special analytical software (DS-3, Konica Minolta Sensing Inc., Japan), and 2%, 3% or 4% oxygen desaturation index (ODI) (the average number of oxygen desaturation events at least 2%, 3% or 4% below baseline level per hour), lowest SpO 2 during the measurement period, and CT90 (cumulative percentage time at SpO 2 below 90% during the measurement period) were calculated.
Statistics
Univariate analyses were carried out for all measured parameters. Since it could not be assumed that the parameters have normal distributions, Friedman’s test was used to determine whether changes in each parameter have significance in their groups. After the significance of the parameters was proved, Wilcoxon’s matched-pair signed-rank test was used to evaluate the changes in paired parameters in each group. Data were analysed using SPSS version 10 for Windows (SPSS Japan Inc., Japan).
Results
Cephalometric analyses
Friedman’s test indicated significant changes in nasopharyngeal depth (NPD), distance from H to mandibular line (MPH), distance from H to palatal line (PPH), facial angle (FA), angle between line A–B and facial plane (A–B plane angle), angle between mandibular plane and FH plane (MPA), angle between line S–N and line N–B (SNB), ramus inclination (angle between line Ar–Go and FH plane), gonial angle (angle between mandibular plane and line Ar–Go), facial axis (angle between mandibular plane and FH plane), angle between line S–N and odontoid process tangent through Cv2tg and Cv2ip (SNL/OPT), and angle between line S–N and cervical vertebral tangent through Cv2tg and Cv4ip (SNL/CVT).
In the two jaw surgery group, Friedman’s test indicated significant changes in NPD, MPH, PPH, FA, A–B plane angle, MPA, SNA, SNB, gonial angle and facial axis. In the one jaw group, Friedman’s test indicated significant changes in MPH, PPH, FA, A–B plane angle, MPA, SNB, ramus inclination, gonial angle, facial axis, SNL/OPT and SNL/CVT.
The maxilla was displaced forward and downward at surgery and was displaced backward and upward by 6 months after surgery. The mandible was displaced backward and downward at surgery and was displaced forward and upward by 6 months after surgery. The hyoid bone moved backward and downward in the period T0–T1 and had returned to a position slightly backward from the original position at T2 ( Tables 1–3 ).
| T1–T0 | T1–T2 | ||
|---|---|---|---|
| ANS | Horizontal | 1.0 ± 2.0 | −0.4 ± 1.7 |
| Vertical | 0.7 ± 1.4 | −0.4 ± 1.2 | |
| Pog | Horizontal | −7.1 ± 4.3 | 0.8 ± 2.3 |
| Vertical | 0.2 ± 2.0 | −0.6 ± 1.2 | |
| H | Horizontal | −4.5 ± 5.6 | 1.5 ± 5.5 |
| Vertical | 7.6 ± 6.3 | −7.1 ± 6.5 |
| T1–T0 | T1–T2 | ||
|---|---|---|---|
| ANS | Horizontal | 2.1 ± 2.3 | −0.6 ± 1.8 |
| Vertical | 0.7 ± 1.6 | −0.1 ± 1.4 | |
| Pog | Horizontal | −5.8 ± 4.5 | −0.2 ± 2.6 |
| Vertical | −0.1 ± 1.9 | −0.9 ± 1.3 | |
| H | Horizontal | −4.1 ± 5.5 | 2.6 ± 6.9 |
| Vertical | 7.8 ± 5.2 | −9.6 ± 5.5 |
| T1–T0 | T1–T2 | ||
|---|---|---|---|
| ANS | Horizontal | −0.2 ± 0.8 | −0.3 ± 1.6 |
| Vertical | 0.8 ± 1.1 | −0.8 ± 0.9 | |
| Pog | Horizontal | −8.4 ± 3.9 | 1.7 ± 1.6 |
| Vertical | 0.4 ± 2.1 | −0.4 ± 1.1 | |
| H | Horizontal | −4.9 ± 5.9 | 0.5 ± 3.8 |
| Vertical | 7.5 ± 7.5 | −4.5 ± 6.5 |
In linear measurements, NPD, MPH and PPH were significantly increased in the period T0–T1 by Wilcoxon’s matched-pair signed-rank test, and only MPH was significantly different at T0 and T2. Both MPH and PPH increased in the period T0–T1 and decreased in the period T1–T2, indicating downward and backward displacement of the hyoid bone 6 months after surgery. There was no significant change in posterior airway space (PAS) using Friedman’s test. Compared with controls, there was no difference between subjects ( Tables 4–6 ).
Of the linear measurements in the two jaw surgery group, NPD, MPH and PPH were significantly increased in the period T0–T1 using Wilcoxon’s matched-pair signed-rank test, and only PPH was significantly different at T0 and T2. Both MPH and PPH increased in the period T0–T1 and decreased in the period T0–T2. In the one jaw surgery group, MPH and PPH were significantly increased in the periods T0–T1 and T0–T2 using Wilcoxon’s matched-pair signed-rank test. Both MPH and PPH increased in the period T0–T1 and decreased in the period T1–T2. This indicates downward and backward displacement of the hyoid bone 6 months after surgery. There was no significant change in PAS using Friedman’s test in both groups, and compared with controls, there was no difference between subjects in either group ( Tables 4–6 ).
Regarding angular measurements, there were significant changes in parameters indicating mandibular protrusion in the periods T0–T1 and T0–T2. These parameters were significantly different from those of the controls. Craniocervical angles (SNL/OPT and SNL/CVT) increased in the period T0–T1 and decreased in the period T1–T2, and the values for subjects were smaller than those for controls. There were significant differences between subjects at T2 and controls in A–B plane angle, MPA, SNB, gonial angle and ramus inclination ( Tables 7–9 ).
Regarding angular measurements, there were significant changes in parameters indicating mandibular protrusion in the periods T0–T1 and T0–T2, and these parameters were significantly different from those of controls. Craniocervical angles (SNL/OPT and SNL/CVT) increased in the period T0–T1 and decreased in the period T1–T2, and the values for subjects were smaller than those for controls. There were significant differences between subjects at T2 and controls in A–B plane angle, SNA, SNB, gonial angle and ramus inclination in the two jaw surgery group, and in MPA, SNB and gonial angle in the two jaw surgery group ( Tables 7–9 ).
PSG measurements
There was no significant change in AHI in the period T0–T2. Results of pulse oximetry showed that CT90 increased in the period T0–T2 ( Tables 10–12 ). There was no significant difference in the results of PSG and pulse oximetry in either surgical group. Two patients were diagnosed with mild OSA 6 months after surgery because AHI exceeded five events per hour, but they did not have subjective symptoms of OSA. The patient with the worst postoperative AHI value (12.1 events/h) was a 22-year-old male who underwent one jaw surgery (only bilateral sagittal split ramus osteotomy). Although he did not have OSA before surgery (preoperative AHI 4.4 events/h) and although he was not obese (BMI 20.6 kg/m 2 before surgery and 19.8 kg/m 2 6 months after surgery), the amount of mandibular setback at surgery was large (13.7 mm at pogonion). The other patient was an 18-year-old female who was not obese (BMI 21.3 kg/m 2 before surgery and 21.8 kg/m 2 after surgery) and underwent two jaw surgery (Le Fort I osteotomy and bilateral sagittal split ramus osteotomy) but showed a large amount of mandibular setback at surgery (12.6 mm at pogonion). In this patient, AHI increased to 5.4 events/h after surgery from 2.1 events/h before surgery, though there were no significant changes in ODI, lowest SpO 2 and CT90.
| Control | Before surgery | 6 months after surgery | |
|---|---|---|---|
| AHI (event/h) | 1.5 ± 1.6 | 2.9 ± 2.8 | 2.1 ± 1.7 |
| 4%ODI (number/h) | 0.4 ± 0.6 | 0.3 ± 0.4 | 0.3 ± 0.3 |
| 3%ODI (number/h) | 0.1 ± 1.3 | 0.6 ± 1.1 | 0.5 ± 0.6 |
| 2%ODI (number/h) | 3.3 ± 4.6 | 2.1 ± 2.4 | 1.7 ± 1.5 |
| Lowest SpO 2 (%) | 91.6 ± 2.3 | 90.7 ± 3.7 | 93.1 ± 1.5 |
| CT90 (%) | 0.0 ± 0.0 | 0.1 ± 0.2 | 0.0 ± 0.0 |
| Control | Before surgery | 6 months after surgery | |
|---|---|---|---|
| AHI (event/h) | 1.5 ± 1.6 | 2.2 ± 3.3 | 2.7 ± 3.4 |
| 4% ODI (number/h) | 0.4 ± 0.6 | 0.4 ± 0.6 | 0.2 ± 0.3 |
| 3% ODI (number/h) | 0.1 ± 1.3 | 1.0 ± 1.6 | 0.6 ± 0.6 |
| 2% ODI (number/h) | 3.3 ± 4.6 | 3.2 ± 4.9 | 2.6 ± 2.8 |
| Lowest SpO 2 (%) | 91.6 ± 2.3 | 93.1 ± 3.0 | 93.3 ± 2.1 |
| CT90 (%) | 0.0 ± 0.0 | 0.0 ± 0.1 | 0.0 ± 0.0 |
Correlations
Although a positive correlation was found between changes in AHI (difference before and after surgery) and amounts of mandibular setback only in the one jaw surgery group, there was no correlation between AHI and BMI or PAS. Positive correlations were observed between amounts of maxillary anterior movement and changes in NPD (difference between T0 and T1 or difference between T1 and T2) and between amounts of mandibular setback and posterior movement of the hyoid bone ( Tables 13–15 ). Changes in craniocervical angles after surgery showed negative correlations with amounts of anterior movement of the maxilla and posterior movement of the hyoid bone ( Tables 16–18 ). In the two jaw surgery group, positive correlations were observed between the amounts of maxillary anterior movement and inferior movement of the hyoid bone (between T1 and T2), mandibular setback and changes in MPH (difference between T0 and T1), and amounts of inferior movement of the hyoid bone (between T1 and T2). Changes in PAS showed positive correlations with changes of MPH and PPH, and negative correlations with amounts of inferior movement of the hyoid bone ( Tables 13–15 ). Changes in craniocervical angles after surgery showed correlations with changes of MPH and amounts of movement of the hyoid bone ( Tables 16–18 ). In the one jaw surgery group, negative correlations were observed between amounts of maxillaly anterior movement and posterior movement of the hyoid bone (between T0 and T1), between amounts of mandibular setback and posterior movement of the hyoid bone (between T0 and T1), and between changes of PAS and amounts of inferior movement of the hyoid bone (between T1 and T2). Changes in PAS (between T1 and T2) showed positive correlations with changes of NPD ( Tables 13–15 ). Changes in craniocervical angles after surgery showed correlations with changes of PAS, NPD and MPH ( Tables 16–18 ).
