Chapter 13: Obstructive Sleep Apnea Surgery¶

OSA pathophysiology, diagnostic evaluation, maxillomandibular advancement, DOME, SARPE, genioglossus advancement, hypoglossal nerve stimulation, and the multidisciplinary sleep team.

Introduction¶

Obstructive sleep apnea (OSA) affects an estimated 26% of adults aged 30-70 in the United States, with the majority of moderate-to-severe cases remaining undiagnosed (Peppard et al., Am J Epidemiol, 2013). The oral and maxillofacial surgeon occupies a unique position in OSA management: trained in both the skeletal and soft-tissue anatomy of the upper airway, proficient in orthognathic techniques that can fundamentally alter airway dimensions, and increasingly involved in the multidisciplinary sleep team. Maxillomandibular advancement (MMA) is the most effective surgical treatment for OSA, with cure rates exceeding 85% in appropriately selected patients, rivaling or surpassing CPAP adherence-adjusted efficacy.

This chapter covers the pathophysiology and diagnosis of OSA, the role of drug-induced sleep endoscopy (DISE), the full range of surgical interventions (MMA, DOME, SARPE, genioglossus advancement, hyoid suspension), hypoglossal nerve stimulation, oral appliance therapy, and the critical importance of multidisciplinary coordination.

Pathophysiology of OSA¶

Anatomy of Obstruction¶

OSA results from repetitive partial or complete upper airway collapse during sleep. The pharynx is a collapsible muscular tube lacking rigid skeletal support, making it vulnerable to collapse during the negative intraluminal pressure generated by inspiratory effort.

Levels of obstruction (Friedman classification):

Level I (Palatal/Retropalatal): Soft palate, uvula, tonsillar pillars, lateral pharyngeal walls
Level II (Retrolingual): Base of tongue, lingual tonsils, epiglottis
Level III (Hypopharyngeal): Epiglottic collapse, lateral hypopharyngeal wall collapse

Most patients have multilevel obstruction, which is why single-level procedures (e.g., UPPP alone) have historically yielded disappointing results (~40% success rate; Sher et al., Sleep, 1996).

Contributing Factors¶

Factor	Mechanism
Skeletal anatomy	Maxillary/mandibular hypoplasia narrows the skeletal framework
Soft tissue	Macroglossia, enlarged tonsils/adenoids, long soft palate
Neuromuscular	Decreased pharyngeal dilator muscle tone during sleep
Obesity	Parapharyngeal fat deposition, increased tongue volume
Fluid shifts	Nocturnal rostral fluid redistribution from legs to neck
Age/sex	Increased prevalence with age; male predominance (2-3:1)

Pcrit (Critical Closing Pressure)¶

Pcrit is the fundamental measure of pharyngeal collapsibility -- the pressure at which the pharynx collapses. Normal Pcrit is -15 to -5 cm H2O (resistant to collapse). OSA patients have Pcrit values approaching or exceeding 0 cm H2O (atmospheric pressure), meaning the airway collapses easily. MMA decreases Pcrit by approximately 5-6 cm H2O, moving the airway toward a non-collapsible state (Sforza et al., Thorax, 2011).

graph LR
    A[Anatomic Narrowing] --> D[Elevated Pcrit]
    B[Neuromuscular Dysfunction] --> D
    C[Obesity / Soft Tissue Excess] --> D
    D --> E[Airway Collapse During Sleep]
    E --> F[Apnea/Hypopnea]
    F --> G[Hypoxemia & Arousals]
    G --> H[Cardiovascular Morbidity]
    G --> I[Neurocognitive Impairment]
    G --> J[Excessive Daytime Sleepiness]

Diagnosis¶

Clinical Assessment¶

History: Witnessed apneas, snoring, excessive daytime sleepiness (Epworth Sleepiness Scale [ESS]; score >10 suggests significant sleepiness), nocturia, morning headaches, impaired concentration, irritability, decreased libido.

Physical examination:

BMI (obesity is the strongest modifiable risk factor)
Neck circumference (>17 inches male, >16 inches female correlates with increased OSA risk)
Mallampati classification (Class III-IV associated with OSA)
Friedman tongue position
Tonsillar size (Brodsky grading 0-4)
Nasal patency (septal deviation, turbinate hypertrophy, valve collapse)
Maxillomandibular relationship (retrognathia, high arched palate, transverse maxillary deficiency)
Dental examination (wear facets, tooth condition for oral appliance candidacy)

STOP-BANG questionnaire (Chung et al., Anesthesiology, 2008): Validated screening tool:

**S**noring loudly
**T**ired/fatigued during the day
**O**bserved apneas
**P**ressure (treated for hypertension)
**B**MI >35
**A**ge >50
**N**eck circumference >40 cm
**G**ender male

Score >= 5: High probability of moderate-to-severe OSA.

Polysomnography (PSG)¶

In-laboratory attended PSG is the gold standard for OSA diagnosis (AASM Clinical Practice Guideline, Berry et al., JCSM, 2017):

EEG, EOG, EMG (sleep staging)
Nasal pressure transducer and thermistor (airflow)
Respiratory inductance plethysmography (thoracic/abdominal effort)
Pulse oximetry (oxygen saturation)
ECG (cardiac rhythm)
Body position sensor

Key metrics:

Metric	Definition
AHI (Apnea-Hypopnea Index)	Number of apneas + hypopneas per hour of sleep
RDI (Respiratory Disturbance Index)	AHI + RERAs (respiratory effort-related arousals)
ODI (Oxygen Desaturation Index)	Number of >= 3% desaturations per hour
Nadir SpO2	Lowest oxygen saturation recorded
T90	Percentage of sleep time with SpO2 <90%

Severity classification:

Severity	AHI
Normal	<5
Mild	5-14
Moderate	15-29
Severe	>= 30

Home Sleep Apnea Testing (HSAT)¶

HSAT (Type III or IV devices) is appropriate for uncomplicated suspected moderate-to-severe OSA in patients without significant comorbidities (AASM guidelines). HSAT underestimates AHI because it uses recording time rather than total sleep time as the denominator. A negative HSAT in a high-probability patient should be followed by in-lab PSG.

Drug-Induced Sleep Endoscopy (DISE)¶

DISE provides dynamic visualization of upper airway collapse patterns during pharmacologically induced sleep, enabling site-specific surgical planning.

Technique:

Patient in supine position, unintubated
Propofol infusion titrated to achieve light sedation (target BIS 50-70; alternatively, midazolam + propofol TCI)
Flexible nasopharyngoscopy through one nostril
Observation of collapse at palatal, oropharyngeal, tongue base, and epiglottic levels
Assessment of directionality (anteroposterior, lateral, concentric)

VOTE Classification (Kezirian et al., Laryngoscope, 2011):

Structure	Direction of Collapse
Velum (palate)	AP, lateral, concentric
Oropharyngeal lateral walls	Lateral
Tongue base	AP
Epiglottis	AP (trapdoor), lateral

Each level scored as 0 (no obstruction), 1 (partial, >50%), or 2 (complete obstruction).

Clinical Pearl

DISE findings change surgical decision-making in 40-50% of cases compared to awake assessment alone (Carrasco-Llatas et al., Laryngoscope, 2019). For example, a patient with apparent retropalatal obstruction on awake exam may demonstrate primary tongue base or epiglottic collapse on DISE, which would not be adequately addressed by UPPP alone. DISE is strongly recommended before any targeted upper airway surgery.

First-Line Therapy: CPAP¶

Continuous positive airway pressure (CPAP) remains the first-line treatment for moderate-to-severe OSA per AASM guidelines. CPAP acts as a pneumatic splint, maintaining positive transmural pressure to prevent airway collapse. When used consistently, CPAP is highly effective.

The adherence problem: Despite proven efficacy, CPAP adherence (defined as >= 4 hours/night for >= 70% of nights) ranges from only 46-83% at one year (Weaver & Grunstein, Proc Am Thorac Soc, 2008). Long-term adherence declines further. This adherence gap is the primary justification for surgical intervention: a treatment that works perfectly but is not used provides no benefit.

Maxillomandibular Advancement (MMA)¶

Rationale¶

MMA simultaneously advances the maxilla (LeFort I osteotomy) and mandible (bilateral sagittal split osteotomy), expanding the skeletal framework of the upper airway at all levels. This increases the retrolingual, retropalatal, and lateral pharyngeal dimensions, tensions the pharyngeal musculature (particularly the suprahyoid and velopharyngeal muscles), and decreases Pcrit.

MMA is the most effective surgical treatment for OSA, with meta-analytic success rates of 85-100% (defined as AHI <20 with >= 50% reduction) and cure rates (AHI <5) of 38-50% (Holty & Guilleminault, Sleep, 2010; Camacho et al., Sleep Med Rev, 2015).

Indications¶

Primary MMA: CPAP-intolerant patients with moderate-to-severe OSA with favorable skeletal anatomy (retrognathia, maxillary hypoplasia)
Salvage MMA: After failure of CPAP, oral appliance therapy, and/or phase I soft-tissue surgery
Combined with CPAP: MMA can reduce CPAP pressure requirements, improving tolerability

Preoperative Planning¶

Cephalometric analysis (lateral cephalogram):

PAS (posterior airway space): Measured at multiple levels; narrowing at the tongue base level (<11 mm) and palatal level (<11 mm) identifies obstruction sites
SNA/SNB/ANB angles: Quantify maxillary and mandibular position relative to the cranial base
Hyoid position: Hyoid-to-mandibular plane distance (MP-H) >15 mm indicates low hyoid position contributing to tongue base collapse
Soft palate length: >35 mm associated with palatal obstruction

Virtual surgical planning (VSP): 3D CT-based planning is increasingly standard for MMA in OSA (see Chapter 16). VSP allows precise prediction of airway volumetric changes and optimization of advancement vectors.

Orthodontic considerations: Unlike traditional orthognathic surgery, MMA for OSA often employs a "surgery-first" approach without preoperative orthodontics, since the goal is airway enlargement rather than occlusal correction. Minor malocclusion resulting from differential advancement can be accepted or addressed with postoperative orthodontics.

Surgical Technique¶

Standard MMA protocol:

Nasotracheal intubation (or submental intubation if simultaneous nasal surgery planned)
LeFort I osteotomy: Standard down-fracture with 10-12 mm advancement (OSA advancement exceeds typical orthognathic advancement of 4-6 mm). Counter-clockwise rotation of the maxillomandibular complex is preferred, as it maximizes airway opening at the retrolingual level.
BSSO: Sagittal split osteotomies with mandibular advancement to match the maxillary advancement. Rigid fixation with bicortical screws or plates.
Counter-clockwise rotation: The occlusal plane is rotated counter-clockwise (posterior maxillary impaction with anterior downgraft), advancing the pogonion further than the maxilla relative to the vertical dimension. This maximizes the airway effect.
Genioplasty (optional adjunct): Advancement genioplasty increases the genial tubercle attachment, pulling the genioglossus and geniohyoid muscles anteriorly.
Fixation: Bone plates and screws; intermaxillary fixation with guiding elastics for 2-4 weeks.

Surgical Caution

The inferior alveolar nerve is at higher risk in MMA than in standard orthognathic surgery because of the larger advancement distances. Meticulous technique during the sagittal split, with protection of the neurovascular bundle, is essential. Despite this, temporary IAN paresthesia occurs in 30-50% of patients, with permanent neurosensory deficit in 5-10% (Abrahamsson et al., Int J Oral Maxillofac Surg, 2015).

Adjunctive Procedures with MMA¶

Procedure	Indication	Benefit
Genioglossus advancement (GGA)	Retrolingual obstruction	Advances genial tubercle, tensions tongue base
Septoplasty/turbinate reduction	Nasal obstruction	Improves nasal breathing, CPAP tolerance
UPPP / tonsillectomy	Palatine tonsil hypertrophy	Reduces retropalatal soft tissue bulk
Hyoid suspension	Low hyoid, hypopharyngeal collapse	Advances and stabilizes hyoid

Outcomes¶

Meta-analysis data (Holty & Guilleminault, Sleep, 2010; 627 patients):

Mean AHI reduction: 87.9% (from 63.9 to 9.5)
Surgical success rate (AHI <20, >= 50% reduction): 86%
Surgical cure rate (AHI <5): 43.2%
Mean ESS improvement: 13.4 to 4.5
Lowest SpO2 improvement: 73.5% to 87.7%

Long-term stability: Riley et al. (Sleep, 2010) reported stable outcomes at 4+ years post-MMA with no significant relapse in AHI. Weight gain remains the primary cause of late surgical failure.

CPT: 21141 (LeFort I, single piece -- used for maxillary component), 21196 (mandibular osteotomy with distraction, if applicable), 21198-21199 (osteotomy, mandible, segmental), 21193 (BSSO). Note: MMA for OSA is typically billed as 21141 + 21196 or using the orthognathic codes appropriate to the specific osteotomies performed. Prior authorization with PSG documentation of OSA severity is required by most payers.

ICD-10: G47.33 (obstructive sleep apnea)

Distraction Osteogenesis Maxillary Expansion (DOME)¶

Rationale¶

DOME combines surgically assisted rapid palatal expansion (SARPE) with subsequent distraction of the maxilla to address transverse maxillary deficiency, a frequently overlooked contributor to nasal and pharyngeal obstruction in OSA patients. Transverse maxillary deficiency narrows the nasal floor, increases nasal resistance, and forces mouth breathing, lowering tongue posture and contributing to retrolingual obstruction.

Technique¶

SARPE procedure: LeFort I osteotomy (with or without pterygomaxillary disjunction, depending on technique) combined with midpalatal osteotomy to allow transverse expansion
Distraction device: Bone-borne (e.g., MSE -- maxillary skeletal expander) or tooth-borne (Hyrax) distractor activated 0.25-0.5 mm twice daily
Expansion target: 5-12 mm of transverse expansion; monitored clinically and with CBCT
Consolidation: 3-6 months of retention

Evidence¶

A systematic review by Camacho et al. (Laryngoscope, 2017) found that SARPE/DOME produced:

Mean AHI reduction of 55% (from ~20 to ~9)
Significant nasal volume increase on acoustic rhinometry
Improved nasal breathing as measured by NOSE (Nasal Obstruction Symptom Evaluation) scores

Clinical Pearl

DOME is particularly valuable in the non-obese OSA patient with transverse maxillary deficiency, high arched palate, and nasal obstruction. Consider DOME as a staged approach: first expand the maxilla (improving nasal breathing and tongue posture), then reassess OSA severity before proceeding to MMA if needed. In select patients, DOME alone may be sufficient.

Surgically Assisted Rapid Palatal Expansion (SARPE)¶

Indications in OSA¶

SARPE is indicated when transverse maxillary deficiency contributes to nasal obstruction and OSA, particularly in skeletally mature patients (after mid-palatal suture fusion, typically >16-18 years in females and >18-20 years in males):

Transverse maxillary deficiency (intercanine width <33 mm, interpremolar width <37 mm)
High arched palate
Bilateral posterior crossbite
Nasal floor narrowing on CBCT

Technique¶

Classic SARPE involves:

Bilateral LeFort I-level osteotomies (lateral maxillary walls)
Midpalatal osteotomy (or pterygomaxillary disjunction in some protocols)
Placement of bone-borne or tooth-borne expansion device
Activation protocol: latency 5-7 days, then 0.25 mm BID

Miniscrew-Assisted Rapid Palatal Expansion (MARPE) using the MSE (Moon et al., Am J Orthod Dentofacial Orthop, 2015) achieves skeletal expansion through palatal bicortical miniscrews without a formal osteotomy in younger adults (18-30 years). Success depends on suture maturation status.

Comparison: DOME vs. SARPE¶

Feature	DOME	SARPE
Osteotomy	Full LeFort I + midpalatal	Lateral walls + midpalatal (no down-fracture)
Expansion potential	Greater (10-15 mm)	Moderate (5-10 mm)
Airway effect	Nasal + pharyngeal	Primarily nasal
Complexity	Higher	Lower
Can combine with MMA	Staged (expand then advance)	Staged or simultaneous

Genioglossus Advancement¶

Anatomy¶

The genioglossus muscle originates from the superior genial tubercle on the lingual surface of the mandibular symphysis. As the primary tongue protruder, it plays a critical role in maintaining airway patency during sleep.

Technique¶

A rectangular osteotomy of the anterior mandible captures the genial tubercle and its muscular attachment:

Degloving of the anterior mandible via a sublabial incision
Identification of the genial tubercle (CBCT planning confirms its exact location)
Rectangular osteotomy (approximately 10 mm x 10 mm) centered on the genial tubercle, using a reciprocating saw or piezotome
The bony window is advanced anteriorly (10-12 mm) and rotated 90 degrees to prevent retrodisplacement
Fixation with a miniplate or lag screw

Alternative: Mortised genioplasty -- a horizontal sliding genioplasty also advances the genial tubercle while improving chin projection (Riley et al., Otolaryngol Head Neck Surg, 1984).

Outcomes¶

GGA as a standalone procedure has limited efficacy (success rate ~35-60%). It is most effective as an adjunct to MMA, UPPP, or hyoid suspension as part of a multilevel surgical protocol.

CPT: 21199 (osteotomy, mandible, unilateral or bilateral, segmental -- may be used for GGA)

Hyoid Suspension¶

Rationale¶

The hyoid bone serves as an anchor point for the tongue base (genioglossus, hyoglossus) and pharyngeal constrictors. In OSA patients, the hyoid is often positioned inferiorly (>15 mm below the mandibular plane), contributing to tongue base and hypopharyngeal collapse.

Techniques¶

Hyothyroidopexy: Suture fixation of the hyoid to the superior border of the thyroid cartilage (Riley et al., Otolaryngol Head Neck Surg, 1994)
Hyomandibular suspension: Suture or titanium screw suspension of the hyoid to the inferior mandibular border (more common in current practice)

Evidence¶

Hyoid suspension as an isolated procedure has modest efficacy. Song et al. (Laryngoscope, 2016) reported AHI reduction from 42 to 24 (43% reduction) with hyoid suspension alone. It is most valuable as an adjunct to other procedures.

Hypoglossal Nerve Stimulation¶

Inspire System (Inspire Medical Systems)¶

The Inspire Upper Airway Stimulation (UAS) system received FDA approval in 2014 and represents a paradigm shift in OSA treatment for CPAP-intolerant patients with moderate-to-severe OSA.

Mechanism: A neurostimulator implanted in the right infraclavicular region delivers electrical impulses via a cuff electrode on the medial branch (protrusor fibers) of the hypoglossal nerve, timed to inspiration (detected by a sensing lead on the intercostal muscles). Stimulation causes tongue protrusion and stiffening, opening the retrolingual airway.

Indications (FDA-approved):

Age >= 18 years
AHI 15-100 (updated from initial 15-65)
BMI <= 40 kg/m² (updated from initial <= 32)
CPAP failure or intolerance
Absence of complete concentric collapse at the palatal level on DISE (this is the critical selection criterion; concentric collapse predicts poor response)

Implantation procedure:

Three incisions: infraclavicular (pulse generator pocket), submandibular (hypoglossal nerve dissection and cuff electrode placement), lateral chest wall (sensing lead on intercostal muscles between ribs 4-5)
Hypoglossal nerve identified deep to the posterior belly of the digastric muscle; the medial (protrusor) branches are isolated and the stimulating cuff is placed selectively
Tunneling of leads and connection to pulse generator
Intraoperative testing confirms tongue protrusion with stimulation

Activation: Device is activated 1 month postoperatively, with titration PSG to optimize settings.

Outcomes (STAR trial, 5-year data; Woodson et al., Otolaryngol Head Neck Surg, 2018):

Mean AHI: 29 to 6.2 (78% reduction)
Surgical success (AHI <20, >= 50% reduction): 75%
Surgical cure (AHI <5): 44%
ESS: 11.6 to 6.0
Stable outcomes at 5 years with high patient satisfaction

Clinical Pearl

The DISE finding of complete concentric collapse (CCC) at the velum is the primary contraindication to Inspire therapy, as the device does not address palatal obstruction. However, partial concentric collapse or anteroposterior palatal collapse does not preclude success. Recent data suggest that concurrent palatal procedures (expansion sphincter pharyngoplasty) combined with Inspire may address this limitation (Mahmoud et al., Sleep, 2023).

Role of OMS in Hypoglossal Nerve Stimulation¶

While Inspire implantation has been primarily performed by otolaryngologists, OMS surgeons with appropriate training and credentialing are increasingly performing this procedure. The OMS familiarity with the submandibular space, hypoglossal nerve anatomy, and perioperative management of the upper airway makes this a natural extension of practice.

CPT: 64568 (implantation of cranial nerve neurostimulator electrode array -- hypoglossal nerve), 64590 (insertion of peripheral/gastric neurostimulator pulse generator)

Oral Appliance Therapy¶

Mandibular Advancement Devices (MADs)¶

Oral appliances that advance the mandible anteriorly during sleep represent the primary alternative to CPAP for mild-to-moderate OSA and as a CPAP adjunct or alternative for severe OSA (AASM Practice Parameters, Ramar et al., JCSM, 2015).

Mechanism: Mandibular protrusion increases retrolingual airway space, tensions the genioglossus and lateral pharyngeal walls, and reduces pharyngeal collapsibility.

Device types:

Custom, titratable (standard of care): Fabricated from dental impressions or digital scans; allow progressive mandibular advancement via titration mechanism. Examples: SomnoDent (SomnoMed), Herbst-style devices, TAP (Thornton Adjustable Positioner), EMA (Myerson).
Thermoplastic "boil-and-bite": OTC devices; inferior retention, comfort, and efficacy. Not recommended for definitive therapy.

Titration protocol:

Initial setting: 50-60% of maximum protrusion
Advance 0.25-0.5 mm per week until symptoms resolve or maximum tolerable protrusion is reached
Confirm efficacy with follow-up PSG or HSAT at therapeutic position
Annual dental/TMJ follow-up to monitor for bite changes

Efficacy: MADs reduce AHI by approximately 50% on average, with complete response rates (AHI <5) of 30-40% for mild-moderate OSA (Sutherland et al., Sleep Med Rev, 2014). They are less effective than CPAP on a per-night basis but have higher adherence, making the effective clinical efficacy comparable for mild-moderate disease.

Side effects:

Temporomandibular joint discomfort (10-30%, usually temporary)
Excessive salivation or dry mouth
Dental side effects: Progressive mandibular incisor proclination, reduction in overjet and overbite, development of posterior open bite. These changes are slow and cumulative; long-term follow-up is mandatory.
Morning jaw stiffness

Surgical Caution

OMS surgeons are ideally positioned to screen for TMJ pathology before prescribing oral appliance therapy. Patients with active TMJ internal derangement (Wilkes III-V), severe degenerative joint disease, or limited mandibular range of motion are poor candidates for MAD therapy and may experience worsening of TMJ symptoms with forced protrusion.

CDT Codes:

D5999 (unspecified maxillofacial prosthesis, by report) or
E0486 (oral device/appliance used to reduce upper airway collapsibility, custom fabricated) -- HCPCS for medical billing

Multilevel and Staged Surgical Approaches¶

Riley-Powell-Stanford Protocol¶

The original staged surgical approach (Riley, Powell, Guilleminault, Otolaryngol Head Neck Surg, 1993):

Phase I (soft tissue):

UPPP (uvulopalatopharyngoplasty) or lateral pharyngoplasty
Genioglossus advancement
Hyoid suspension
Radiofrequency tongue base reduction

Phase II (skeletal -- if Phase I fails):

MMA

Success rates: Phase I alone ~60%; Phase I + Phase II combined ~95% (Riley et al., 1993).

Contemporary Approach¶

The trend has shifted away from staged protocols toward primary MMA in appropriate candidates, recognizing that:

Staged approaches subject patients to multiple surgeries with cumulative morbidity
Phase I procedures have modest individual efficacy
MMA addresses the fundamental skeletal etiology
Outcomes are superior with primary MMA compared to Phase I salvage scenarios

The 2022 AASM Position Statement acknowledges MMA as a viable first-line surgical option for CPAP-intolerant patients with skeletal deficiency.

Special Considerations¶

Pediatric OSA¶

Adenotonsillectomy is the first-line surgical treatment for pediatric OSA (Marcus et al., Pediatrics, 2012). When adenotonsillectomy fails (residual OSA in 20-40% of cases), the OMS surgeon may contribute:

Rapid maxillary expansion (orthodontic or surgically assisted in older children)
Distraction osteogenesis for micrognathic children (e.g., Pierre Robin sequence; see Chapter 11)
MMA in adolescents with skeletal deficiency

Obesity and OSA Surgery¶

BMI is the strongest modifiable predictor of surgical failure. Patients with BMI >35 have lower MMA success rates. Bariatric surgery referral should be considered for morbidly obese OSA patients, with MMA reserved for those who achieve meaningful weight loss or who have significant skeletal deficiency independent of obesity.

OSA and Orthognathic Surgery¶

Every patient undergoing orthognathic surgery should be screened for OSA, particularly those with mandibular setback procedures planned. Mandibular setback reduces the posterior airway space and can precipitate or worsen OSA. If mandibular setback is necessary (Class III correction), consider maxillary advancement rather than mandibular setback whenever possible to preserve airway dimensions.

Critical Safety

Mandibular setback procedures have been clearly documented to reduce posterior airway space by 25-30% on average and can precipitate new-onset OSA. Preoperative sleep screening (minimum: STOP-BANG questionnaire; ideally: PSG) is mandatory before any planned mandibular setback. If the patient already has OSA or borderline AHI, alternative surgical plans (maxillary advancement only, or differential advancement) must be considered (Gokce et al., J Oral Maxillofac Surg, 2012).

Postoperative Management¶

MMA-Specific Postoperative Care¶

Airway monitoring: ICU or step-down unit observation for 24-48 hours. Nasal trumpets, head-of-bed elevation, and avoidance of sedatives
Edema management: Dexamethasone 8-10 mg IV perioperatively, ice packs, head elevation
Diet: Liquid diet for 2 weeks, soft diet for 6 weeks
Elastics: Light guiding elastics for 2-4 weeks; no rigid IMF (airway safety)
Follow-up PSG: At 3-6 months postoperatively (once edema has resolved and the patient has returned to baseline weight) to document surgical efficacy

Outcome Measures¶

Measure	Definition of Success
Sher criteria	AHI <20 AND >= 50% reduction from baseline
Surgical cure	AHI <5
ESS normalization	ESS <10
Quality of life	FOSQ (Functional Outcomes of Sleep Questionnaire) improvement
Partner outcomes	Snoring resolution, bed partner sleep quality

Coding and Reimbursement¶

Procedure	CPT Code	Notes
LeFort I osteotomy (MMA maxillary component)	21141-21160	Based on complexity
BSSO (MMA mandibular component)	21196	With or without distraction
Genioglossus advancement	21199	Segmental mandibular osteotomy
SARPE	21141 + 21196 (varies)	May require unlisted code
Hyoid suspension	21685	Hyoid myotomy and suspension
Hypoglossal nerve stimulator implantation	64568 + 64590	Electrode + generator
Polysomnography	95810	In-lab, attended
Home sleep apnea test	95800-95801	Unattended
DISE	42975	Drug-induced sleep endoscopy
Oral appliance (medical billing)	E0486	HCPCS code

Clinical Pearl

Medical necessity documentation for MMA in OSA requires: (1) diagnostic PSG with AHI >= 15, (2) documented CPAP failure or intolerance (>= 90 days of attempted use with adherence data from the CPAP device), (3) BMI documentation, (4) cephalometric analysis demonstrating skeletal contribution to airway obstruction. Including DISE findings strengthens the authorization request. Use ICD-10 G47.33 as the primary diagnosis.

Key References¶

Peppard PE, Young T, Barnet JH, et al. Increased prevalence of sleep-disordered breathing in adults. Am J Epidemiol. 2013;177(9):1006-1014.
Holty JE, Guilleminault C. Maxillomandibular advancement for the treatment of obstructive sleep apnea: a systematic review and meta-analysis. Sleep Med Rev. 2010;14(5):287-297.
Camacho M, Teixeira J, Zaghi S, et al. Maxillomandibular advancement and tracheostomy for morbidly obese obstructive sleep apnea: a systematic review and meta-analysis. Otolaryngol Head Neck Surg. 2015;152(4):619-630.
Sher AE, Schechtman KB, Piccirillo JF. The efficacy of surgical modifications of the upper airway in adults with obstructive sleep apnea syndrome. Sleep. 1996;19(2):156-177.
Woodson BT, Strohl KP, Soose RJ, et al. Upper airway stimulation for obstructive sleep apnea: 5-year outcomes. Otolaryngol Head Neck Surg. 2018;159(1):194-202.
Kezirian EJ, Hohenhorst W, de Vries N. Drug-induced sleep endoscopy: the VOTE classification. Eur Arch Otorhinolaryngol. 2011;268(8):1233-1236.
Riley RW, Powell NB, Guilleminault C. Maxillomandibular advancement for treatment of obstructive sleep apnea: a review of 306 consecutively treated patients. J Oral Maxillofac Surg. 2000;58(2):320-324.
Ramar K, Dort LC, Katz SG, et al. Clinical practice guideline for the treatment of obstructive sleep apnea and snoring with oral appliance therapy. JCSM. 2015;11(7):773-827.
Camacho M, Certal V, Abdullatif J, et al. Myofunctional therapy to treat obstructive sleep apnea: a systematic review and meta-analysis. Sleep. 2015;38(5):669-675.
Chung F, Yegneswaran B, Liao P, et al. STOP questionnaire: a tool to screen patients for obstructive sleep apnea. Anesthesiology. 2008;108(5):812-821.
AAOMS. Parameters of Care: Clinical Practice Guidelines for Oral and Maxillofacial Surgery (ParCare 6^th ed). 2017; Section VII.
Moon W, Wu KW, MacGinnis M, et al. The efficacy of maxillary protraction protocols with the micro-implant-assisted rapid palatal expander (MARPE) and the novel N2 mini-implant. Angle Orthod. 2015;85(1):164-174.