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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4421_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Contents
- •Contributors
- •1.6 Mixed Disorders
- •1.7 Isolated Symptoms
- •1.7.1 Snoring
- •1.7.2 Catathrenia
- •1.8 Summary
- •References
- •1.1 Introduction
- •1.2 Obstructive Sleep Apnea
- •1.2.1 Obstructive Sleep Apnea, Adult
- •1.2.2 Obstructive Sleep Apnea, Pediatric
- •1.3 Central Sleep Apnea
- •1.3.5 Primary Central Sleep Apnea
- •1.5 Sleep-Related Hypoxemia Disorder
- •2.7 Summary
- •References
- •3: Health Consequences of Obstructive Sleep Apnea
- •3.1 Cardiovascular Consequences
- •3.1.1 Chronic Heart Failure
- •3.1.2 Systemic Hypertension
- •3.1.3 Coronary Heart Disease
- •3.1.4 Arrhythmias
- •3.1.5 Cerebrovascular Disease
- •3.2 Respiratory Consequences
- •3.2.1 Asthma
- •3.2.3 Pulmonary Embolism
- •3.2.4 Pulmonary Hypertension
- •3.3.1 Diabetes Mellitus
- •3.3.2 Metabolic Syndrome
- •3.3.3 Sexual Dysfunction
- •3.4 Gastrointestinal Consequences
- •3.4.2 Nonalcoholic Fatty Liver Disease
- •3.5 Obstetric Outcomes
- •3.5.2 Gestational Diabetes
- •3.5.4 Maternal Surgical Complications
- •3.6 Perinatal Outcomes
- •3.6.1 Impaired Fetal Growth
- •3.6.2 Preterm Birth
- •3.6.4 Stillbirth
- •3.6.5 NICU Admission
- •3.7 Perioperative Outcomes
- •3.8 Accident-Related Consequences
- •3.9 Cancer-Related Outcomes
- •3.10 Survival Outcomes
- •3.10.1 Overall Mortality
- •3.10.2 Cardiovascular Death
- •3.10.4 Perioperative Mortality
- •References
- •4.1 Patient Case
- •4.2 Introduction
- •4.3 History
- •4.4.1 Oxygen
- •4.4.2 Vascular
- •4.4.3 Endocrine
- •4.6.1 Attention & Executive Function
- •4.6.4 Visual-Spatial
- •4.7 Summary
- •References
- •5.1 Introduction
- •5.2 Obesity
- •5.3 Hypertension
- •5.4 Diabetes Mellitus
- •5.5 Fatty Liver Disease
- •5.6 Conclusions
- •References
- •6.1 Background
- •6.2 History Taking
- •6.3 Physical Examination
- •6.4 Conclusion
- •References
- •Further Reading
- •7.1 Background
- •7.2.2 Screening Tools
- •7.2.3 Diagnostic Tests
- •7.2.7 Clinical Guidelines
- •7.3 Home Sleep Apnea Test (HSAT)
- •7.3.1 Advantages
- •7.3.2 Disadvantages
- •7.3.3 Patient Selection
- •7.3.4 Data Obtained
- •7.3.8 Recommended Follow-Up
- •7.3.9 Clinical Outcomes
- •7.4 Polysomnography (PSG)
- •7.4.1 Patient Selection
- •7.4.4 Follow-Up
- •7.5 Conclusions
- •Further Reading
- •8.1 Introduction
- •8.4 CBCT and OSA
- •8.5.1 CPAP
- •8.5.2 Oral Appliances
- •8.5.3 Maxillomandibular Advancement
- •8.6 Upper Airway Stimulation
- •8.7 Summary
- •References
- •9.1.1.1 Cranial Base Lengthening
- •9.1.1.2 Cranial Base Flexion
- •9.1.5.3 Tongue Growth
- •References
- •10.2.1.1 Cranial Base
- •10.2.1.2 Facial Height
- •10.2.1.4 Pharyngeal Airway Space
- •10.2.1.6 Hyoid Bone Position
- •10.3.1 Maxillary Expansion
- •10.3.1.4 RME for OSA
- •References
- •11.2 Pathophysiology
- •11.3 Clinical Exam
- •11.5 Treatment
- •11.6 Summary
- •References
- •12.1 Introduction
- •12.5 Mask Options
- •12.6.1 Dry Mouth
- •12.6.2 Tangled Tubing
- •12.6.3 Condensation
- •12.6.4 Headgear Problems
- •12.6.6 Ramp
- •12.6.7 Cleaning Equipment
- •12.6.8 Skin Irritation
- •12.6.9 Nasal Congestion
- •12.6.10 Aerophagia
- •12.7 Cleaning Equipment
- •12.7.1 Travel Options
- •References
- •13: Oral Appliance Therapy
- •13.1 Introduction
- •13.2 Terminology
- •13.3.2 Device Designs
- •13.4 Methodology
- •13.7.2 Device Design
- •13.7.5 Non-anatomical Traits
- •13.7.6 Disease Severity
- •13.7.7 Supine Dependency
- •13.12.3 Adherence
- •13.12.4 Mean Disease Alleviation
- •13.13 Long-Term Outcomes
- •13.16 Guidelines
- •References
- •14.1 Introduction
- •14.2 Positional Therapy
- •14.2.1 Weight Loss
- •14.2.2 Nasal EPAP Therapy
- •14.2.3 Oral Pressure Therapy
- •14.2.4 Hypoglossal Nerve Stimulation
- •References
- •15.1 Introduction: Background Information
- •15.4 Preoperative Assessment
- •15.4.1 Physical Examination
- •15.4.2 Polysomnography
- •15.4.3 Clinical History
- •15.5 Preoperative Consent
- •15.6 Preoperative Assessment
- •15.6.1 Surgical Setting
- •15.8 Instrumentation
- •15.8.1 Tonsillectomy
- •15.8.2 Adenoidectomy
- •15.9 Postoperative Management
- •15.9.1 Pain
- •15.9.2 Diet
- •15.9.3 Follow-Up
- •15.10 Expected Outcomes by Population
- •15.10.1 General Population
- •15.10.2 Complex Children
- •15.10.2.1 Obese Children
- •15.10.2.2 Down Syndrome
- •15.10.2.3 Craniofacial Syndromes
- •15.10.2.4 Synchronous Airway Lesion
- •15.11.3 Cardiovascular Parameters
- •15.13 Conclusion
- •References
- •Further Reading
- •16.1 Introduction
- •16.3.1 Anatomic Factors
- •16.8 Summary
- •References
- •17: Palatal Surgery for OSA Patients
- •17.1 Introduction
- •17.2.2 Nasopharyngeal Endoscopy
- •17.2.3 Cephalometrics
- •17.3.1.1 Success Rate of UPPP
- •17.3.1.2 Limitations of UPPP
- •17.3.1.3 Impact of UPPP
- •17.3.1.4 Complications of UPPP
- •17.3.2.2 Z-Palatopharyngoplasty
- •17.3.2.3 Expansion Sphincter Pharyngoplasty
- •References
- •18: Hypopharyngeal Surgery for OSA Patients
- •18.1 Introduction
- •18.2 Historical Perspective
- •18.3 Patient Selection
- •18.4 Physical Exam
- •18.5 Imaging I
- •18.5.1 Imaging
- •18.6 Drug-Induced Sedated Endoscopy
- •18.7 Treatment Algorithm
- •18.8 Procedures
- •18.8.1 Transoral Robotic Surgery
- •18.8.2 Radiofrequency Ablation (RFA)
- •18.8.3 Genioglossus Advancement
- •18.8.4 Tongue Base Suspension
- •18.8.5 Hyoid Suspension
- •18.8.7 Hypoglossal Nerve Stimulators
- •18.9 Future Directions
- •References
- •Suggested Reading
- •19.1.1 Imaging
- •19.2.1.1 Pierre Robin Sequence
- •19.2.1.2 Craniofacial Microsomia
- •19.2.2.1 Crouzon’s Syndrome
- •19.2.2.2 Apert Syndrome
- •19.2.3.1 Treacher Collins Syndrome
- •19.2.3.2 Goldenhar Syndrome
- •19.3 Surgical Correction
- •Bibliography
- •20.1 Introduction
- •20.4.2 Surgical Technique (DOME)
- •20.4.4 Consolidation Phase
- •20.6 Discussion
- •References
- •21.3.3 Maxillomandibular Setback
- •References
- •22.1 Introduction
- •22.3 Results
- •22.3.1 Success Rate
- •22.4 Cases
- •22.5 Discussion
- •22.6 Conclusion
- •References
- •23.1 Patient Evaluation
- •23.1.1 Patient Concerns
- •23.1.4 Facial Evaluation
- •23.1.5 Lateral View
- •23.1.6 Oral Examination
- •23.1.7 Periodontal Evaluation
- •23.1.8 Tongue Assessment
- •23.1.9 Temporomandibular Joint
- •23.1.10 The Nose
- •23.1.11 Oropharyngeal Airway Assessment
- •23.2 Radiographic Evaluation
- •23.2.2 Lateral Cephalometric Radiograph
- •23.2.5 Cephalometric Analysis
- •23.3 Dental Model Analysis
- •23.3.1 Arch Length Measurements
- •23.3.2 Tooth Size Analysis
- •23.3.3 Tooth Position
- •23.3.4 Arch Width Analysis
- •23.3.6 Cuspid-Molar Position
- •23.3.7 Tooth Arch Symmetry
- •23.3.10 Ankylosed Teeth
- •23.4 Summary
- •References
- •24.1 TMJ Articular Disc Displacement
- •24.3 Reactive Arthritis (ReA)
- •24.5 Trauma
- •24.6 TMJ Ankylosis
- •24.7 Other End-Stage TMJ Conditions
- •24.8 Summary
- •References
- •25.1 Background
- •25.2 Treatment Planning Maxillary Surgery
- •25.2.1 Bone Anatomy
- •25.2.2 Vascular Anatomy
- •25.5 Adjunct Procedures
- •25.6 Complications
- •References
- •26: Mandibular Surgical Procedures
- •26.1 Genioplasty Procedures
- •26.2 Osseous Genioplasty
- •26.2.1 Anteroposterior Augmentation
- •26.2.2 Surgical Procedure
- •26.2.3 Anteroposterior Reduction
- •26.2.4 Vertical Augmentation (Downgraft)
- •26.2.5 Vertical Reduction
- •26.3 Alloplastic Augmentations
- •26.3.1 Surgical Procedure
- •26.4 Genioplasty Complications
- •26.5 Mandibular Subapical Procedures
- •26.5.3 Possible Complications
- •26.6 Mandibular Body Surgery
- •26.7.1 Nonunion or Malunion
- •26.7.3 Infections
- •26.7.4 Periodontal Defects
- •26.7.5 Nerve Damage
- •26.8 Mandibular Ramus Surgery
- •26.9 Vertical Ramus Osteotomy
- •26.11.1 Early Relapse
- •26.11.2 Condylar Sag
- •26.11.4 Unfavorable Splits or Fractures
- •26.11.6 Periodontal Defects
- •26.11.8 Nerve Injury
- •26.11.9 Infections
- •26.11.10 Nonunion
- •26.11.11 Bleeding Problems
- •References
- •27.1 Occlusal Plane Alteration
- •27.1.1 History
- •27.2 Corrected Frankfort Horizontal Plane
- •27.3 High Occlusal Plane (HOP) Facial Type
- •27.3.6 MRI Evaluation
- •27.3.7 TMJ Disc Displacement
- •27.3.9 Reactive Arthritis
- •27.3.11 Other End-Stage TMJ Pathologies
- •27.6 Summary
- •References
- •28: Maxillomandibular Advancement
- •28.1.1 Symptoms
- •28.1.3.1 Noninvasive Treatments
- •28.1.3.2 Surgical Interventions
- •28.4.1 Preoperative Medical Assessment
- •28.5 Procedure
- •28.5.1.2 Plates Vs. Screws
- •28.7 Post-MMA Follow-Up Care
- •28.8 Conclusion
- •References
- •29.2.1 CASS Adoption Widespread
- •29.2.2 Overall CASS Accuracy
- •29.2.2.1 Soft-Tissue Prediction Simulators
- •29.2.3 Cost
- •29.4.1 Overall CASS Process
- •29.4.1.1 Step 1: Patient Referral
- •29.4.1.7 Step 7: Procedure
- •29.4.4 Case 3
- •29.5 Conclusion
- •References
- •30.1 Introduction
- •30.2 Preoperative Considerations
- •30.2.1 Surgical Facility
- •30.2.2 Medical Clearance
- •30.2.3 Anesthesia Considerations
- •30.3 Inpatient Postoperative Management
- •30.3.1 Immediate Postoperative Course
- •30.3.2 Acute Pain Management
- •30.3.5 DVT Prophylaxis
- •30.3.6 Nutrition
- •30.3.7 Antibiotics
- •30.4.1 Follow-Up Regimen
- •30.4.2 Postoperative Occlusal Guidance
- •30.5 Conclusion
- •References
- •31.1 Paradigm
- •31.2 Preoperative
- •31.3 Acute Post-surgical
- •31.4 Long-Term Post-surgical
- •References

362
L. Wolford
24
Magnetic resonance imaging (MRI) is one of the most
important tools available to the oral and maxillofacial surgeon for diagnosis and treatment planning of
patients with temporomandibular joint (TMJ) disorders.
However, it is estimated that 40–60% of TMJ MRIs are
misread by radiologists. Therefore, it is very important
for the oral and maxillofacial surgeon to be able to interpret TMJ MRIs. This chapter incorporates magnetic
resonance imaging (MRI) into the diagnostic evaluation of obstructive sleep apnea (OSA) patients that
also have temporomandibular joint (TMJ) pathology.
TMJ pathology may coexist with the dentofacial deformity or may be the etiology of the jaw deformity that is
responsible for creating the OSA.This chapter will present the MRI ndings of the common TMJ pathologies
associated with OSA.TMJ pathologies associated with
mandibular condylar hyperplasia, benign, or malignant
tumors will not be discussed, as they do not contribute
to OSA.
One of the primary factors contributing to sleep
apnea is a decreased oropharyngeal airway. Using lateral cephalometric analysis, the normal A-P dimension
of the oropharyngeal airway from the posterior pharyngeal wall to the soft palate and posterior pharyngeal
wall to the base of the tongue should be 11mm, plus
or minus 2mm. OSA patients commonly have a high
occlusal plane angle facial morphology that includes a
retruded mandible and maxilla as well as a decreased
oropharyngeal airway. A normal occlusal plane angle
to the Frankfort horizontal plane is 8 degrees, plus or
minus 4 degrees, but OSA patients commonly have a
signicantly increased occlusal plane angle. There is a
triad of factors that are commonly observed in OSA
patients, and they include: (1) high occlusal plane angle
facial morphology associated with retruded maxilla and
mandible, (2) nasal airway obstruction related to hypertrophied turbinates and/or nasal septal deviation or
spurring, and (3) TMJ pathology. Patients with the high
occlusal plane angle facial morphology should routinely
be assessed for nasal airway obstruction, decreased oropharyngeal airway, and TMJ pathology.
For many OSA patients, the most highly predictable surgical treatment is to advance the maxilla and
mandible in a counterclockwise direction [1–4], which
opens up the oropharyngeal airway signicantly [5–10].
The counterclockwise rotation of the maxillomandibular complex usually provides the best facial aesthetic
balance while maximizing the increase of the oropharyngeal airway dimensions. The traditional method of
straightforward or clockwise advancement of the maxilla and mandible that most surgeons perform may compromise the esthetic outcome and decrease the potential
increase of the oropharyngeal airway.
Many OSA patients have TMJ issues that need to be
surgically addressed in order for the orthognathic surgery
to be successful and provide a stable, predictable outcome. Preexisting TMJ pathology, if ignored, can result
in postsurgery condylar resorption and mandibular
relapse with skeletal instability, malocclusion, pain, and
decrease of the oropharyngeal airway that was achieved
from the orthognathic surgery [11–21]. As the maxillary
and mandibular complex is advanced forward in a counterclockwise direction in the presence of healthy TMJs
or surgically corrected TMJs, the overall facial balance
is predictably improved, skeletal and occlusal stability
is established, jaw function is enhanced, the oropharyngeal airway is opened, and pain is eliminated.
To evaluate the presence or absence of TMJ pathology, radiographic evaluation is very helpful in the diagnostic process and cone-beam CT (CBCT) technology
makes accessibility to low-cost, low-radiation CT scans,
but are primarily methods to evaluate hard-tissue structures. MRI allows evaluation of hard and soft tissues of
the TMJ, such as condyle, fossa, and disc position, morphology, mobility, extent of joint bone and soft-tissue
degenerative changes, inammation, condylar resorption, tumors, and connective tissue/autoimmune diseases [22, 23]. Additional imaging such as panograms,
cephalometric radiographs, CT scans, CBCT scans,
bone scans, 3D imaging, and 3D modeling may also be
indicated for some OSA patients.
MRIs can help in the diagnosis of TMJ pathology
in the silent joint where disc displacement and degenerative changes can be present but may not make noise
and may not be particularly uncomfortable or painful,
and therefore, clinicians often ignore the TMJ issues. If
untreated in a patient requiring orthognathic surgery
for maxillary/mandibular advancement (MMA) with
or without counterclockwise rotation (CCWR) to correct OSA, surgery could result in a poor outcome relative to function, skeletal and occlusal stability, airway,
and pain. The MRI provides a method to identify these
patients and the associated TMJ pathologies.
Dr. Raymond Damadian is credited with the
development of the MRI imaging technology, and
on July 3, 1977, the rst human MRI exam was performed. Superconducting magnets from 1.5 to 3.0 tesla
(15,000–30,000 gauss) are required to achieve the imaging. Interestingly, the earth’s magnetic eld is equal to
0.5gauss. There are radiofrequency coils that transmit
waves into the body. Superconducting magnets align
the protons head to feet. The radiofrequency magnets
change the rotation of the protons causing resonance
at Larmor frequency. There are three gradient magnets
within the machine that create the image slices. The signals generated are picked up by special TMJ coils and
sent to a computer, and Fourier transform formula maps
the tissues and then integrates into 2D or 3D images.
Contrast materials can be injected as normal and abnormal tissues will react differently. There are no known

MRI Evaluation forPatients withTMJ Disorders andObstructive Sleep Apnea
363
24
biological hazards; however, it is not recommended during pregnancy. Dangers include magnetic coding will be
erased from such devices as credit cards, etc. Pacemakers
may malfunction. Aneurysm clips in the brain could
move, and magnetic materials around or in the patient
can cause serious or life-threatening damage.
MRI requirements for TMJ imaging include the fol-
lowing:
1. A closed 1.5–3.0 tesla MRI machine.
2. TMJ coils are highly recommended to enhance the
imaging. The coils, particularly in the lower grade
machines (1.5 tesla), will signicantly enhance the
imaging. Without the coils, the imaging may be
unreadable and nondiagnostic.
3. MRI is best done prior to the application of orthodontic appliances as the metal devices can create distortion and interference of the TMJ anatomy,
although in the presence of orthodontic appliances,
an adequate MRI of the TMJ can usually be acquired.
However, the more metal that may be associated with
the orthodontic appliances and additional nonremovable metal devices, the greater the risk of interference
of the MRI imaging. Any metal orthodontic appliances or devices must be nonmagnetic.
The recommended TMJ views for adequate MRI interpretation include the following:
1. Coronal Closed Views– in centric relation, maximum
closure, without splints.
2. Sagittal Closed Views– in centric relation, maximum
closure, without splints.
3. Sagittal Open Views– with maximum jaw opening.
4. Sagittal Dynamic Views– from a slight open position
(to accommodate the ratchet device) to maximum
open position. The dynamic views are often helpful
in determining the point at which the displaced discs
may or may not reduce mobility of the condyle and
disc, presence of adhesions, etc. However, it is important to understand that the “dynamic” views are not
acquisitioned with the patient’s normal voluntary
jaw opening. On the contrary, the opening is achieved
with the patient in a supine position using an opening ratchet device placed between the maxillary and
mandibular incisors. This opens the bite to accommodate the device so that the dynamic imaging
begins with the jaws slightly open, unless the patient
has an anterior open bite. The device opens the jaw
in increments with MRI data recorded at each increment of opening until the maximum opening is
achieved with the device still in place. The MRI data
gathered at the various increments are integrated to
appear as a continuous motion from the slight open
position to maximum opening. This may or may not
duplicate the patients normal jaw function when the
patient is in an upright position.
In the MRI, different tissues are contrasted dependent
of the tissue properties (proton density), and the pulse
sequence parameters are usually dened as a T1- or
T2-weighted image. In general, T1 images are helpful in
identifying disc position, the presence of alteration in
bone and soft-tissue structures, and interrelationships
of the bony and soft-tissue anatomy. T2 MRI images
are more helpful in identifying inammatory responses
in the TMJ.The importance of disc position cannot be
overemphasized, and the MRI is the best diagnostic tool
to determine disc position, TMJ pathology, quality, and
salvageability of the disc and condyle, as well as will
dictate the treatment protocol, particularly if surgery is
indicated.
With a normal healthy TMJ (. Fig.24.1), the con-
dyle should have a uniform shape and consistent thickness of cortical bone. The condyle should be positioned
in the fossa with equal joint space between the condyle
and fossa posteriorly, superiorly, and anteriorly. The
articular disc should sit on top of the condyle with the
posterior band at about the 12 o’clock position. The disc
should have a bowtie shape with increased thickness of
the posterior band and anterior band and a thinner area
for the intermediate zone. The articular eminence should
have a moderate inclination, although the articular eminence may be quite variable in steepness. There should
be no joint effusion, inammation, or synovitis evident.
On opening, the condyle and disc should translate down
and forward as a unit beneath the articular eminence.
The MRI imaging can be correlated to CBCT and CT
scan imaging of the TMJs for joint space and greater
interpretation of bony pathology.
24.1 TMJ Articular Disc Displacement
The most common type of disc displacement is anterior
as seen in . Fig.24.2a. The posterior band of the disc
is anterior to the condylar head. When opening, the disc
may (. Fig.24.2b) or may not reduce. Upon reduction,
there is usually a palpable and sometimes audible pop
in the joint as the head of the condyle comes downward
and forward over the back end of the posterior band
as the condyle reduces onto the disc (.
The mandible may then open the rest of the way with
a normal condyle–disc relationship. Upon closing, the
condyle may slide back off the posterior band of the
disc, making a reciprocal closing click. As TMJ disease
progresses, on opening the disc may not reduce back
in position creating a silent joint, as the disc remains
anterior throughout jaw function. Displacement of the
articular disc can initiate a cascade of events leading to
arthritis.
The anteriorly displaced disc may eventually become
deformed and nonreducing but still be mobile, or
Fig. 24.2b).

24
ab
364
L. Wolford
. Fig. 24.1 MRI sagittal view of a normal healthy TMJ. a The
joint space is equal posterior, superior, and anterior with the posterior band of the disc at 12 o’clock position relative to the condyle.
become adherent to the articular eminence and/or fossa
The condyle has a smooth regular contour. b On opening, the condyle and disc translate down and forward as a unit beneath the articular eminence
24.1.1 Silent TMJ withDisc Displacement
limiting the translation abilities of the condyle and disc
creating the “closed lock” phenomenon (. Fig.24.2c).
It is not uncommon to see a lateral rotational disc displacement where the disc may be anteriorly displaced at
the lateral aspect of the joint, but toward the medial, the
disc is in a more normal position, thus the importance
of the evaluation of sagittal MRI views from lateral to
medial in a sequential fashion. Since the lateral attachment of the disc to the condyle is weaker compared to
the medial attachment, the disc more commonly can displace at the lateral aspect of the joint initially and then
progress toward the medial side. This also can cause the
disc to displace medially, so the disc becomes anteromedially displaced.
Medial displacement of the disc can occur where
the disc is dislocated to the medial aspect of the joint
and lacks coverage of the lateral portion of the condyle. There is typically a decreased lateral joint space,
more evident on the coronal view (. Fig.24.3a). This
can result in a condition called lateral capsular impingement, where the disc displaces medially and the capsule
is pulled over between the lateral pole and the fossa,
which can create pain issues. Discs can also be displaced
laterally (. Fig. 24.3b), but this is less common than
anterior and/or medial displacement. There is a breakdown of the attachment at the medial pole, and the disc
is displaced lateral to the condyle and can cause pain
and dysfunction.
There are a number of TMJ pathological processes
where the disc is displaced, but yet, the disc is silent with
function. An MRI can determine the following silent
joint disorders: (1) anterior displaced disc that does not
reduce on opening (. Fig.24.4a, b); (2) steep articular
eminence where the articular disc is anteriorly displaced,
but in a vertical orientation so that upon opening, there
is an immediate reduction of the disc as it is in a “preclick” position (. Fig. 24.5a); (3) medial or lateral
disc displacements (. Fig.24.3a, b); (4) certain pathological conditions such as adolescent internal condylar
resorption (AICR) where there may be thickening of
the bilaminar tissues so that there is a smooth transition from the thickened bilaminar tissue onto the displaced disc (.
Fig.24.5b); (5) long-term splint therapy
with downward and forward posturing of the mandibular condyle with thickening of the bilaminar tissues so
that there is a smooth transition onto the disc (similar
to . Fig. 24.5b); and (6) Class II mechanics that may
articially pull the condyle down and forward onto the
disc, but in an unstable position relative to the condylar
centric relation.
When discs are anteriorly displaced for an extended
time period, the discs may become deformed with loss
of the intermediate zone and thickening of the posterior
and anterior bands with progressive arthritis, rendering the discs and possibly the condyles nonsalvageable

MRI Evaluation forPatients withTMJ Disorders andObstructive Sleep Apnea
365
24
a
c
b
. Fig. 24.2 a In the closed position, the condyle is positioned pos-
terior in the fossa and the disc is anteriorly displaced with the posterior band at about the 10 o’clock position. b On opening, the disc
reduces into a normal position. c The disc is severely deformed and
(. Fig.24.2c). Also, there may be a degenerative process developing in the discs where there is a breakdown
of the cartilaginous substance with vascular invasion
and degeneration. When discs advance to a certain level
of deformation and degeneration, they become nonsalvageable. When discs are displaced and nonreducing,
the deformation and degenerative processes progress
more rapidly as compared to displaced discs that reduce.
Bony degenerative changes occur as well. An MRI will
help determine the degree and progression of the degen-
anteriorly displaced. On opening, the disc will not reduce. If the disc
becomes adhered to the articular eminence, it can cause a “closed
lock” situation
erative and deformation changes to the joint structures
and indicate the corrective surgical procedures that will
provide the most predictable outcome for each patient’s
specic presentation. When discs are salvageable, a surgical option is to reposition and stabilize the disc into
a normal position with a Mitek bone anchor and articial ligaments (Mitek anchor technique) (.
Fig.24.6)
[24–33]. For success of this technique, specic criteria
must be met. The MRI is strategic in determining if this
technique will be benecial.

366
L. Wolford
24
ab
. Fig. 24.3 a MRI coronal view demonstrates a medially displaced articular disc. Notice the decreased vertical joint space toward the lat-
eral aspect of the fossa. b Coronal view demonstrates lateral displacement of the articular disc. Medial joint space may be narrowed
a
. Fig. 24.4 a Sagittal view of an anteriorly displaced disc. Green
arrows identify the disc and “C” indicates the condyle. b In the open
view, the condyle translates forward beneath the articular eminence,
b
but the disc remains anteriorly displaced without reduction. Green
arrows identify the disc and “C” indicates the condyle

MRI Evaluation forPatients withTMJ Disorders andObstructive Sleep Apnea
a b
367
24
. Fig. 24.5 a Sagittal view with the white arrow pointing to the
posterior band of the disc that is anteriorly displaced but in a vertical orientation. The red arrow points to the condyle–disc interface.
As the mandible is opened, there is a smooth transition between the
condyle and disc rendering an opening without a click or pop. This
is a silent joint with a displaced disc, but can cause pain and dysfunction. b There is signicant thickening of the bilaminar tissues in this
. Fig. 24.6 Mitek anchor
technique. a The disc is
anteriorly displaced (green
arrow). The bilaminar tissue on
top of the condyle is excised and
the disc is mobilized. b The disc
is repositioned over top of the
condyle. The Mitek anchor is
inserted into the posterior head,
and articial ligaments
(0-Ethibond suture) are used to
secure the disc in position. c
Illustrates the Mitek anchor and
the placement of two 0-Ethibond
sutures through the eyelet that
will act as articial ligaments. d
Posterior view of the condyle
showing the insertion of the
Mitek anchor lateral to the mid
sagittal plane and the placement
of the sutures (articial
ligaments) through the posterior
aspect of the posterior band of
the disc to secure it in position
a
c
Mitek mini anchor
0-Ethibond suture
TMJ with AICR.The thickening of the bilaminar tissues can occur
with certain pathologies as well as long-term splint therapy. A thickened bilaminar tissue can result in a smooth transition of the condyle onto the disc rendering a silent joint. The red arrows identify the
position of the disc and “C” indicates the condyle. The distance
between the head of the condyle and the fossa identies the hyperplastic bilaminar and synovial tissues
b
d
1.8 × 5 mm
Mitek
anchor
Posterior view

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L. Wolford
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24.1.2 Criteria forArticular Disc
Repositioning withtheMitek Anchor
Technique
1. Anterior, medial, or lateral disc displacement.
2. Fouryears or less since initial disc displacement.
3. Salvageable disc and condyle.
4. No other joints involved (no polyarthritis).
5. No reactive arthritis.
6. No connective tissue/autoimmune disease.
7. No intracapsular adhesions.
8. No history of recurrent infections, such as sexually
transmitted diseases; upper respiratory or pulmonary
infections; urinary tract infections; genital infections
or history of endometriosis or other gynecological
pathologies; gastrointestinal problems such as irritable bowel syndrome, GERD, and Crohn’s disease;
and eye infections. These conditions can cause a reactive arthritis, where patients may not do well, even
with an ideal surgical disc repositioning as the pathological process may continue to progress postsurgery.
24.1.3 Implications fortheOSA Patient
is some distortion of the MRI imaging because of the
metal anchor in the head of the condyle, but the reduced
position of the disc is noted.
OSA patients that fall out of the criteria for disc
repositioning will benet from custom-tted total joint
prostheses [8, 34–55] where the prostheses are used to
reconstruct the TMJ as well as advance the mandible
for MMA (.
Fig.24.8). Virtual surgical planning (VSP)
In OSA patients that have TMJ disc displacement, but
meet the criteria for disc repositioning, and if the procedure is properly performed prior to or concomitant
with MMA with or without CCWR, surgical treatment
should provide skeletal and occlusal stability, improved
jaw function, signicant decrease or elimination of
pain, and improved dimension of the oropharyngeal
airway. Postsurgical MRI sagittal view of a repositioned
disc with a Mitek anchor is seen in . Fig.24.7. There
ab
.Fig. 24.7 MRI demonstrates the position of the articular disc over
top of the condyle, secured by the Mitek anchor and articial ligaments.
The Mitek anchor creates some image distortion because of the metal
content. The articular disc is the ideal position relative to the condyle
. Fig. 24.8 a Preparation of the stereolithic model for a patient
undergoing bilateral TMJ total joint prostheses reconstruction and
maxillary osteotomies for counterclockwise rotation and advancement of the maxillomandibular complex. The condyle has been
removed, and a 20mm gap has been created to accommodate the
prosthesis. Coronoidectomy must also be performed in order to
achieve the counterclockwise rotation. b TMJ concepts customtted total joint prostheses have been manufactured to t this
patient’s specic anatomical requirements with the jaws repositioned
to achieve the nal desired result

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has improved the accuracy and the projected surgical
outcome and the custom adaptation of the prostheses
to each patient’s specic anatomical requirements [49,
56–59]. With orthognathic surgery only, without cor-
rective TMJ surgery, the negative effects that can occur
include development or worsening of TMJ pain, myofascial pain, headaches, ear symptoms, etc. There is
an 84% chance of developing pain postsurgery and a
signicant increase of the postsurgical pain level (84%
increase) compared to presurgery. There is a risk (30%)
that condylar resorption can occur postsurgery [11].
24.2 Adolescent Internal Condylar
Resorption (AICR)
Adolescent internal condylar resorption (AICR) has a
relatively classic MRI presentation. This hormonally
mediated condition is initiated usually between the ages
of 11 and 15years and predominantly in females (ratio
8:1 females to males); there is no genetic predisposition;
only the TMJ joints are involved with no other joints
affected; discs are anteriorly displaced; condyles progressively decrease in size; and the mandible is retruded.
Following the onset of the process, the rate of condylar resorption is about 1.5mm per year. The mandible
will slowly retrude into a Class II occlusal and skeletal
relationship with a tendency toward anterior open bite.
These patients all have high occlusal plane angle facial
morphological proles [60–63].
MRIs of these cases present with a condyle that is
slowly becoming smaller in size in all three planes of
space. In some cases, there is a signicant thinning of the
cortical bone on top of the condyle contributing to the
inward collapse of the condylar head in this pathological
process (. Fig.24.9). Interestingly, the brocartilage on
the condylar head and in the fossa remains intact. This
is the only form of condylar resorption where the brocartilage remains intact. The articular discs are anteriorly displaced and may or may not reduce on opening.
Nonreducing discs will degenerate and deform at a more
rapid rate as compared to discs that reduce.
24.2.1 Implications fortheOSA Patient
Treatment considerations for OSA patients with AICR
usually require MMA with or without CCWR including disc repositioning with Mitek anchor versus total
joint prostheses. Consideration for disc repositioning
with Mitek anchors follows the guidelines previously
described for TMJ disc displacement. Our studies
[60–63] demonstrate that AICR can be arrested if the
articular discs are put back into position on top of the
condyle and stabilized with the Mitek anchor technique
(.
Fig.24.6) [24–33]. Results are best for AICR if the
TMJ surgery is performed within 4 years of the onset
of the TMJ pathology. After 4years, the discs may not
be salvageable. Patients that fall outside of these criteria
will be candidates for total joint prostheses [8, 34–59],
resulting in a signicantly greater outcome predictability relative to stability, improved function, and airway,
as well as decrease in pain.
OSA patients that have AICR undergoing MMA
without appropriate TMJ surgically management will
have predictably unstable skeletal and occlusal out-
ab
. Fig. 24.9 a MRI of TMJ AICR. The disc is anteriorly displaced.
Notice the thinning of the cortical bone on top of the condyle and
the loss of condylar vertical dimension. The disc is anteriorly dis-
placed (red arrow). b On opening, the articular disc commonly
remains anteriorly displaced without reduction (red arrow) in AICR

370
L. Wolford
24
comes because of the condylar resorption. A common
approach of many surgeons is to follow the patient
until the “condylar resorption burns-out” and then perform the MMA with clockwise rotation of the MMA
by increasing the occlusal plane even greater than the
already high occlusal plane angulation. However, with
MMA, the TMJs will have increased loading and could
reinitiate the condylar resorption process. Additional
negative effects of MMA on this patient population
may result in development or worsening TMJ pain,
myofascial pain, headaches, ear symptoms, etc. Also,
the amount of advancement required to correct the
OSA would dictate that the maxilla would need to be
advanced a greater amount in order to advance the
mandible enough to open the oropharyngeal airway
creating major and unaesthetic compromises in the
facial appearance. Additional surgery may be required
that would include total joint prostheses (. Fig.24.8)
and repeat orthognathic surgery to correct the original
failed surgery, as well as MMA and CCWR to correct
the TMJ pathology, restore facial balance, increase the
oropharyngeal airway, and eliminate residual pain.
24.3 Reactive Arthritis (ReA)
such as tissue necrosis factor alpha, nitric oxide, cytokines, chemokines, and interleukins (IL-1, IL-6, IL-8),
and may be the primary source of pain experienced by
many TMJ patients [1, 6–8]. Currently, there are no predictable nonsurgical treatments to eliminate this TMJ
pathology although some promising techniques may be
developing.
MRI of ReA may initially show a localized area of
uid effusion, inammation, and synovitis, with or without disc displacement and with or without erosion of
the condyle and/or fossa. As the disease progresses, it
can present as a more profuse inammatory process surrounding the disc and through the bilaminar tissues and
capsule (. Fig. 24.10). The ReA can cause signicant
destruction of the TMJ structures. The MRI may show
the presence of disc displacement as well as joint effusion, synovitis, and inammation with the soft tissues in
association with condylar degeneration that can include
resorption. However, in low-grade inammatory conditions, bone deposition may occur on the condyle and
fossa that could lead to osteophytes, heterotopic bone
deposition, and ankylosis (.
24.3.1 Implications fortheOSA Patient
Fig.24.11).
Reactive arthritis (ReA), or seronegative spondyloarthropathy, is an inammatory disease in joints usually
caused by venereal and respiratory bacteria. ReA is
one of the most common forms of arthritis, but least
understood. In the TMJ, ReA commonly develops in
the late- teens through the fourth decade, predominately
in females, and can cause TMJ pain, arthritis, and
condylar resorption. Systemic symptoms of ReA may
include joint pain, fever, fatigue, back pain, degenerative joint disease, polyarthritis, and dysfunction of the
immune system. The most common bacteria that cause
ReA are from two genera: chlamydia and mycoplasma.
The specic species identied contributory to knee and
TMJ ReA include C. trachomatis, C. pneumoniae, C.
psittaci, M. genitalium, M. pneumoniae, and M. fermentans [64–75].
The plausible theory for chlamydia- and mycoplasma-induced TMJ ReA begins with a triggering
infectious site established elsewhere in the body that is
often asymptomatic. Host cells such as macrophages
and monocytes become infected. When an injury or
inammatory reaction occurs in the TMJ, the host cells
respond, transport the bacteria through the hemopoietic
system, inltrate the synovial and bilaminar tissues, and
colonize the bacteria; the TMJ infection is initiated; and
bone and cartilage degeneration begins, as well as the
production of pain. Chlamydia and mycoplasma bacteria stimulate pro-inammatory and pain mediators,
Surgical options to treat ReA include arthroscopy and
arthrocentesis that may reduce symptoms temporarily
but will not eliminate the bacteria. Open joint debridement and disc repositioning may be effective in the very
early stages, but will be ineffective with more advanced
disease. The most predictable TMJ treatment option
for OSA patients with ReA requiring MMA is customtted total joint prostheses to reconstruct the TMJs and
advance the mandible in conjunction with the MMA
with CCWR (. Fig.24.8) [8, 34–59]. This approach will
usually provide the best outcome predictability relative
to skeletal and occlusal stability, improved jaw function,
increased the airway dimension, decreased pain, and
maximized facial balance.
OSA patients that have ReA undergoing MMA
with or without CCWR, and without appropriate TMJ
surgically management, may have predictably unstable
skeletal and occlusal outcomes if the ReA has caused
presurgery condylar resorption or the surgery initiates the resorption. A common approach of many surgeons is to follow the patient until “condylar resorption
burns- out” and then perform the MMA.However, the
MMA will load the TMJs and could reinitiate the condylar resorption process. Additional negative effects of
MMA on this patient population without TMJ surgical management may result in the development of, or
worsening TMJ pain, myofascial pain, headaches, ear
symptoms, etc.

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a
c
b
d
. Fig. 24.10 a The disc is anteriorly displaced (red arrows) with an
inammatory process (reactive arthritis – ReA) within the joint as
illustrated by the whitish tissue (green arrow) surrounding the disc
and in the bilaminar tissues. The condyle (yellow arrow) is undergoing degenerative changes at the anterosuperior aspect. b ReA in a
more advanced form. The blue arrows point out the inammatory
tissue within the joint. The yellow arrow indicates the condyle with
evidence of erosion and loss of vertical height. There may be some
remnants of the disc, but for the most part, it has been destroyed by
24.4 Connective Tissue andAutoimmune
Diseases (CT/AI)
The common CT/AI diseases that can affect the TMJs
include juvenile idiopathic arthritis (JIA), rheumatoid
arthritis, psoriatic arthritis, ankylosing spondylitis,
Sjogren’s syndrome, systemic lupus erythema, scleroderma, mixed connective tissue disease, etc. Multiple
systems are commonly involved with these diseases.
Peripheral joints are usually affected bilaterally and
symmetrically inamed, resulting in progressive destruction of articular structures. Facial deformity can occur
the inammatory process. c Severe ReA that has caused signicant
destruction of the condyle (green arrow) with large mass of reactive
tissue within the joint space as outlined by the white arrows. Even the
articular eminence has been resorbed. d This MRI demonstrates a
post-Mitek anchor repositioning of the articular disc in a patient
with ReA.The disc (red arrow) is slowly being resorbed by the reactive tissue surrounding it (the grayish tissue) as well as causing
arthritic changes to the condylar head
with TMJ involvement with associated condylar resorption. Clinical and radiographic features include the following: (1) retruded mandible, (2) posterior maxillary
vertical hypoplasia, (3) progressive worsening facial and
occlusal deformity, (4) high occlusal plane angle facial
morphology, (5) Class II occlusion and anterior open
bite, and (6) TMJ symptoms such as noises, pain, jaw
dysfunction, headaches, and ear symptoms [45, 76].
MRI features include loss of condylar vertical
dimension, signicant mediolateral condylar narrowing
but the residual condylar stumps may mushroom and
become broad in the A-P direction; articular eminence
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