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402 PART V ORAL AND MAXILLOFACIAL SURGERY
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9. How long does it take the bone in the distraction zone to achieve 90% of normal
bony structure?
Eight months.
10. What are the etiologies of failure in distraction osteogenesis?
• Ischemic fibrogenesis: Inadequate blood supply leads to fibrous formation.
• Cystic degeneration: Venous congestion leads to a distraction gap filled with cystic cavity.
• Fibrocartilage nonunion: This is caused by unstable fixation. Cartilage is filled in the distraction gap.
• Buckling of regenerate is caused by premature removal of distraction device.
11. What is the primary advantage of an external distraction device versus an internal
distraction device?
Better control of the distraction vector.
12. How does the stability of moderate (5 to 10 mm) maxillary advancement with
distraction osteogenesis compare to that with conventional orthognathic surgery?
Distraction osteogenesis has not been proven to be superior in stability to conventional orthognathic
surgery for moderate maxillary movement. As a result, maxillary distraction is mostly reserved for
>10 mm advancement and patients with cleft palate.
13. Which Kaban subtype of hemifacial microsomia will benefit from distraction
osteogenesis?
Kaban’s classification (Class I, IIa, IIb, and III) describes temporomandibular joint defects found in
patients with hemifacial microsomia. The type I patient has a mild deficiency that usually does not
require surgery, whereas the type III patient has too little bone stock for osteotomy and distractor
placement. The type IIa patient can be treated predictably with orthognathic surgery and bone graft.
The type IIb patient will benefit the most from distraction osteogenesis.
14. What is included in the clinical assessment of patients for mandibular distraction?
Cephalometric analysis, facial nerve function, dental evaluation, photography, and possibly a three-
dimensional CT scan.
15. What incision and osteotomy are used for mandibular distraction?
Extra-oral skin incision (Risdon incision) with inverted-L osteotomy is by far the most common tech-
nique in making mandibular osteotomy and placement of distractor.
16. What are the possible complications related to mandibular distraction?
• Facial scar
• Loosening of hardware
• Facial nerve injury
• Sensory deficits of inferior alveolar nerve
• Tooth bud injury in young patient
• Noncompliance
17. Who are the candidates for neonatal mandibular distraction?
• Syndromic patients with poor mandibular growth
• Beyond 9 months and continued airway compromise secondary to tongue base obstruction
• Candidates for tracheostomy
• Failure of nonsurgical management
18. For neonatal mandibular distraction, what are the physical signs that indicate
adequate distraction?
When the lower alveolar crest is anterior to the maxillary alveolar crest or minimal episodes of oxygen
desaturation during close monitoring are good indications of adequate distraction.
19. For alveolar distraction in the mandible, what is the minimal bone height you need?
The minimal bone needed for proper placement of a distraction device is 3 to 4 mm. One millimeter of
bone will be removed for the osteotomy, and the remaining bone will be needed for screw fixation of
the distraction device in the proximal and distal bony segments.
20. What are the disadvantages of craniofacial distraction?
Prolonged treatment time, required external device, multiple clinical visits, and close postoperative
follow-ups are needed.
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21. What is the average age of the patient who needs to undergo midface
distraction?
Unless there is a severe upper airway obstruction from midface hypoplasia, midface distraction should
not be performed until approximately 3.5 years of age to ensure that there is adequate bone stock to
perform the procedure successfully.
22. What orthodontic measures can be practiced during activation and consolidation
to achieve the optimal occlusion?
During the activation and consolidation phases, the newly generated bone can be molded and shaped
by using guiding elastics to help establish the optimal occlusion. In unilateral mandibular distraction,
an intraoral splint can be used to maintain a posterior open bite during the distraction process. The
open bite will later close orthodontically by extruding the maxillary dentoalveolus with serial reduction
of the bite plate.
23. Where is the area of most bone formation after maxillary distraction?
Most bone formation occurs in the pterygomaxillary region.
SLEEP APNEA AND SNORING
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Robert A. Strauss, Kenneth J. Benson, Roman G. Meyliker
CHAPTER 41
1. How is snoring defined?
Snoring is a partial airway and pharyngeal flow obstruction that does not cause the individual to have
an arousal from sleep. Movement of air through the partially obstructed airway creates vibration and
thus the snoring sound.
2. Does snoring always indicate the presence of obstructive sleep apnea syndrome
(OSAS)?
No. Although patients who have OSAS are typically loud snorers, and snoring usually indicates some
degree of obstructed breathing, not all people who snore have OSAS. In fact, about 25% of adult
males snore, and this number increases with age, reaching about 60% at age 60 years. Most snoring
is not pathologic and may be reduced or prevented by lifestyle changes. However, with age and
weight gain, snoring can eventually degrade into sleep apnea.
3. Can a snoring patient with excessive daytime somnolence, but without other clas-
sic symptoms, have OSAS?
Yes. The lack of other classic symptoms of OSAS does not mean the diagnosis of OSAS can be ruled
out. Approximately 30% of sleep apnea patients have no other symptoms other than snoring. Because
snoring is an indication of partial airway obstruction, understanding the potential of the process to
worsen over time is important.
4. What is the surgical management of snoring?
Laser-assisted uvulopalatoplasty (LAUP) and Bovie-assisted uvulopalatoplasty (BAUP) are the most
commonly used surgical procedures for the treatment of snoring. Both procedures involve amputation
of the uvula and approximately 1 cm of the soft palate. After healing, the soft palate stiffens, reducing
its ability to vibrate, and thus reduces snoring. Occasionally the procedure is repeated to resect more
tissue without involving the levator muscle and causing velopharyngeal insufficiency. As long as
obstructive sleep apnea has been ruled out, the procedure can usually be done under local anesthesia
in the office. The advantage of LAUP over BAUP is the prevention of deeper tissue damage and possibility of less postoperative pain, but both procedures are equally effective.
5. What is obstructive sleep apnea (OSA)?
OSA is repetitive, discrete episodes of decreased airflow (hypopnea) or complete cessation of airflow
(apnea) for at least a 10 second duration, in association with >2% decrease in oxygen hemoglobin
saturation, and that causes an arousal from sleep.
6. Is there a difference between OSA and OSAS?
Yes. These are not the same processes. OSA is an objective lab finding. OSAS involves OSA combined
with signs and symptoms of disease.
7. What are the differences between apnea and hypopnea?
Apnea is the cessation of airflow lasting for more than 10 seconds. Hypopnea refers to a greater than
two-thirds decrease in tidal volume. Both show a decrease in oxygen saturation of at least 2%.
8. How many sleep stages are there in normal sleep patterns?
There are five sleep stages: one rapid eye movement (REM) stage and four non-REM stages.
9. During which sleep stages do most obstructive events occur?
Stages III and IV and the REM stage, which are the deeper stages of sleep. Pharyngeal wall collapse is
more common during these stages because the muscles are most relaxed.
10. What factors may contribute to OSA events?
Anything that effectively causes patient drowsiness or muscle relaxation may contribute to OSA.
Alcohol, sedatives, and narcotics are good examples. Weight gain can also potentiate OSA events, as
can allergies and upper respiratory infections.
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CHAPTER 41 SLEEP APNEA AND SNORING 405
AHI = apneas + hypopneas/total sleep time × 60
RDI = AHI + RERA
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11. What is the primary symptom of OSAS?
Excessive daytime sleepiness.
12. What other symptoms of OSAS may be present?
• Loud snoring
• Morning headache
• Depression
• Impotence
• Restless sleep and frequent arousal at night
• Hypertension
13. What are the important elements of the physical exam of a patient suspected of
having OSA?
A thorough head and neck exam, including diagnostic nasopharyngoscopy, should be performed
in any patient who presents with possible OSA. Exam should include the nose for signs of
obstruction or septal deviation, hypertrophic turbinates, and allergic rhinitis. The oral cavity should be examined for large tonsils, redundant soft palate and uvula, redundant lateral
pharyngeal walls, macroglossia, and retrognathia. The neck should be evaluated for a thick neck
and laryngeal obstruction. The patient should also be screened for signs of hypothyroidism, cor
pulmonale, and hypertension.
14. What is the main objective test for diagnosing OSAS?
Polysomnography is the most commonly performed evaluation for diagnosis of OSAS. It comprises the
following tests:
• Electroencephalography (EEG)
• Thoracic and abdominal efforts
• Electrooculography (EOG)
• Pulse oximetry
• Chin and leg electromyography (EMG)
• Electrocardiography (ECG)
• Nasal and oral airflow
In some cases, a less formal home sleep study (which can still be very accurate) and multiple sleep
latency tests (MSLTs) to confirm daytime sleepiness may also be included.
15. What are the Apnea/Hypopnea Index (AHI) and the Respiratory Disturbance Index
(RDI)?
The AHI represents the number of obstructive respiratory events per hour of sleep. The AHI
along with oximetry is the primary clinical indicator in the diagnosis of OSAS. The RDI is the
AHI plus any respiratory effort-related arousals (RERA), arousals associated with breathing that
do not meet the technical criteria for an apnea or hypopnea (e.g., greater than 10 seconds in
duration).
16. How are the AHI and RDI calculated?
An AHI of 5 is the upper limit of normal.
17. What is the modified Muller technique?
While undergoing fiberoptic nasopharyngoscopy, the patient performs an inspiratory effort against a
closed mouth and nose (reverse Valsalva) with the scope first above the soft palate and then secondarily above the base of the tongue. The examiner observes the degree of closure at the oropharyngeal
and hypopharyngeal levels.
18. How are lateral cephalograms used in evaluation of patients for OSAS?
Cephalometric analysis helps confirm physical exam and fiberoptic nasopharyngoscopy exam
results. The following are normal measurements of the cephalogram:
• Posterior nasal spine–tip of palatal uvula (PNS-P): 35 mm or less
• Mandibular plane–hyoid (MP-H): 15 mm or less
• Posterior airway space (PAS): 11 mm or greater
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19. What is Fujita’s classification of upper airway obstruction?
Type I Fujita: upper pharyngeal obstruction including palate, uvula, and tonsils; normal base of tongue
Type II Fujita: type I obstruction plus base of tongue obstruction
Type III Fujita: obstruction at tongue base, supraglottis, and hypopharynx; normal palate
20. What are the classes of sleep apnea?
Obstructive, central, and mixed.
21. What is the difference between OSA and central sleep apnea?
With OSA, there is a normal inspiration effort, but upper airway obstruction causes intermittent ces-
sation of airflow. Central sleep apnea is marked by a lack of inspiratory effort secondary to failure
of respiratory centers in the central nervous system to provide the phrenic nerve with appropriate
afferent information to activate the diaphragm.
22. What is the prevalence of OSA in the general population in the United States?
OSA is present in approximately 6% to 13% of the general US population.
23. Is there a relationship between the prevalence of OSA and chronic obstructive
pulmonary disease (COPD)?
According to one study, OSA is highly prevalent in moderate to severe COPD patients. These patients
have a greater than expected sleep disordered breathing that can be an important contributory factor
to morbidity and mortality of these patients.
24. Who usually treats central sleep apnea?
Neurologists and sleep specialists.
25. How is OSA classified?
The combination of AHI/RDI and lowest oxyhemoglobin desaturation (SaO2) is a good parameter for
scoring OSA severity (Table 41-1).
26. What are some systemic complications associated with OSAS?
• Cor pulmonale
• Hypertension
• Daytime somnolence
• Hypoxia
• Death
• Polycythemia vera
• Depression
• Stroke
27. What are the criteria for the cure of OSAS?
The surgical cure should have respiratory and sleep results equal to the second night of continuous
positive airway pressure (CPAP) titration.
• Although many articles use a postoperative AHI reduction of at least 50% with a maximum of 20
• Postoperative SaO2 that is normal or with only a few brief falls below 90%
• Normalization of sleep architecture
For patients on CPAP, a nonsurgical treatment, cure is determined as:
(i.e., an AHI of 26 should be reduced to 13, and an AHI of 80 should be reduced to 20), this can still
represent significant OSA. Currently, most experts agree that true cure is only achieved when the
AHI is less than 10 regardless of where it began.
Table 41-1. Classification of OSA
RDI SAO
Mild OSA 10-30 >90%
Moderate OSA 30-50 <85%
Severe OSA >50 <60%
OSA, obstructive sleep apnea; RDI, respiratory disturbance index.
2
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28. What are the nonsurgical treatment methods for OSAS?
Nasal CPAP is the most effective nonsurgical treatment for OSAS. It usually consists of an airtight
mask held over the nose by a strap wrapped around the patient’s head. CPAP is maintained by a
machine that is similar to a ventilator. Although nasal CPAP is nearly 100% effective in relieving OSAS,
it is very poorly tolerated. Even when it is initially successful, many patients (30% to 50%) eventually
stop using it because of discomfort or intolerance.
Mandibular positioning devices are another effective nonsurgical method of treating OSAS. These
devices open the airway by holding the mandible, and hence the tongue, forward during sleep. These
devices are used with patients with mild to moderate OSA, in patients with lesser degree of oxygen
saturation, relatively less daytime sleepiness, low frequency of apnea, and intolerant to CPAP or those
who refuse surgery. As with CPAP, discomfort and poor compliance are major problems. Behavioral
modifications, such as weight loss and avoidance of alcohol and sedatives, may also reduce OSAS.
Again, patient compliance is a major stumbling block.
29. What are the potential complications of CPAP?
Mask Related Pressure/Airflow Related
Skin rash Rhinorrhea
Conjunctivitis from air leak Nasal dryness/congestion
30. What are the surgical options for the management of OSAS?
• Tracheotomy
• Mandibular osteotomy with genioglossus advancement
• Uvulopalatopharyngoplasty (UPPP) or laser-assisted UPPP (LA-UPPP)
• Hyoid suspension
• Robotic base of tongue reduction
• Maxillary and mandibular advancement (MMA)
31. What is a “U-triple-P”?
UPPP is a surgical procedure performed to enlarge the oropharyngeal airway in an anterior-superior
and lateral direction. The tonsils are removed (if they have not been removed previously), along with
the posterior edge of the soft palate, including the uvula. The tonsillar pillars are then sewn together,
and the mucosa on the nasal side and oral side of the cut edge of the soft palate are sewn together.
This was historically the most common surgical procedure performed for treatment of OSAS, although
it is actually only moderately effective.
32. What are the results of UPPP in the treatment of OSAS?
UPPP offers promising results to many patients suffering from OSAS, but success rates vary:
• Elimination of snoring in 80% to 100% of cases
• Subjective decrease and improvement in excessive daytime somnolence in 80% to 100% of cases
• Measured RDI decrease by approximately 50% in 50% of patients
Despite having an approximate 50% reduction in RDI, a patient may still have significant OSA; there-
fore UPPP may not improve an OSA patient enough to decrease mortality. CPAP and tracheostomy are
still the gold standards to decrease OSA mortality rates. However, MMA has now been shown to be
highly effective as a surgical cure.
33. What are the potential complications of UPPP?
Bleeding is the most common postoperative complication. Velopharyngeal insufficiency occurs in 5%
to 10% of patients but is rarely permanent. Nasopharyngeal stenosis is rare but can be a complication. Other minor complaints include dry mouth, tightness in the throat, and an increased gag reflex.
34. What is the role of LAUP in OSAS?
LAUP is highly effective in the treatment of snoring, with successful results in 85% to 90% of patients.
However, the effectiveness of standard LAUP in the treatment of OSAS has been well established to be
poor and, in some cases, detrimental. Snoring and OSAS probably represent a continuum of a similar
Chest discomfort
Sinus discomfort
Tympanic membrane rupture (rare)
Massive epistaxis (rare)
Pneumothorax (rare)
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pathology, but it is still difficult to determine where LAUP is effective and where it is not. Therefore the
current recommendation is that all patients should undergo a sleep study before surgery for snoring
or OSAS. LAUP should only be used on patients who have no OSA.
35. What is an appropriate phase I surgical treatment plan for an OSAS patient with a
nasooropharyngeal site of obstruction?
In patients with less severe OSA, phase I or targeted surgical procedures may be attempted. UPPP
is excellent for snoring but has only a 40% success rate with OSAS at this obstruction site. Other
procedures include nasal surgery and palatal advancement procedures.
36. What phase I treatment would be appropriate for OSAS in the presence of oropharyngeal and hypopharyngeal obstruction?
UPPP or nasal surgery and genioglossus advancement with or without hyoid myotomy and suspension
are options for this level of obstruction. Newer types of tongue base and hyoid advancements that use
sutures around the base of the tongue or hyoid and connected to screws on the inferior border of the
mandible may also be effective, especially when used in combination with other phase I procedures.
37. What is the next step after phase I treatment?
CPAP treatment is continued for 6 months, at which time the patient is reevaluated with polysom-
nography. If phase I treatment is unsuccessful, then phase II surgery would be appropriate. Phase II
surgery involves orthognathic surgery, which consists of combined MMA. For patients with severe
OSA, many surgeons bypass phase I surgery and advance immediately to the more effective phase II
surgery (MMA).
38. What is the most effective surgical management of OSAS?
Tracheostomy. More recently, MMA has been shown to be highly effective as a surgical treatment with
much less morbidity than tracheostomy.
39. What is the success rate of MMA in the treatment of OSAS?
Many consider MMA the most promising surgical alternative to tracheostomy. Long-term studies
and recent evidence suggest approximately 85% to 95% effectiveness of MMA based on polysomnographic data. Quality of life indicators are also highly correlated. MMA is very effective because it
increases the entire airway space.
40. What are the complications of untreated childhood OSAS?
• Failure to thrive
• Growth impairment
• Behavior and learning problems
• Cardiopulmonary complications
41. What are the signs and symptoms of childhood OSAS?
• Snoring
• Nighttime sweating
• Restlessness
• Unusual sleeping positions
• Chest retraction
• Paradoxical breathing
• Use of accessory muscles
• Paradoxical rib cage motion during inspiration
• Enuresis
• Hyponasal speech
• Nasal obstruction
• Mouth breathing
42. What remains the first-line surgical treatment for OSAS in children?
Adenotonsillectomy has been shown to have high cure rates in healthy children with OSAS.
BiBliography
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Hausfeld JN: Snoring and sleep apnea syndrome. In American Academy of Otolaryngology—Head and Neck Surgery
Foundation: common problems of the head and neck, Philadelphia, 1992, Saunders.
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Munoz A: Sleep apnea and snoring. In Jafek BW, Stark AK, editors: ENT secrets, Philadelphia, 1996, Hanley & Belfus.
Nelson PB, Riley RW: A surgical protocol for sleep disordered breathing, Oral Maxillofac Clin North Am 7:345–356, 1995.
Nimkam Y, Miles P, Waite P: Maxillomandibular advancement surgery in obstructive sleep apnea syndrome patients: long-
term stability, J Oral Maxillofac Surg 53:1414–1418, 1995.
Prinsell J: Maxillomandibular advancement surgery: a site-specific treatment approach for obstructive sleep apnea in 50
consecutive patients, Chest 116:1519–1520, 1999.
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23:593–605, 1990.
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surgery, ed 5, St Louis, 2010, Elsevier.
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1531–1547, 1992.
FACIAL PAIN AND MYOFASCIAL
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DISORDERS
Bhavik S. Desai, Steven G. Gollehon, Gregory M. Ness
CHAPTER 42
1. How are the treatment modalities to manage temporomandibular joint (TMJ) pain
and dysfunction classified?
The treatment of TMJ pain and dysfunction is divided into irreversible and reversible modalities.
Reversible therapy consists of patient education, medication, physical therapy, and splint therapy.
Occlusal adjustments, prosthetic restoration, orthodontic treatment, orthognathic surgery, and TMJ
surgery are irreversible therapies that involve permanent changes in the function or morphology of the
masticatory system.
2. What is the most common form of pain and discomfort associated with TMJ
disorders?
Masticatory myalgia or myofascial pain.
3. How is the etiology of muscle pain categorized?
• Muscle hyperactivity (functional and dysfunctional)
• Muscle inflammation (myositis) secondary to injury or infection
• Myalgia associated with muscle hyperactivity
In contrast to episodic myofascial pain, myofascial pain dysfunction (MPD) syndrome is chronic
and self-perpetuating. Sustained muscular hyperactivity results in increased loading of the articular
surfaces, and microtrauma leads to inflammation, arthralgia, reflex muscle splinting, and continued
myospasm.
4. What is a differential diagnosis of conditions that can cause pain of non-odontogenic
origin in the head and neck region?
• Temporomandibular joint disorders including capsular, bony, and disc pathologies
• Myofascial pain to muscles of mastication
• Referred pain from maxillary sinus
• Pain of traumatic origin (including iatrogenic trauma)
• Trigeminal neuralgia
• Neurovascular pain such as migraines and tension headaches
• Trigeminal autonomic cephalgias such as cluster headaches, paroxysmal hemcrania, and
SUNCT (Short-lasting, Unilateral Neuralgiform-headache attack with Conjunctival injection and
Tearing)
• Pain secondary to salivary gland pathology such as infections and neoplasms
• Persistent idiopathic facial pain (atypical facial pain)
• Burning mouth syndrome (stomatodynia/glossodynia)
5. What are the hallmarks of trigeminal neuralgia?
Trigeminal neuralgia, briefly, is characterized by recurring episodes of severe, sharp, stabbing, lanci-
nating or electric shock-like pain along the V1, V2, or V3 branches of the trigeminal nerve. Symptoms
are typically unilateral, and the highest incidence of the condition is in middle-aged adults with a
female predilection. Pain is episodic, lasts seconds to a few minutes, and may occur multiple times a
day with refractory periods between pain episodes. It may occur spontaneously or may be triggered
by touching the face, exposure to wind, or by intraoral stimuli, such as tooth brushing and flossing.
A small percentage of cases are associated with central tumors. A patient with symptoms of trigeminal neuralgia under age 40 should be evaluated for multiple sclerosis. It is recommended to obtain
an MRI of the brain in suspected cases of trigeminal neuralgia. Medical management includes use of
anticonvulsant and neuropathic medications.
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6. What are some salient features of migraine headaches an oral surgeon or dentist
should be aware of?
Migraines are a group of episodic, recurring headache disorders of neurovascular origin. They have a
mean age of incidence in the second to fourth decades of life and are more common in females than
males. A migraine episode is typically characterized by severe, throbbing unilateral pain supraorbital
or localized in the periorbital region that could radiate to the frontalis and temples. Some patients can
identify triggering factors, such as alcohol, caffeine, food products, noises, etc., that may precipitate
a migraine attack. An episode of migraine may accompany gastric discomfort or nausea, and some
patients report prodromal symptoms prior to the onset of pain. An episode of migraines can last for a
few hours to days and is followed by a recovery phase. Medical management of migraines includes
use of medications such as triptans, neuropathic and anticonvulsant medications, and painkillers
along with avoidance of triggering factors when possible. It is pertinent for an oral surgeon or dental
provider to include migraines, especially those on the midface and temples, in the differential diagnosis of temporomandibular joint disorders, myofascial pain, and trigeminal neuralgia.
7. What are cluster headaches?
Cluster headaches are a well-characterized group of recurring headaches within the neurovascular
group of trigeminal autonomic cephalgias that also includes paroxysmal hemicrania and SUNCT. It
is characterized by intense, stabbing pain episodes in the ocular region and frontal/temporal region
lasting minutes to a few hours and accompanied by autonomic signs on the ipsilateral side such as
conjunctival tearing and rhinorrhea. It is more common in male patients than female, and peak incidence is during the second and third decades of life. Its medical management is very similar to that of
migraines.
8. What is the relationship between TMJ disc displacement and clinical symptoms
of pain and discomfort?
Despite the clinical evidence supporting the existence of TMJ disc derangement, many questions
remain unanswered, raising doubts about its clinical significance. Because pain is usually aggravated
by functional and parafunctional movements, it would appear that pain originates from pressure and
traction on the disc attachments. However, many, and perhaps the majority of, patients with displaced
discs have no pain, whereas some have severe pain. Studies by Kircos et al. (1987) and Westesson
et al. (1989) show a 30% incidence of disc displacement in asymptomatic patients with normal TMJ
exams and an 88% incidence of disc displacement in the contralateral asymptomatic joint in patients
with unilateral pain and discomfort, respectively. These findings make it clear that disc displacement
is not necessarily related to pain.
9. Does preemptive analgesia reduce postsurgical pain and chronic pain following
surgery in patients with TMJ disorders?
Recent studies have demonstrated that dynamic processing by neurons in the affected pathway may
facilitate nociception. The old view that nociceptive pathways are merely static conductors of signals
generated by noxious stimuli appears to be invalid. As a result, preemptive analgesic techniques may
reduce postsurgical pain and, perhaps, reduce the possibility of chronic pain in the operated patient.
10. What is the main goal in the postoperative management of patients with TMJ
dysfunction?
Chronic pain and restricted jaw movement are the most common complaints of multiply operated TMJ
dysfunction patients. Typically, pain restricts the patient’s ability to comply with postsurgical physical
therapy, contributing to a gradual decline in jaw mobility. Therefore the major management objective
should be adequate pain control coupled with effective physical therapy to maintain jaw function.
11. What are the management strategies used to treat pain and discomfort in the
multiply operated patient with TMJ dysfunction?
Strategies include pharmacologic approaches, behavioral modification techniques, psychiatric
counseling, and physical therapy. Obviously, the success of any approach will depend on an accurate
assessment of the patient’s physical and emotional status. Furthermore, combination therapies (provided by a coordinated, multidisciplinary team of qualified health care providers) are often required to
optimize the patient’s condition. Further surgery is ineffective at reducing pain in the multiply operated
patient and is not indicated unless a specific mechanical obstruction to function is identifiable and
amenable to surgical correction (e.g., ankylosis). In such cases, the patient must understand that
improvements in range of motion and function are not likely to be accompanied by pain reduction.
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