Differential Diagnosis and Management of TMDs










Key Points
8
Temporomandibular disorders (TMDs) rarely result in dis-
abling conditions.
There is no single cause for all TMDs. Benign TMD signs and
symptoms are very common among the general population
and are generally self-limiting.
Only 3.6% to 7% of the general population has TMDs severe
enough that they seek treatment. Patients with pain-free
TMJ clicking generally do not need treatment; reassurance
and education about this benign condition usually sufces.
Management of TMDs should include the control of contrib-
uting factors such as parafunctional oral habits.
Smoking habits and certain disorders may inuence TMD
symptoms and prognosis, so these factors should be
addressed.
Management of TMDs may include self-management instruc-
tions, oral appliances, pharmacotherapy, and physical therapy.
Generally, invasive surgical management is indicated only
after reasonable nonsurgical efforts have failed and when the
patient’s quality of life is signicantly affected.
Radiographic structural changes consistent with degenera-
tive joint disease (DJD) should not be used as the sole guide
for treatment decisions.
Differential
Diagnosis and
Management of
TMDs

144
Dierential Diagnosis and Management of TMDs
8
Anatomy of the Masticatory
Structures
Temporomandibular articulation occurs in the
temporomandibular joints (TMJs), two of the
most complex joints of the body. The TMJ is
technically considered a ginglymoarthrodial
joint because each TMJ provides for both
hinging or rotation movement in one plane
(a criterion for a ginglymoid joint) and for glid-
ing or translation movements (a criterion for
an arthrodial joint).
1
The TMJ is formed by the
mandibular condyle tting into the mandibular
(glenoid) fossa of the temporal bone (Fig 8-1).
1
Separating these two bones from direct con-
tact is the interposed articular disc (sometimes
inappropriately called a meniscus). The articu-
lar portion of the healthy disc is composed of
dense brous connective tissue, devoid of any
nerves or vessels; conversely, the posterior at-
tachment of the disc is richly vascularized and
innervated.
2–4
Collateral ligaments attach the
disc to the condyle both medially and laterally.
These ligaments permit rotational movement
of the disc on the condyle during opening and
closing of the mouth.
This so-called condyle-disc complex trans-
lates out of the fossa during extended mouth
opening (Fig 8-2).
1
Therefore, in the normal
joint, rotational movement occurs between the
condyle and the inferior surface of the disc dur-
ing early opening (the inferior joint space), and
translation takes place in the space between
the superior surface of the disc and the fossa
(the superior joint space) during later opening.
Movement of the joint is lubricated by synovial
uid, which also acts as a medium for trans-
porting nutrients and waste products to and
from the articular surfaces. Unlike most syno-
vial joints, the articulating surfaces of the TMJs
are lined with dense brocartilage instead of
hyaline cartilage.
5
This is an important feature
because brocartilage has a greater ability to
repair itself than hyaline cartilage. This implies
that the management of arthritic conditions of
the TMJ may be different from that of other
synovial joints.
6
Movement of the TMJs is achieved by a
group of skeletal muscles called the muscles of
mastication. These muscles are comparable to
other skeletal muscles in physiology and ergo-
nomics.
7
Although the muscles of mastication
are the primary muscles that provide mandibu-
lar movement, other associated muscles of the
head and neck furnish secondary support during
mastication. The masticatory muscles include
the masseter, medial pterygoid, and temporalis
muscles, which predominantly elevate the man-
dible (mouth closing); the digastric muscles,
which assist in mandibular depression (mouth
opening); the inferior lateral pterygoid muscles,
which assist in protruding and lateral move-
ments of the mandible; and the superior lateral
pterygoid muscles, which provide stabilization
for the condyle and disc during function.
8–11
The masticatory muscles perform a variety of
functional behaviors that include talking, chew-
ing, and swallowing.
12
A number of muscle be-
haviors are nonfunctional (ie, parafunctional),
dened under the broad term of bruxism,
and include grinding, clenching, or rhythmic
chewing-like, empty-mouth movements.
13,14
Dening TMDs
TMDs encompass a group of musculoskeletal
and neuromuscular conditions that involve the
TMJs, the masticatory muscles, and all asso-
ciated tissues, and they have been identied
as a major cause of nondental pain in the oro-
facial region.
15,16
TMDs represent clusters of
related disorders in the masticatory system
with many common symptoms. The most
frequent presenting symptom is pain, usually
localized in the muscles of mastication or the
preauricular area. Chewing or other mandibular
activities usually aggravate the pain. In addi-
tion to complaints of pain, patients with these
disorders frequently have limited mandibular
movements and TMJ sounds that are most fre-

145
Fig 8-1 Normal anatomy of the
TMJ. ACL, anterior capsular liga-
ment (collagenous); AS, articular
surface; IRL, inferior retrodiscal
lamina (collagenous); RT, retro-
discal tissues; SC and IC, supe-
rior and inferior joint cavities;
SLP and ILP, superior and inferior
lateral pterygoid muscles; SRL,
superior retrodiscal lamina (elas-
tic). (Reproduced with permis-
sion from Okeson.
1
)
Fig 8-2 Normal functional movement of the condyle and disc during the full range of opening and closing.
Note that the disc is rotated posteriorly on the condyle as the condyle is translated out of the fossa. The closing
movement is the exact opposite of opening. (Reproduced with permission from Okeson.
1
)
ACL
ASSC
SRL
IC
RT
IRL
SLP
ILP
1
3
5
7
2
4
6
8
Defining TMDs

146
Dierential Diagnosis and Management of TMDs
8
quently described as clicking, popping, grating,
or crepitus.
Common patient complaints include jaw
ache, earache, headache, and facial pain. Non-
painful masticatory muscle hypertrophy and
abnormal occlusal wear associated with oral
parafunction such as bruxism (eg, clenching
and grinding) may be related problems. Pain
or dysfunction due to nonmusculoskeletal
causes such as otolaryngologic, neurologic,
vascular, neoplastic, or infectious disease in
the orofacial region is not considered a primary
TMD even though secondary musculoskeletal
pain may be present.
Epidemiology of TMDs
Reports on prevalence of TMDs from cross-
sectional epidemiologic studies vary consider-
ably from study to study because of differ ences
in terminology, operational denitions, data col-
lection, analytic approaches (eg, single-factor
versus multiple-factor analysis) and bias. A sys-
tematic review including only studies adopt-
ing the Research Diagnostic Criteria for TMDs
(RDC/TMD) reported a prevalence of up to
13% for masticatory muscle pain, up to 16%
for disc derangement disorders, and up to 9%
for TMJ pain disorders in the general popula-
tion.
17, 1 8
While the prevalence of the different
diagnoses in TMDs within patient populations
varied widely, the results of a meta-analysis
showed a prevalence of 45%, 41%, and 30%
for muscle disorders, disc derangement dis-
orders, and joint pain disorders, respectively.
18
Data from the National Health Interview Survey
from 2009 show that 5% of the US adult popu-
lation (11.5 million people) self-reported jaw or
face pain in the preceding 3 months.
19
Other
studies show that TMDs are primarily a condi-
tion of young and middle-aged adults, rather
than of children or the elderly, and are approxi-
mately twice more common in women than in
men.
19–21
According to a population-based sur-
vey, the report of symptoms are 50% more
prevalent in African-Americans, and longitudi-
nal data show that the rate of TMD symptoms
was higher and the rate of TMD diagnosis
was 52% higher in this population, although
the persistency of the symptoms is higher in
whites.
22
In addition, TMDs are often remit-
ting, self-limiting, or uctuating over time; the
progression to a potentially more serious non-
reducing disc status or chronic and disabling
intracapsular TMJ disease is relatively uncom-
mon.
23–27
In fact, recent data demonstrated
that 76% and 71% of soft and hard tissue
diagnoses, respectively, remained stable after
an 8-year follow up.
24,27,28
Only 3.6% to 7% of individuals with TMDs
are estimated to require treatment, and the an-
nual incidence rate is estimated to be 2%.
29–34
For painful TMDs specically, the most recent
estimate for rst onset was 3.9%, with 50%
of the cases maintaining the condition after 6
months.
22,30,35,36
Because joint sounds are com-
mon, often pain free, and not progressive, it
is important to avoid overtreatment of benign
chronic reducing and nonreducing disc dis-
placement in the absence of pain and impaired
function.
27
According to magnetic resonance
imaging (MRI) studies, it is estimated that up
to 35% of asymptomatic individuals appear to
have disc displacements.
37
Painful TMD conditions such as myofascial
pain and arthralgia have been associated with
facial trauma, third molar removal, clenching,
physical symptoms (somatization), and female
sex.
38
Cigarette smoking has been associated
with increased risk of TMDs in young adults,
and higher levels of pain, psychosocial dis-
tress, and sleep disturbances are reported in
TMD patients.
39,40
The relationship between
painful TMDs and comorbid conditions has
been evaluated by several investigators. Myo-
fascial pain patients self-report more severe
headaches, fainting and dizzy spells, gastric
acid reux, bromyalgia, anxiety, depression
psychiatric treatments, phobias, and frequent
sore throats compared with arthralgia (both
diagnoses based on the RDC/TMD).
41
Indi-
147
Etiology of TMDs
viduals developing TMDs are also more likely
to describe comorbidities such as headaches,
muscle soreness, and other body pains.
42
In a more integrated model, it was investi-
gated if the presence of comorbid conditions
further modies the phenotype of individuals
with TMDs. This relationship was evaluated im-
plementing a Multisystem Dysregulation Index
that included sensory, autonomic, inamma-
tory, and psychologic domains due to their
contribution in pain amplication.
43
Among
individuals without comorbid persistent pain
(only 8% among cases of the study popula-
tion), the predominant dysregulation was in
the sensory domain, which represented the
presence of generalized somatic sensitiza-
tion. Among those with one persistent pain-
ful comorbid condition (49%), the psychologic
dysregulation was the only domain associated
with the increased risk of having a TMD. For
those individuals with two or more comorbid
conditions (42%), a multisystem dysregulation
was observed including sensory, psychologic,
and autonomic domains, indicating that multi-
system dysregulation is associated with com-
mon persistent pain conditions.
43
International comparisons of comorbid pain
conditions among women with TMD pain were
evaluated among women from Italy, Sweden,
and Saudi Arabia. Using a case-control design
and age-matched in the respective centers,
it was found that comorbid pain prevalence,
intensity, and disability differ among women
from these cultures. The comorbid conditions
studied were head, chest, back, and abdominal
pain, and all comorbid conditions were consis-
tently higher among the cases than the con-
trols. The prevalence of back pain was higher
among women from Saudi Arabia. Saudi Ara-
bian women had more interference from the
back pain than women from Sweden and Italy.
Headache did not differ among the groups, but
the intensity was lower among the women
from Sweden.
44
Etiology of TMDs
No unambiguous universal cause of TMDs has
been identied because determining causation
requires more than phenotyping the condi-
tions under study and/or describing their dis-
tribution based on observational studies. Nev-
ertheless, the methodologic quality of such
observational studies is key to determine their
internal and external validity and therefore to
transfer such knowledge to clinical care. For
this reason, most of the factors discussed in
this section are not proven causal, but associ-
ated with TMDs. Factors that may cause the
onset of TMDs are called initiating factors, fac-
tors that increase the risk of TMDs are called
predisposing factors, and factors that interfere
with healing or enhance the progression of
TMDs are called perpetuating factors. Under
different circumstances, individual factors may
serve any or all of these roles. There is not a
single etiologic factor or a unique theoretical
model that can explain the onset of TMDs.
Bone and TMJ soft tissue remodeling and
muscle tone regulation are all adaptive physi-
ologic responses to injury or change. Loss of
structural integrity, altered function, or biome-
chanical stresses in the system can compro-
mise adaptability and increase the likelihood
of dysfunction or pathology.
45
Direct extrinsic
trauma to any component of the mastica-
tory system can spontaneously initiate loss
of structural integrity and concomitantly alter
function, thereby reducing the adaptive capac-
ity in the system. In addition, there are other
contributing anatomical, systemic, pathophysi-
ologic, and psychosocial factors that may suf-
ciently reduce the adaptive capacity of the
masticatory system and result in TMDs.
Trauma
Trauma is described as any force applied to
the mastication structures that exceeds that
of normal functional loading. Most trauma can
be divided into three types: (1) the result of a

148
Dierential Diagnosis and Management of TMDs
8
sudden and usually isolated blow to the struc-
tures (direct trauma), (2) that associated with
a sudden blow but without direct contact to
the affected structures (indirect trauma), and
(3) the result of prolonged, repeated force over
time (microtrauma).
Direct trauma
There is general agreement that direct trauma
(ie, macrotrauma) to the mandible or the
TMJ produces injury via impact and is ac-
companied in close temporal proximity with
signs and symptoms of inammation. If the
forces lead to structural failure, loss of func-
tion may quickly follow. Direct trauma result-
ing in mandibular fracture in adults has been
associated with increased signs and symp-
toms of TMDs; however, these may not result
in patients seeking treatment.
46
In children,
condylar and subcondylar fractures in girls,
but not boys, were associated with increased
TMD symptoms over time.
47
More signi-
cant fractures may result in disc displace-
ment.
48
Patients with TMDs report physical
trauma more often than non-TMD patients.
49
The accuracy of recall of TMD symptoms as-
sociated with a traumatic event may be com-
promised, making it difcult to clearly link the
traumatic event with the symptom onset.
50
Other forms of trauma such as wide or pro-
longed mouth opening, third molar extrac-
tion, and intubation have been reported as
associated with TMDs.
51,52
Self-reported jaw
injury due to yawning or prolonged opening
is signicantly higher in patients with TMDs.
49
Transient and permanent dysfunction of the
TMJ after upper airway management proce-
dures has been reported, but controlled trials
and longitudinal studies are not available in
the English-language literature.
53,54
Indirect trauma
Acceleration-deceleration (exion-extension)
injury (ie, whiplash) with no direct blow to the
face may cause symptoms consistent with
TMDs, but signicant controversy persists
as to whether there could be a direct causal
relationship. Prospective controlled studies
both link and show limited risk for the devel-
opment of TMD symptoms after whiplash.
55,56
Review of the literature has highlighted these
controversies; however, there is some evi-
dence that postwhiplash TMDs can have a dif-
ferent and potentially more protracted clinical
course than non-trauma-associated TMDs.
57–59
Although symptoms in the mandible may be
referred from injured cervical structures, a di-
rect causal relationship between mandibular
symptoms and indirect trauma has yet to be
established.
56,60,61
However, reports seem to
indicate increased risk to developing orofacial
pain, especially with increased severity of the
indirect trauma.
62
Computer simulation suggests that
low-velocity rear-end impact does not cause
mandibular movement or stresses beyond
the physiologic range.
63
In support of this nd-
ing, human volunteers in simulated rear-end
crash tests failed to demonstrate mandibular
movement beyond physiologic limits.
64
Thus,
while evidence is lacking for a mandibular
strain without a direct blow to the mandible
following a low-velocity motor vehicle acci-
dent, there are recognized pathways of het-
erotopic pain from the cervical area to the
trigeminal area.
16,65
It is therefore not uncom-
mon to observe symptoms of TMDs following
acceleration-deceleration injury to the neck
without direct trauma to the face or jaw. The
etiologic signicance of nonimpact injuries is
uncertain, and much misinformation is being
provided to patients without scientic studies
to support the claims.
Microtrauma
Microtrauma has been hypothesized to origi-
nate from sustained and repetitious adverse
loading of the masticatory system through
postural imbalances or from parafunctional
habits. It has been suggested that pos-
tural habits such as forward head position
or phone-bracing may create muscle and joint
149
Etiology of TMDs
strain and lead to musculoskeletal pain—
including headache—in the TMD patient.
66
Parafunctional habits have been most fre-
quently assessed by indirect means such as
self-report, questionnaires, reports by a bed-
room partner, or tooth wear. These indirect
measures of parafunctional habits have pro-
vided conicting reports as to the relationship
between TMD symptoms and the presence of
parafunctional habits. When myofascial TMD
patients were compared with controls using
polysomnography, the tests did not conrm
the patientsself-reports of more sleep brux-
ism than the controls.
67
Parafunctional habits
such as teeth clenching, tooth grinding, lip bit-
ing, and abnormal posturing of the mandible
are common and usually do not result in TMD
symptoms, but they have been suggested as
initiating or perpetuating factors in certain sub-
groups of TMD patients.
14,68–75
Although the
available research and clinical observations gen-
erally support this contention, the exact role of
parafunctional habits in TMDs remains unclear
because few studies have directly assessed
these behaviors. Attrition severity secondary to
bruxism cannot distinguish TMD patients from
asymptomatic individuals, and muscle hyper-
activity has not been shown to be associated
with arthrogenous TMJ disorders.
76–78
Further-
more, clenching does not cause neuromuscu-
lar fatigue because muscles compensate for
sustained muscle activity by derecruitment of
motor neurons or through slower ring rates.
79
Despite the lack of evidence that nonex-
perimentally induced parafunction or clenching
can cause TMDs, some studies have shown
that experimentally induced parafunction can
result in transient pain similar to that reported
by patients with TMDs.
72,80–82
The impact of
these studies is limited by their small sam-
ple size. The intensity and frequency of oral
parafunctional activity may be exacerbated
by stress and anxiety, sleep disorders, and
medications (eg, neuroleptics, alcohol, and
other substances), although the relationship
between sleep bruxism and psychologic fac-
tors has been questioned.
14,83,84
Some forms
of masticatory muscle hyperactivity have been
associated with emotional behavior and may
be mediated via the cortex through the hypo-
thalamus.
85
Intense and persistent parafunc-
tion can also occur in patients with neurologic
disorders (eg, cerebral palsy) and extrapyra-
midal disorders (eg, orofacial dyskinesia and
epilepsy).
86
Conversely, sleep bruxism has not
been related to facial type or head form.
87
The most commonly believed indication of
past sleep bruxism severity is dental attrition.
88
However, dental attrition can also be partly ex-
plained by overbite and overjet changes that
correlate with age and sex, protrusive guid-
ance schemes, dentofacial morphology, ero-
sive diets, the bite force ability, and environ-
mental factors.
89–97
In addition, it is not clear
whether sleep bruxism is a pathogenic disor-
der or a normal physiologic process. Recent
evidence suggests that sleep bruxism may be
associated with increasing salivation during
sleep, resulting in lubrication of oropharyngeal
structures, or with increasing the space of the
upper airways to aid with airway patency, or
both.
98–101
Furthermore, it has been suggested
that sleep bruxism plays a protective role as
a compensatory mechanism to protect the
airway during sleep-related breathing disor-
ders.
102
Therefore, the issue of whether or not
sleep bruxism requires management without
the presentation of signicant problems is de-
batable. A more pragmatic approach may be to
view this as an issue regarding “consequence
management,” taking into account risk or side
effect/benet ratio.
103
Another problem arises
when attrition is used to suggest current brux-
ism levels.
71
Attrition appears to be episodic
in nature and occurs in bursts caused by as
yet unspecied factors, and thus any noted
attrition may not necessarily represent ongo-
ing habits.
25,104
Continued research with more
direct measurements of parafunction (eg, por-
table electromyography, sleep laboratory, and
direct observation) will be necessary to clarify
the specic role of current parafunction.
105–107

150
Dierential Diagnosis and Management of TMDs
8
Anatomical factors
Skeletal factors
Skeletal factors include adverse biomechanical
relationships that can be genetic, developmen-
tal, or iatrogenic in origin. Severe skeletal malfor-
mations, interarch and intraarch discrepancies,
and past injuries to the teeth may play a role in
TMDs, but this role may be less strong than pre-
viously believed. For example, while it is known
that disc displacement is common in children
with facial skeletal abnormalities such as ret-
rognathia, it cannot be said that these anatomi-
cal anomalies are etiologic.
108
In addition, TMD
patients with a disc displacement as well as
other TMD patients generally do not have an in-
creased prevalence of forward head posture.
109
A steep articular eminence has also been
proposed as an etiologic factor in internal de-
rangement of the TMJ. In asymptomatic indi-
viduals, a steeper eminence was associated
with an increased posterior rotation of the
disc, posing a potential anatomical risk fac-
tor.
110
However, several studies have shown
that in TMJs with disc displacement without
reduction and TMJs with osseous changes,
the eminence was less steep than in TMJs
with disc displacement with reduction or TMJs
without osseous changes, indicating adaptive
remodeling.
111 113
In addition, unilateral joint
sounds were associated with the side with the
less steep condylar movement path.
114
Occlusal relationships
The dental profession has historically viewed
occlusal variation as a primary etiologic factor
for TMDs. Occlusal features such as work-
ing and nonworking posterior contacts and
discrepancies between the retruded contact
position (RCP) and intercuspal position (ICP)
have been commonly identied as predispos-
ing, initiating, and perpetuating factors. The
current available evidence suggests that the
inuence of the occlusion on the onset and
development of TMDs is low.
115, 116
Among the
occlusal factors evaluated, loss of posterior
support and unilateral crossbite show some
association across studies.
115
Several occlusal factors (eg, large overjet,
minimal anterior overlap and anterior skeletal
open bite, unilateral posterior crossbite, oc-
clusal slides greater than 2 mm, and lack of
rm posterior tooth contact) were found to be
more prevalent in patients than in convenience
samples. However, this is possibly due to con-
dylar positional changes following intracapsu-
lar alterations associated with the disease pro-
cess itself. Therefore, these occlusal factors
may be the result rather than the cause of the
disease.
115, 117, 118
Previous studies have lacked
reliable occlusal measurement techniques and
data collection methods, which may explain
the diversity of some ndings. Nevertheless,
whether considered individually or simultane-
ously, little evidence is available to implicate
occlusal factors in TMD etiology despite the
historic views.
118
Pathophysiologic factors
Systemic factors
Systemic pathophysiologic conditions may
inuence local TMDs and should generally
be managed in cooperation with the patient’s
primary care physician or other medical spe-
cialists. These conditions can include degen-
erative, endocrine, infectious, metabolic,
neoplastic, neurologic, rheumatologic, and
vascular disorders. Systemic factors can act
simultaneously at a central and local (ie, pe-
ripheral) level.
119,120
Generalized joint laxity (ie, hypermobility)
has been cited as a possible contributing fac-
tor to TMDs and has proven to be signicantly
more prevalent in patients with internal de-
rangements than with other types of TMDs or
in normal controls.
25,121–125
Altered collagen me-
tabolism may also play a role in joint laxity, and
the collagen composition in TMJs with pain-
ful disc displacement compared with asymp-
tomatic joints has been found to differ.
123,126
151
Etiology of TMDs
Nevertheless, there is only a weak correlation
between the mobility of peripheral joints or the
trunk and mandibular mobility, and research
has yet to demonstrate that joint laxity can
predict the potential for developing TMDs.
127
Local (peripheral) factors
Local pathophysiologic factors of TMDs such
as masticatory efciency appear to be multi-
factorial and involve such a large span of indi-
vidual variation that it is difcult to establish
norms.
128
In addition, chewing force is also
inuenced by sex, age, and pain levels.
129–135
Masticatory muscle tenderness is not al-
ways related to variation in muscle activity or
the site or side of reported tenderness.
120,136–138
While the masseter muscle may react to
proximal muscle pain, the anterior temporalis
muscle does not, and any associations may
be parallel developments rather than etiologic.
Muscle tenderness does not appear to be the
result of inammation but is probably related
to prolonged central hyperexcitability and al-
tered CNS processing following peripheral tis-
sue injury.
138
Cervical muscle activity has been
shown to inuence masticatory muscle activ-
ity, probably involving a primary afferent reex
response.
139–141
Thus, a primary cervical or TMJ
disorder may precipitate a secondary mastica-
tory muscle condition. Muscle hyperalgesia
can also result from TMJ inammation.
142
Of great concern to the clinician is the
distinction between pathologic and adaptive
responses to disease in the TMJ. Histologic
studies suggest that cartilage thickness and
composition adapt to shearing stresses during
functional loading.
143,144
Maintenance of an in-
tact articular surface is to be expected, even in
the face of osteoarthritic changes, allowing for
both stable morphologic relationships and his-
tologic compatibility between the articulating
components.
118,145,146
Therefore, even though
morphologic change is mostly irreversible, it
usually achieves and maintains stability and
should be considered adaptive.
147
The goal
of treating osteoarthritic changes in this light
should not be to restore earlier morphology
but to encourage the body’s adaptive response
to pathophysiologic processes.
In early disc derangements, signs of osteo-
arthritis are not apparent. Disc derangements
with reduction may persist for many years
without development of radiographically visible
changes or symptoms.
148
Disc derangements
in later stages with osteoarthritic changes
occur possibly parallel but may also represent
independent processes, and 50% will show
some active cellular osteoblastic or osteoclas-
tic activity.
149,150
Osteoarthritic changes, altera-
tions in synovial uid viscosity, and inadequate
or altered lubrication may initiate derangement
of the TMJ articular disc.
151,152
Synovial uid
analyses attempting to correlate biochemi-
cal signs of inammation with pain reveal
abnormal concentrations of plasma proteins
or neurotransmitters and inammatory cyto-
kines.
153–158
While still controversial, cytokine
proles of patients with intracapsular TMDs
do appear to be different from controls.
159
With these as well as animal model studies,
additional research in this area could have the
potential for targeted therapeutic treatments
in a subset of individuals with TMDs.
Frictional “sticking” of the disc has been
proposed to cause internal derangement of the
TMJ with the forces dependent on the type
of clenching task, with the greater impact at
ICP and during a unilateral molar clench.
73,160,161
According to experimental models and animal
studies, the forces are also increased by re-
duced congruity between the opposing sur-
faces and by at unrounded surfaces.
161–165
The
forces are affected by disc thickness and area
and by mandibular deformation during clench-
ing.
164,166
Interestingly, nonworking tooth con-
tacts have been hypothesized to reduce loads
within the joint and act as a stress breaker for
the clenching forces.
161
Intracapsular pressure
may also affect TMDs.
167,168
With joint move-
ment, the alternating pressure acts as a pump
for joint lubrication, nutrition, blood supply,
drug delivery, waste removal, and even con-

152
Dierential Diagnosis and Management of TMDs
8
dylar growth. Thus, any interruption through
immobilization or prolonged clenching might
have the potential to initiate or advance TMD
signs and symptoms.
Female hormones might play a role in TMJ
disc disease, but this has not been proven be-
cause the presence of both estrogen and pro-
gesterone receptors within the articular disc
has been both conrmed and denied.
169,170
Clinical randomized controlled trials (RCTs)
indicate that estrogen does not play a role in
the etiology of TMDs, whereas cohort stud-
ies and case-control studies show contrast-
ing results.
171–174
The etiologic explanations for
progression from disc displacement to osteo-
arthritis and osteoarthritic changes are multi-
factorial and include failure of the reparative ar-
ticular chondrocyte response due to metabolic
dysfunction and relative or absolute overload-
ing due to excessive mechanical forces leading
to articular cartilage biochemical failure.
45,175
Remodeling, in contrast, is a physiologic re-
sponse to accommodate an altered disc posi-
tion.
118
Thus, it is probable that a mechanical
breakdown in the articular disc (eg, a perfora-
tion) rather than an unusual disc position leads
to osteoarthritis and/or osteoarthritic changes
following disc displacement.
176
It is not certain,
however, that all gross abnormalities of disc
morphology will lead to osteoarthritis because
one experimental animal study suggests
that the TMJ may be capable of healing disc
perforations within a relatively short time.
177
Mechanical stress may also lead to the accu-
mulation of damaging free radicals in affected
articular tissues of susceptible individuals. This
condition is called oxidative stress.
178
Dijkgraaf
et al
179
have proposed that free radicals may be
responsible for the formation of adhesions in
the TMJ by cross-linking of proteins.
Genetic factors
While the body of literature available with
regard to genetic susceptibility for TMDs is
an expanding eld, genetic association stud-
ies have been limited. The relationship be-
tween catechol-O-methyltransferase (COMT)
polymorphism, pain sensitivity, and the risk
of TMD development has been evaluated,
and three genetic variants (haplotypes) of the
gene encoding COMT were identied and des-
ignated as “low pain sensitivity,“average pain
sensitivity,” and “high pain sensitivity.
180
The
haplotypes were associated with experimen-
tal pain sensitivity, and the presence of even
a single “low pain sensitivity” haplotype was
shown to reduce the risk of developing myog-
enous TMDs. Furthermore, the gene–environ-
ment interaction was illustrated by the signi-
cant role of stress, which doubles the rate of
TMDs among those with low-activity COMT
haplotypes.
22
The most current data from the
Orofacial Pain: Prospective Evaluation and Risk
Assessment (OPPERA) trial did not demon-
strate signicant variation in TMD incidence by
genetic polymorphisms from a panel of candi-
dates’ putative genes but found evidence for
genetic associations in several pronociceptive
intermediate phenotypes and their contribut-
ing role.
181
Single-nucleotide polymorphisms
(SNPs) representing 358 genes involved in
biologic systems associated with pain percep-
tion were identied. Specically, SNPs had
stronger associations with nonspecic orofa-
cial symptoms, global psychologic symptoms,
stress and negative affect, and heat and tem-
poral summation. These included the following:
The glucocorticoid receptor gene, which
suggests a role of the hypothalamic-
pituitary-adrenal system in chronic TMDs
The serotonin receptor gene, indicating
the inuence in nociceptive and affective
pathways
The gene encoding the α subunit of the
voltage-gated sodium channel NaV 1.1,
which is involved in the generation and
propagation of action potentials in sen-
sory nerves
A variation in a gene encoding angioten-
sin I-converting enzyme implicated in
hypertension
153
Etiology of TMDs
The prostaglandin-endoperoxide syn-
thase 1 gene, a regulator of nociception
and inammatory response
A variation in the gene encoding amyloid
β (A4) precursor protein, which inuences
synapse formation and neuronal plasticity
Multiple PDZ domain protein gene, in-
uencing G-protein-coupled receptors
involved in nociception and analgesia
These most extensive panel-related candi-
date genes support the strong indication that
multiple genetic and biologic pathways contrib-
ute to the risk for TMDs.
181
Psychosocial factors
Psychosocial factors include individual, inter-
personal, and situational variables that impact
the patient’s capacity to function adaptively.
General distress is the most salient single fac-
tor across most individuals with chronic TMD
pain.
182
General distress is readily assessed
(see chapters 2 and 12), and certainly other
factors may contribute actively to the mea-
sured distress, such as personality character-
istics, enduring stressors, a physical response
style to stress, or limited coping skills.
183–188
There is evidence that some patients with
TMDs experience more anxiety than healthy
control groups and that some TMDs and oro-
facial pain symptoms may be only one of sev-
eral somatic manifestations of emotional dis-
tress.
189–192
Some muscle pain may in fact be
caused by excessive sympathetic nervous sys-
tem activity as an overresponse to life stress-
ors, and the attention focused on the pain can
adversely affect the intensity of the pain.
193–196
Patients with such complaints often have a
history of other stress-related disorders.
192
Depression and anxiety related to other major
life events may alter the patient’s perception
of and tolerance of physical symptoms, caus-
ing them to seek more care for what is pre-
sented as a problem of the body.
197
Patients
with chronic TMDs have been found to have
psychosocial and behavioral characteristics
similar to patients with lower back pain and
headache.
198,199
In general, TMD patients are
not signicantly different from healthy individu-
als in personality type, and they do not differ
from other pain patients in response to illness,
attitudes toward health care, or ways of coping
with stress.
69,188,200–202
Any psychologic impair-
ment may be merely associated with the pres-
ence of pain persistence.
131,197,203
Environmental contingencies can greatly
complicate treatment by affecting an indi-
vidual’s perception of and responses to pain
and disease. Some patients may experience a
lessening of distress to the extent that psycho-
genic symptoms decrease or resolve preexist-
ing psychologic and interpersonal conicts.
This primary gain of symptom formation is
distinguished from the secondary gain of so-
cial benets experienced by patients once a
disorder is established.
204–206
Secondary gain
includes being exempt from ordinary daily re-
sponsibilities; being compensated monetarily
from insurance or litigation; using the rational-
ization of “being ill” to avoid unpleasant tasks;
and gaining attention from family, friends, or
health care workers.
206,207
What the clinician
interprets as pain (eg, in response to a clini-
cal examination procedure designed to evoke
pain) may be less related to any local nocicep-
tive mechanisms and more a function of pain
behavior: how the individual presents his or
her distress as motivated by factors beyond
the stated complaint.
From the psychosocial domain, the OPPERA
study group evaluated 26 psychosocial mea-
sures; among them, the frequency of somatic
symptoms was the strongest predictor for
TMD onset. Other contributors to a lesser
degree were psychologic stress, anxiety,
obsessive-compulsive feelings, and pain cop-
ing strategies.
208
Using a case-control analyti-
cal approach as a foundation for their research,
the OPPERA group reported that TMD cases
are different than controls across multiple phe-
notypic domains including sociodemographic

154
Dierential Diagnosis and Management of TMDs
8
factors, clinical variables, psychologic function-
ing, pain sensitivity, autonomic responses, and
genetic associations. All of these elements
are providing leading-edge information to the
biologic pathways that may elucidate TMD
pathophysiology.
209
Diagnostic Classication of TMDs
The classication of TMDs is hampered by lim-
ited knowledge of the etiology and the natu-
ral progression of these disorders, and yet
advancement in our knowledge is dependent
on an accepted taxonomy and corresponding
diagnostic criteria.
17
Diagnostic criteria allow
comparisons of patient populations in different
studies and provide a common language for
developing a conceptual framework to use in
the clinic.
210
Any classication scheme or tax-
onomy must be considered an evolving frame-
work that will be modied by new ndings and
with increased level of understanding. The fol-
lowing outlines are based on the Diagnostic
Criteria for Temporomandibular Disorders (DC/
TMD; a revision of the RDC/TMD), which in-
clude the most common TMDs with sensitivity
and specicity values, and the expanded tax-
onomy, which includes less common TMDs
without validity estimates (Box 8-1).
211,212
TMJ disorders
Joint pain (ICD-10 M26.62)
Previously described as synovitis, capsulitis,
and retrodiscitis, joint pain has been explained
in the biomedical model as an inammatory
process of the synovial lining of the TMJ that
can be due to infection, an immunologic con-
dition secondary to cartilage degeneration, or
trauma. Joint pain is characterized by localized
pain that is exacerbated by function and para-
function. On occasion, there may be a uctu-
ating swelling that decreases the ability to oc-
clude on the ipsilateral posterior teeth.
Arthralgia (ICD-10 M26.62)
This is pain of joint origin affected by jaw move-
ment, function, or parafunction and replication
of this pain with provocation testing, either
during mandibular movement or palpation of
the TMJs. Sensitivity is 0.89, and specicity is
0.98.
History is positive for both of the following:
In the past 30 days, pain in the jaw, tem-
ple, in front of the ear, or in the ear with
examiner conrmation of pain location in
a masticatory structure
Pain altered with jaw movement, func-
tion, or parafunction
Conrmation of the pain location in the
TMJ area includes at least one of the follow-
ing tests:
Palpation of the lateral pole (0.5 kg pres-
sure) or around the lateral pole (1.0 kg
pressure)
Maximum unassisted or assisted open-
ing, right or left lateral movements, or
protrusive movements
Examination of the TMJ elicits a report of
familiar pain (dened as similar or like the pain
the patient has experienced in the masticatory
area palpated during the last 30 days).
Arthritis
This is pain of joint origin with clinical charac-
teristics of inammation or infection: edema,
erythema, and/or increased temperature.
It may arise in association with trauma. As-
sociated symptoms can include occlusal
changes such as ipsilateral posterior open bite
if intra-articular swelling is present unilater-
ally. This disorder has also been referred to as
synovitis or capsulitis; however, these terms
limit the sites of nociception. With this local-
ized condition, there should be no history of
systemic inammatory disease. Sensitivity
and specicity have not been established.

155
Diagnostic Classification of TMDs
Note: This box was adapted from work performed by the International RDC-TMD Consortium sponsored by the International
Association for Dental Research and the Special Interest Group on Orofacial Pain of the International Association for the
Study of Pain.
Temporomandibular joint disorders
1. Joint pain (ICD-10 M26.62)
A. Arthralgia
B. Arthritis
2. Joint disorders
A. Disc-condyle complex disorders (ICD-10
M26.62)
i. Disc displacement with reduction
ii. Disc displacement with reduction with
intermittent locking
iii. Disc displacement without reduction
with limited opening
iv. Disc displacement without reduction
without limited opening
B. Other hypomobility disorders (ICD-10
M26.61)
i. Adhesions/adherence
ii. Ankylosis
a. Fibrous ankylosis
b. Osseous ankylosis
C. Hypermobility disorders
i. Subluxation (ICD-10 S03.0XXA)
ii. Luxation (ICD-10 S03.0XXA)
a. Closed dislocation (ICD-10
S03.0XXA)
b. Recurrent dislocation (ICD-10
M26.69)
c. Ligamentous laxity (ICD-10 M24.20)
3. Joint diseases
A. Degenerative joint diseases (ICD-10
M19.91)
i. Osteoarthrosis
ii. Osteoarthritis
B. Condylysis (ICD-10 M26.69)
C. Osteochondritis dissecans (ICD-10 M93.20)
D. Osteonecrosis (ICD-10 M87.08)
E. Systemic arthritides (rheumatoid arthritis:
ICD-10 M06.9)
F. Neoplasm (benign: ICD-10 D16.5;
malignant: ICD-10 C41.1)
G. Synovial chondromatosis (ICD-10 D48.0)
4. Fractures
A. Closed fracture of condylar process (ICD-10
S02.61XA)
B. Closed fracture of subcondylar process
(ICD-10 S02.62XA)
C. Open fracture of condylar process (ICD-10
S02.61XB)
D. Open fracture of subcondylar process (ICD-
10 S02.62XB)
5. Congenital/developmental disorders
A. Aplasia (ICD-10 Q67.4)
B. Hypoplasia (ICD-10 M27.8)
C. Hyperplasia (ICD-10 M27.8)
Masticatory muscle disorders
1. Muscle pain limited to the orofacial region
A. Myalgia (ICD-10 M79.1)
i. Local myalgia
ii. Myofascial pain
iii. Myofascial pain with referral
B. Tendonitis (ICD-10 M67.90)
C. Myositis
i. Noninfective (ICD-10 M60.9)
ii. Infective (ICD-10 M60.009)
C. Spasm (ICD-10 M62.838)
2. Contracture
A. Muscle (ICD-10 M62.40)
B. Tendon
3. Hypertrophy (ICD-10 M62.9)
4. Neoplasms
A. Jaw
i. Malignant (ICD-10 C41.1)
ii. Benign (ICD-10 D16.5)
B. Soft tissues of head, face, and neck
i. Malignant (ICD-10 C49.0)
ii. Benign (ICD-10 D21.0)
5. Movement disorders
A. Orafacial dyskinesia
i. Abnormal involuntary movements
(ICD-10 R25.1 [tremor unspecied];
R25.2 [cramp and spasm]; R25.3
[fasciculations])
ii. Ataxia, unspecied (ICD-10 R27.0);
muscular incoordination (ICD-10 R27.9)
iii. Subacute, due to drugs; oral tardive
dyskinesia (ICD-10 G24.01)
B. Oromandibular dystonia
i. Acute, due to drugs (ICD-10 G24.02)
ii. Deformans, familial, idiopathic, and
torsion dystonia (ICD-10 G24.1)
6. Masticatory muscle pain attributed to
systemic/central disorders
A. Fibromyalgia (ICD-10 M79.7)
B. Centrally mediated myalgia (ICD-10 M79.1)
Masticatory muscle disorders
1. Headache attributed to TMDs (ICD-10 G44.89
or ICD-10 R51)
Associated structures
1. Coronoid hyperplasia (ICD-10 M27.8)
Box 8-1 Expanded TMD taxonomy

156
Dierential Diagnosis and Management of TMDs
8
History is positive for arthralgia as dened
above as well as one of the following:
Swelling, redness, and/or increased tem-
perature in front of the ear
Dental occlusal changes resulting from
articular inammatory exudate (eg, pos-
terior open bite)
Examination is positive for arthralgia as de-
ned above as well as one of the following:
Presence of edema, erythema, and/or in-
creased temperature over the TMJs
Reduction in dental occlusal con-
tacts noted between two consecutive
measurements
Unilateral or bilateral posterior open bite
must not be attributable to other causes. The
patient is negative for rheumatologic disease,
including those in systemic arthritides. The
pain is not better accounted for by another
pain diagnosis.
Joint disorders
Articular disc displacement is the most com-
mon TMJ arthropathy and is characterized
by several stages of clinical dysfunction that
involve the condyle-disc relationship. It is
characterized by an abnormal relation or mis-
alignment of the articular disc relative to the
condyle. Although posterior and mediolateral
displacements of the articular disc have been
described, the usual direction for displacement
is in an anterior or anteromedial direction.
213–220
Nevertheless, pain or mandibular movement
symptoms are not specic for disc derange-
ment disorders, and the disc position is not
related to any presenting symptoms.
221,222
The causes of disc displacement are not
agreed upon; however, it is postulated that in
the majority of cases, elongated or torn liga-
ments binding the disc to the condyle permit
the disc to displace.
223
Lubrication impairment
is also suggested as a possible etiologic factor
of disc displacement.
73,152
Disc displacement is
subdivided into disc displacement with reduc-
tion and disc displacement without reduction.
Disc-condyle complex disorders
Disc displacement with reduction (ICD-10
M26.63)
This is an intracapsular biomechanical disor-
der involving the condyle-disc complex: In the
closed mouth position, the disc is in an anterior
position relative to the condyle, and the disc re-
duces upon opening of the mouth. Medial and
lateral displacement of the disc may also be
present. Clicking, popping, or snapping noises
may occur with disc reduction. Using MRI as
the reference standard, sensitivity is 0.34, and
specicity is 0.92. Although not required for
this diagnosis and without diagnostic validity,
elimination of the opening and closing noise, if
present, with protrusion can help corroborate
this diagnosis.
History is positive for the following:
In the last 30 days, any noise(s) pres-
ent with jaw movement or function, or
patient report of joint sounds during the
examination
Examination is positive for at least one of
the following:
Both an opening and closing clicking,
popping, or snapping noise detected with
palpation during at least one of three rep-
etitions of jaw opening and closing
Either an opening or closing clicking, pop-
ping, or snapping noise detected with
palpation during at least one of three
repetitions of opening and closing and a
clicking, popping, and/or snapping noise
detected with palpation during at least
one of three repetitions of left lateral,
right lateral, or protrusive movements
157
Diagnostic Classification of TMDs
When this diagnosis needs to be conrmed,
then imaging analyses criteria, using TMJ MRI,
are positive for both of the following:
In the maximum intercuspal position, the
posterior band of the disc is located an-
terior to the 11:30 position, and the inter-
mediate zone of the disc is anterior to the
condyle and the articular eminence.
On full opening, the intermediate zone of
the disc is positioned between the con-
dyle and the articular eminence.
Disc displacement with reduction with
intermittent locking (ICD-10 M26.63)
This is an intracapsular biomechanical disor-
der involving the condyle-disc complex: In the
closed mouth position, the disc is in an anterior
position relative to the condyle, and the disc in-
termittently reduces with opening of the mouth.
When the disc does not reduce with opening
of the mouth, intermittent limited mandibular
opening occurs. When the limited opening oc-
curs, a maneuver may be needed to unlock the
TMJ. Medial and lateral displacement of the
disc may also be present. Clicking, popping, or
snapping noises may occur with disc reduction.
Although not required for this diagnosis, occur-
rence of intermittent closed lock during the
clinical examination can help corroborate this
diagnosis. Using MRI as the reference stan-
dard, sensitivity is 0.38, and specicity is 0.98.
History is positive for both of the following:
In the last 30 days or during the examina-
tion itself, any noises present with jaw
movement or function
In the last 30 days, report of intermittent
locking with limited opening or evidence
of intermittent locking during clinical
examination
Examination is positive for the following:
Disc displacement with reduction as de-
ned above
When this diagnosis needs to be conrmed,
the imaging analysis criteria are the same as
for disc displacement with reduction. If locking
occurs during imaging, then an imaging-based
diagnosis of disc displacement without reduc-
tion will be rendered, and clinical conrmation
of reversion to intermittent locking is needed.
Disc displacement without reduction with
limited opening (ICD-10 M26.63)
This is an intracapsular biomechanical disor-
der involving the condyle-disc complex: In
the closed mouth position, the disc is in an
anterior position relative to the condyle and
the disc does not reduce with opening of the
mouth. Medial and lateral displacement of the
disc may also be present. This disorder is as-
sociated with limited mandibular opening that
does not reduce with the clinician or patient
performing a manipulative maneuver. This is
also referred to as closed lock. Using MRI as
the reference standard, sensitivity is 0.80, and
specicity is 0.97.
History is positive for both of the following:
Jaw lock or catch so that it will not open
all the way
Limitation in jaw opening severe enough
to interfere with the ability to eat
Examination is positive for the following:
Maximum assisted opening (passive
stretch) < 40 mm including vertical inci-
sal overlap
When this diagnosis needs to be conrmed,
then imaging analysis criteria, using TMJ MRI,
are positive for both of the following:
In the maximum intercuspal position, the
posterior band of the disc is located an-
terior to the 11:30 position, and the inter-
mediate zone of the disc is anterior to the
condyle and the articular eminence.

158
Dierential Diagnosis and Management of TMDs
8
On full opening, the intermediate zone
of the disc is positioned anterior to the
condyle.
Disc displacement without reduction without
limited opening (ICD-10 M26.63)
This is an intracapsular biomechanical disor-
der involving the condyle-disc complex: In
the closed mouth position, the disc is anterior
relative to the condyle, and the disc does not
reduce with opening of the mouth. Medial and
lateral displacement of the disc may also be
present. This disorder is not associated with
limited mandibular opening. Using MRI as the
reference standard, sensitivity is 0.54, and
specicity is 0.79.
History is the same as dened for disc
displacement without reduction with limited
opening.
Examination is positive for the following:
Maximum assisted opening (passive
stretch) > 40 mm including vertical inci-
sal overlap
When this diagnosis needs to be con-
rmed, then imaging analysis criteria are the
same as for disc displacement without reduc-
tion with limited opening.
Other hypomobility disorders (ICD-10
M26.61)
Intra-articular brous adhesions and ankyloses
are characterized by a restricted mandibular
movement with deection to the affected side
on opening that may occur as a long-term se-
quela of trauma, including mandibular fracture.
In case of bilateral involvement, asymmetries
in mandibular movements during clinical exam-
ination will be less pronounced or absent. The
diagnostic criteria of mandibular movement
asymmetries are for unilateral causes of hypo-
mobility. Hypomobility is rm and unyielding
because of intra-articular brous adhesions,
more widespread brotic changes in the cap-
sular ligaments (brous ankylosis), and/or, less
frequently, the formation of a bony mass that
results in fusion of the joint components (bony
ankylosis). The condition is usually not asso-
ciated with pain. The most frequent cause of
TMJ ankylosis is macrotrauma; less frequent
causes are infection of the mastoid or middle
ear, systemic disease, and inadequate surgical
treatment of the condylar area.
Adhesions and adherence
Fibrous adhesions within the TMJ are thought
to occur mainly in the superior compartment
of the TMJ. They produce decreased move-
ment of the disc-condyle complex. Adhesions
may occur secondary to joint inammation
that results from direct trauma, excessive
loading, or systemic conditions such as a poly-
arthritic disease. They are typically associated
with disc-condyle complex disorders.
History is positive for both of the following:
No history of TMJ clicking (historically
to differentiate from disc displacement
without reduction with limited opening)
History of loss of jaw mobility
Examination is positive for all of the
following:
Limited range of motion on opening
Uncorrected deviation of the jaw to
the affected side on opening if present
unilaterally
Marked limited laterotrusion to the con-
tralateral side if unilateral
When this diagnosis needs to be con-
rmed, arthrography, MRI, or arthroscopy may
show the presence of adhesions. Sensitivity
and specicity have not been established.
Ankylosis
TMJ ankyloses are differentiated by the type of
tissues that are causing them: brous or bony.
In brous ankylosis, there are no gross bony
changes and no radiographic ndings other
159
than absence of ipsilateral condylar translation
on opening. Bony ankylosis is characterized by
the union of the bones of the TMJ as a result
of bone cell proliferation; this may cause com-
plete immobility of that joint. It is characterized
by radiographic evidence of bone proliferation
with marked deection to the affected side
and marked limited laterotrusion to the contra-
lateral side. Sensitivity and specicity have not
been established for these disorders.
Fibrous ankylosis
History is positive for the following:
History of progressive loss of jaw mobility
Examination is positive for all of the
following:
Severe limited range of motion on
opening
Uncorrected jaw deviation to the affected
side
Marked limited laterotrusion to the con-
tralateral side
Computed tomography (CT) or cone beam
CT (CBCT) is positive for both of the following:
Imaging ndings of decreased ipsilateral
condylar translation on opening
Imaging ndings of a joint space be-
tween ipsilateral condyle and eminence
Bony ankylosis
History is positive for the following:
History of progressive loss of jaw mobility
Examination is positive for the following:
Absence of or severely limited jaw mobil-
ity with all movements
CT/CBCT is positive for the following:
Imaging-based evidence of bone prolif-
eration with obliteration of part or all of
the joint space
Hypermobility disorders (closed
dislocation: ICD-10 S03.0XXA; recurrent
dislocation: ICD-10 M26.69; ligamentous
laxity: ICD-10 M24.20)
Hypermobility disorders include two types of
TMJ dislocations in which the disc-condyle
complex is positioned anterior to the articular
eminence and is unable to return to a closed
position without a specic maneuver by the
patient (ie, subluxation or partial dislocation) or
by the clinician (ie, luxation or dislocation). The
latter disorder is also referred to as open lock.
Note that the condyle is frequently anterior to
the eminence at full mouth opening and thus
by itself is not a predictor of hypermobility dis-
orders. The duration of dislocation may be mo-
mentary or prolonged. Pain may occur at the
time of dislocation with residual pain following
the episode.
Subluxation (ICD-10 S03.0XXA)
This is a condition involving the disc-condyle
complex and the articular eminence. In the
open mouth position, the disc-condyle com-
plex is positioned anterior to the articular emi-
nence and is unable to return to normal closed
mouth position without a manipulative ma-
neuver by the patient. When the patient needs
the assistance of the clinician to reduce the
dislocation and normalize the jaw position, it
is called luxation or open lock. Using history
only, sensitivity is 0.98, and specicity is 1.00.
History is positive for both of the following:
In the last 30 days, jaw locking or catch-
ing in a wide open mouth position, even
for a moment, so the patient could not
close from the wide open position
Diagnostic Classification of TMDs

160
Dierential Diagnosis and Management of TMDs
8
Inability to close the mouth from wide
opening without a self-maneuver
No examination ndings are required. If the
patient presents with this disorder, he or she
is then found clinically positive for inability to
return to a normal closed mouth position with-
out manipulative patient maneuver.
Luxation (ICD-10 S03.0XXA)
This is a condition in which the disc-condyle
complex is positioned anterior to the articular
eminence and is unable to return to the fossa
without a specic manipulative maneuver by
a clinician. This is also referred to as open
lock. Sensitivity and specicity have not been
established.
History is positive for both of the following:
Report of inability to close from wide
opening
Report that mouth closing can be
achieved only with a specic mandibular
maneuver by the clinician
Examination is positive for one of the fol-
lowing persistent presentations:
Wide open mouth
Protruded jaw position
Lateral position to the contralateral side
if unilateral
When this diagnosis needs to be con-
rmed, CT/CBCT or MRI scans are positive for
the following:
The condyle is anterior to the articular
eminence with the patient attempting to
close the mouth.
Joint diseases
Osteoarthritis (ie, osteoarthrosis or DJD) is de-
ned as a degenerative condition of the joint
characterized by deterioration and abrasion
of articular tissue and concomitant remodel-
ing of the underlying subchondral bone due to
overload of the remodeling mechanism. The
progressive loss of articular cartilage in the os-
teoarthritic TMJ results from an imbalance be-
tween predominantly chondrocyte-controlled
reparative and degradative processes.
224
The
process accelerates as proteoglycan deple-
tion, collagen ber network disintegration,
and fatty degeneration weaken the functional
capacity of the articular cartilage. Different
kinds of biochemical markers have been de-
termined in the synovial uid of TMJs with
osteoarthritis. These include interleukin-6
(IL-6), tissue inhibitor metalloproteinase-1
(TIMP-1), matrix metalloproteinases, heat
shock protein (HSP), transforming growth
factor β 1 (TGF-β1), bone morphogenetic pro-
tein 2 (BMP-2), chondroitin-4-sulfate (C4S)
and chondroitin-6-sulfate (C6S), keratan sulfate
(KS), and human leucocyte antigen D related
(HLA-DR).
225–235
The clinical and diagnostic
value of these markers remains to be evalu-
ated because similar markers have also been
present in other joint diseases. Radiographic
evidence typically lags behind articular tissue
changes.
236
The early changes in the synovial
membrane, such as synovial intima hyperpla-
sia, cell hypertrophy with subsequent loss of
brous material in the intima matrix, and ar-
ticular cartilage are only detectable with biopsy
and arthroscopy.
175,237,238
Thus, osteoarthrosis
frequently escapes early clinical detection.
239
DJD (ICD-10 M19.91; localized/primary)
Degenerative disorders involving the joint are
characterized by deterioration of articular tis-
sue with concomitant osseous changes in the
condyle and articular eminence. Using CT/
CBCT as the reference standard, sensitivity is
0.55, and specicity is 0.61.
History is positive for one of the following:
In the past month, any joint noises pres-
ent with jaw movement or function
Patient report of any noises during the
examination
161
Diagnostic Classification of TMDs
Examination is positive for the following:
Crepitus detected with palpation during
at least one of the following: maximum
unassisted opening, maximum assisted
opening, right or left lateral movements,
or protrusive movements
CT/CBCT is positive for at least one of the
following:
Subchondral cyst
Erosion
Generalized sclerosis
Osteophyte
Flattening and/or cortical sclerosis are con-
sidered indeterminate ndings for DJD and
may represent normal variation, aging, remod-
eling, or a precursor to frank DJD.
Condylysis/idiopathic condylar resorption
(ICD-10 M26.69)
This is an idiopathic degenerative condition
leading to the loss of condylar height and a
progressive anterior open bite. The condi-
tion occurs spontaneously, is mainly bilateral,
and occurs primarily in adolescent and young
adult females.
212
The presence of pain or joint
sounds is variable. In early stages, dental oc-
clusal changes may not be evident, but imag-
ing ndings would be positive. It has been
suggested that it may be a severe form of
DJD and that low estrogen levels may be im-
plicated.
240
Sensitivity and specicity have not
been established.
History is positive for the following:
Progressive dental occlusal changes
Examination is positive for both of the
following:
Anterior open bite
Evidence of progressive dental occlusal
changes with either occlusal facets that
cannot be approximated or change in se-
quential occlusal measurement over time
based on overbite, overjet, or intercuspal
contacts
Imaging includes CT/CBCT evidence of
partial or total condylar resorption or change
with sequential imaging over time from lat-
eral cephalometric images, which may include
clockwise mandibular rotation, increase in
mandibular plane angle, or increased A point–
nasion–B point. Serologic tests for rheumato-
logic disease, including systemic arthritides,
must be negative.
Osteochondritis dissecans (ICD-10 M93.20)
This is a joint condition in which a piece of car-
tilage and a small bone fragment break loose
from the end of the bone and result in loose
osteochondral fragments within the joint. The
pathophysiology is unclear. It usually occurs
in the knee and elbow and is often related to
sports. Case reports describe the condition in
the TMJ, but little is known about signs and
symptoms. Sensitivity and specicity have not
been established.
History is positive for any of the following:
Arthralgia as previously dened
Joint noises with mandibular movement
or swelling
Examination is positive for one of the
following:
Same clinical ndings as operationalized
for arthralgia
Crepitus detected by the examiner dur-
ing palpation or reported by patient dur-
ing mandibular movements
Maximum assisted opening plus vertical
overlap < 40 mm
Swelling around the affected joint
CT/CBCT will provide positive ndings for
loose osteochondral fragments within the

162
Dierential Diagnosis and Management of TMDs
8
joint. Serologic tests for rheumatologic dis-
ease, including systemic arthritides, must be
negative.
Osteonecrosis (ICD-10 M87.08)
Osteonecrosis is a painful condition most
commonly affecting the ends of long bones
such as the femur. Other common sites in-
clude the humerus and the knees. The condi-
tion is found in the mandibular condyle on MRI
as decreased signal in T1-weighted or proton
density images and on T2-weighted images
(sclerosis pattern) and can be combined with
increased signal on T2 images (edema). The
cause, clinical signicance, and the need for
treatment are unknown.
To diagnose osteonecrosis, the patient
must fulll criteria for arthralgia as previously
dened, and imaging must show a decreased
signal in T1-weighted or proton density MR im-
ages and can be combined with an increased
signal on T2-weighted images. In addition, lab-
oratory testing will conrm negative serologic
results for rheumatologic disease. Sensitivity
and specicity have not been established.
Systemic arthritides (rheumatoid arthritis:
ICD-10 M06.9)
This is joint inammation resulting in pain or
structural changes caused by a generalized
systemic inflammatory disease, including
rheumatoid arthritis, juvenile idiopathic ar-
thritis, spondyloarthropathies (eg, ankylosing
spondylitis, psoriatic arthritis, infectious ar-
thritis, Reiter syndrome), and crystal-induced
disease (eg, gout, chondrocalcinosis). Other
rheumatologically related diseases that may
affect the TMJ include autoimmune disorders
and other mixed connective tissue diseases
(eg, scleroderma, Sjögren syndrome, lupus
erythematosus).
241
This group of arthritides
therefore comprises multiple diagnostic cat-
egories that are best diagnosed and managed
by rheumatologists regarding the general or
systemic therapy. Clinical signs and symp-
toms of an ongoing chronic TMJ inammation
are variable between patients and within a pa-
tient over time. They can vary from no signs
or symptoms to only pain to only swelling and
exudate to only tissue degradation to only
growth disturbance. Resorption of condylar
structures may be associated with malocclu-
sion such as a progressive anterior open bite.
A diagnostic instrument should aim to identify
patients with chronic inammation early and
accurately, should not exclude patients with
chronic arthritis of long duration, and should
not only cover rheumatoid arthritis but the
whole range of chronic inammatory states.
Imaging in early stages may not demonstrate
osseous ndings. Sensitivity and specicity
have not been established.
History is positive for both of the following:
Rheumatologic diagnosis of a systemic
inammatory joint disease
TMJ pain or noises present in the past
month or TMJ pain that worsens with the
episodes and exacerbations of the sys-
temic inammatory joint disease
Examination is positive for both of the
following:
Rheumatologic diagnosis of a systemic
joint disease
Arthritis signs and symptoms as dened
previously or crepitus detected with pal-
pation during maximum unassisted and
assisted opening, lateral, and protrusive
movements
Imaging criteria are the same as for DJD;
CT/CBCT is positive for at least one of the
following:
Subchondral cyst
Erosion
Generalized sclerosis
Osteophyte

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Key Points8◊ Temporomandibular disorders (TMDs) rarely result in dis-abling conditions.◊ There is no single cause for all TMDs. Benign TMD signs and symptoms are very common among the general population and are generally self-limiting. ◊ Only 3.6% to 7% of the general population has TMDs severe enough that they seek treatment. Patients with pain-free TMJ clicking generally do not need treatment; reassurance and education about this benign condition usually sufces.◊ Management of TMDs should include the control of contrib-uting factors such as parafunctional oral habits.◊ Smoking habits and certain disorders may inuence TMD symptoms and prognosis, so these factors should be addressed.◊ Management of TMDs may include self-management instruc-tions, oral appliances, pharmacotherapy, and physical therapy. ◊ Generally, invasive surgical management is indicated only after reasonable nonsurgical efforts have failed and when the patient’s quality of life is signicantly affected.◊ Radiographic structural changes consistent with degenera-tive joint disease (DJD) should not be used as the sole guide for treatment decisions.Differential Diagnosis and Management of TMDs 144Dierential Diagnosis and Management of TMDs8Anatomy of the Masticatory StructuresTemporomandibular articulation occurs in the temporomandibular joints (TMJs), two of the most complex joints of the body. The TMJ is technically considered a ginglymoarthrodial joint because each TMJ provides for both hinging or rotation movement in one plane (a criterion for a ginglymoid joint) and for glid-ing or translation movements (a criterion for an arthrodial joint).1 The TMJ is formed by the mandibular condyle tting into the mandibular (glenoid) fossa of the temporal bone (Fig 8-1).1 Separating these two bones from direct con-tact is the interposed articular disc (sometimes inappropriately called a meniscus). The articu-lar portion of the healthy disc is composed of dense brous connective tissue, devoid of any nerves or vessels; conversely, the posterior at-tachment of the disc is richly vascularized and innervated.2–4 Collateral ligaments attach the disc to the condyle both medially and laterally. These ligaments permit rotational movement of the disc on the condyle during opening and closing of the mouth.This so-called condyle-disc complex trans-lates out of the fossa during extended mouth opening (Fig 8-2).1 Therefore, in the normal joint, rotational movement occurs between the condyle and the inferior surface of the disc dur-ing early opening (the inferior joint space), and translation takes place in the space between the superior surface of the disc and the fossa (the superior joint space) during later opening. Movement of the joint is lubricated by synovial uid, which also acts as a medium for trans-porting nutrients and waste products to and from the articular surfaces. Unlike most syno-vial joints, the articulating surfaces of the TMJs are lined with dense brocartilage instead of hyaline cartilage.5 This is an important feature because brocartilage has a greater ability to repair itself than hyaline cartilage. This implies that the management of arthritic conditions of the TMJ may be different from that of other synovial joints.6Movement of the TMJs is achieved by a group of skeletal muscles called the muscles of mastication. These muscles are comparable to other skeletal muscles in physiology and ergo-nomics.7 Although the muscles of mastication are the primary muscles that provide mandibu-lar movement, other associated muscles of the head and neck furnish secondary support during mastication. The masticatory muscles include the masseter, medial pterygoid, and temporalis muscles, which predominantly elevate the man-dible (mouth closing); the digastric muscles, which assist in mandibular depression (mouth opening); the inferior lateral pterygoid muscles, which assist in protruding and lateral move-ments of the mandible; and the superior lateral pterygoid muscles, which provide stabilization for the condyle and disc during function.8–11 The masticatory muscles perform a variety of functional behaviors that include talking, chew-ing, and swallowing.12 A number of muscle be-haviors are nonfunctional (ie, parafunctional), dened under the broad term of bruxism, and include grinding, clenching, or rhythmic chewing-like, empty-mouth movements.13,14Dening TMDsTMDs encompass a group of musculoskeletal and neuromuscular conditions that involve the TMJs, the masticatory muscles, and all asso-ciated tissues, and they have been identied as a major cause of nondental pain in the oro-facial region.15,16 TMDs represent clusters of related disorders in the masticatory system with many common symptoms. The most frequent presenting symptom is pain, usually localized in the muscles of mastication or the preauricular area. Chewing or other mandibular activities usually aggravate the pain. In addi-tion to complaints of pain, patients with these disorders frequently have limited mandibular movements and TMJ sounds that are most fre- 145Fig 8-1 Normal anatomy of the TMJ. ACL, anterior capsular liga-ment (collagenous); AS, articular surface; IRL, inferior retrodiscal lamina (collagenous); RT, retro-discal tissues; SC and IC, supe-rior and inferior joint cavities; SLP and ILP, superior and inferior lateral pterygoid muscles; SRL, superior retrodiscal lamina (elas-tic). (Reproduced with permis-sion from Okeson.1)Fig 8-2 Normal functional movement of the condyle and disc during the full range of opening and closing. Note that the disc is rotated posteriorly on the condyle as the condyle is translated out of the fossa. The closing movement is the exact opposite of opening. (Reproduced with permission from Okeson.1)ACLASSCSRLICRTIRLSLPILP13572468Defining TMDs 146Dierential Diagnosis and Management of TMDs8quently described as clicking, popping, grating, or crepitus.Common patient complaints include jaw ache, earache, headache, and facial pain. Non-painful masticatory muscle hypertrophy and abnormal occlusal wear associated with oral parafunction such as bruxism (eg, clenching and grinding) may be related problems. Pain or dysfunction due to nonmusculoskeletal causes such as otolaryngologic, neurologic, vascular, neoplastic, or infectious disease in the orofacial region is not considered a primary TMD even though secondary musculoskeletal pain may be present.Epidemiology of TMDsReports on prevalence of TMDs from cross- sectional epidemiologic studies vary consider-ably from study to study because of differ ences in terminology, operational denitions, data col-lection, analytic approaches (eg, single-factor versus multiple-factor analysis) and bias. A sys-tematic review including only studies adopt-ing the Research Diagnostic Criteria for TMDs (RDC/TMD) reported a prevalence of up to 13% for masticatory muscle pain, up to 16% for disc derangement disorders, and up to 9% for TMJ pain disorders in the general popula-tion.17, 1 8 While the prevalence of the different diagnoses in TMDs within patient populations varied widely, the results of a meta-analysis showed a prevalence of 45%, 41%, and 30% for muscle disorders, disc derangement dis-orders, and joint pain disorders, respectively.18 Data from the National Health Interview Survey from 2009 show that 5% of the US adult popu-lation (11.5 million people) self-reported jaw or face pain in the preceding 3 months.19 Other studies show that TMDs are primarily a condi-tion of young and middle-aged adults, rather than of children or the elderly, and are approxi-mately twice more common in women than in men.19–21 According to a population-based sur-vey, the report of symptoms are 50% more prevalent in African-Americans, and longitudi-nal data show that the rate of TMD symptoms was higher and the rate of TMD diagnosis was 52% higher in this population, although the persistency of the symptoms is higher in whites.22 In addition, TMDs are often remit-ting, self-limiting, or uctuating over time; the progression to a potentially more serious non-reducing disc status or chronic and disabling intracapsular TMJ disease is relatively uncom-mon.23–27 In fact, recent data demonstrated that 76% and 71% of soft and hard tissue diagnoses, respectively, remained stable after an 8-year follow up.24,27,28Only 3.6% to 7% of individuals with TMDs are estimated to require treatment, and the an-nual incidence rate is estimated to be 2%.29–34 For painful TMDs specically, the most recent estimate for rst onset was 3.9%, with 50% of the cases maintaining the condition after 6 months.22,30,35,36 Because joint sounds are com-mon, often pain free, and not progressive, it is important to avoid overtreatment of benign chronic reducing and nonreducing disc dis-placement in the absence of pain and impaired function.27 According to magnetic resonance imaging (MRI) studies, it is estimated that up to 35% of asymptomatic individuals appear to have disc displacements.37Painful TMD conditions such as myofascial pain and arthralgia have been associated with facial trauma, third molar removal, clenching, physical symptoms (somatization), and female sex.38 Cigarette smoking has been associated with increased risk of TMDs in young adults, and higher levels of pain, psychosocial dis-tress, and sleep disturbances are reported in TMD patients.39,40 The relationship between painful TMDs and comorbid conditions has been evaluated by several investigators. Myo-fascial pain patients self-report more severe headaches, fainting and dizzy spells, gastric acid reux, bromyalgia, anxiety, depression psychiatric treatments, phobias, and frequent sore throats compared with arthralgia (both diagnoses based on the RDC/TMD).41 Indi- 147Etiology of TMDsviduals developing TMDs are also more likely to describe comorbidities such as headaches, muscle soreness, and other body pains.42In a more integrated model, it was investi-gated if the presence of comorbid conditions further modies the phenotype of individuals with TMDs. This relationship was evaluated im-plementing a Multisystem Dysregulation Index that included sensory, autonomic, inamma-tory, and psychologic domains due to their contribution in pain amplication.43 Among individuals without comorbid persistent pain (only 8% among cases of the study popula-tion), the predominant dysregulation was in the sensory domain, which represented the presence of generalized somatic sensitiza-tion. Among those with one persistent pain-ful comorbid condition (49%), the psychologic dysregulation was the only domain associated with the increased risk of having a TMD. For those individuals with two or more comorbid conditions (42%), a multisystem dysregulation was observed including sensory, psychologic, and autonomic domains, indicating that multi-system dysregulation is associated with com-mon persistent pain conditions.43International comparisons of comorbid pain conditions among women with TMD pain were evaluated among women from Italy, Sweden, and Saudi Arabia. Using a case-control design and age-matched in the respective centers, it was found that comorbid pain prevalence, intensity, and disability differ among women from these cultures. The comorbid conditions studied were head, chest, back, and abdominal pain, and all comorbid conditions were consis-tently higher among the cases than the con-trols. The prevalence of back pain was higher among women from Saudi Arabia. Saudi Ara-bian women had more interference from the back pain than women from Sweden and Italy. Headache did not differ among the groups, but the intensity was lower among the women from Sweden.44Etiology of TMDsNo unambiguous universal cause of TMDs has been identied because determining causation requires more than phenotyping the condi-tions under study and/or describing their dis-tribution based on observational studies. Nev-ertheless, the methodologic quality of such observational studies is key to determine their internal and external validity and therefore to transfer such knowledge to clinical care. For this reason, most of the factors discussed in this section are not proven causal, but associ-ated with TMDs. Factors that may cause the onset of TMDs are called initiating factors, fac-tors that increase the risk of TMDs are called predisposing factors, and factors that interfere with healing or enhance the progression of TMDs are called perpetuating factors. Under different circumstances, individual factors may serve any or all of these roles. There is not a single etiologic factor or a unique theoretical model that can explain the onset of TMDs.Bone and TMJ soft tissue remodeling and muscle tone regulation are all adaptive physi-ologic responses to injury or change. Loss of structural integrity, altered function, or biome-chanical stresses in the system can compro-mise adaptability and increase the likelihood of dysfunction or pathology.45 Direct extrinsic trauma to any component of the mastica-tory system can spontaneously initiate loss of structural integrity and concomitantly alter function, thereby reducing the adaptive capac-ity in the system. In addition, there are other contributing anatomical, systemic, pathophysi-ologic, and psychosocial factors that may suf-ciently reduce the adaptive capacity of the masticatory system and result in TMDs.TraumaTrauma is described as any force applied to the mastication structures that exceeds that of normal functional loading. Most trauma can be divided into three types: (1) the result of a 148Dierential Diagnosis and Management of TMDs8sudden and usually isolated blow to the struc-tures (direct trauma), (2) that associated with a sudden blow but without direct contact to the affected structures (indirect trauma), and (3) the result of prolonged, repeated force over time (microtrauma).Direct traumaThere is general agreement that direct trauma (ie, macrotrauma) to the mandible or the TMJ produces injury via impact and is ac-companied in close temporal proximity with signs and symptoms of inammation. If the forces lead to structural failure, loss of func-tion may quickly follow. Direct trauma result-ing in mandibular fracture in adults has been associated with increased signs and symp-toms of TMDs; however, these may not result in patients seeking treatment.46 In children, condylar and subcondylar fractures in girls, but not boys, were associated with increased TMD symptoms over time.47 More signi-cant fractures may result in disc displace-ment.48 Patients with TMDs report physical trauma more often than non-TMD patients.49 The accuracy of recall of TMD symptoms as-sociated with a traumatic event may be com-promised, making it difcult to clearly link the traumatic event with the symptom onset.50 Other forms of trauma such as wide or pro-longed mouth opening, third molar extrac-tion, and intubation have been reported as associated with TMDs.51,52 Self-reported jaw injury due to yawning or prolonged opening is signicantly higher in patients with TMDs.49 Transient and permanent dysfunction of the TMJ after upper airway management proce-dures has been reported, but controlled trials and longitudinal studies are not available in the English-language literature.53,54Indirect traumaAcceleration-deceleration (exion-extension) injury (ie, whiplash) with no direct blow to the face may cause symptoms consistent with TMDs, but signicant controversy persists as to whether there could be a direct causal relationship. Prospective controlled studies both link and show limited risk for the devel-opment of TMD symptoms after whiplash.55,56 Review of the literature has highlighted these controversies; however, there is some evi-dence that postwhiplash TMDs can have a dif-ferent and potentially more protracted clinical course than non-trauma-associated TMDs.57–59 Although symptoms in the mandible may be referred from injured cervical structures, a di-rect causal relationship between mandibular symptoms and indirect trauma has yet to be established.56,60,61 However, reports seem to indicate increased risk to developing orofacial pain, especially with increased severity of the indirect trauma.62Computer simulation suggests that low-velocity rear-end impact does not cause mandibular movement or stresses beyond the physiologic range.63 In support of this nd-ing, human volunteers in simulated rear-end crash tests failed to demonstrate mandibular movement beyond physiologic limits.64 Thus, while evidence is lacking for a mandibular strain without a direct blow to the mandible following a low-velocity motor vehicle acci-dent, there are recognized pathways of het-erotopic pain from the cervical area to the trigeminal area.16,65 It is therefore not uncom-mon to observe symptoms of TMDs following acceleration-deceleration injury to the neck without direct trauma to the face or jaw. The etiologic signicance of nonimpact injuries is uncertain, and much misinformation is being provided to patients without scientic studies to support the claims.MicrotraumaMicrotrauma has been hypothesized to origi-nate from sustained and repetitious adverse loading of the masticatory system through postural imbalances or from parafunctional habits. It has been suggested that pos-tural habits such as forward head position or phone-bracing may create muscle and joint 149Etiology of TMDsstrain and lead to musculoskeletal pain— including headache—in the TMD patient.66Parafunctional habits have been most fre-quently assessed by indirect means such as self-report, questionnaires, reports by a bed-room partner, or tooth wear. These indirect measures of parafunctional habits have pro-vided conicting reports as to the relationship between TMD symptoms and the presence of parafunctional habits. When myofascial TMD patients were compared with controls using polysomnography, the tests did not conrm the patients’ self-reports of more sleep brux-ism than the controls.67 Parafunctional habits such as teeth clenching, tooth grinding, lip bit-ing, and abnormal posturing of the mandible are common and usually do not result in TMD symptoms, but they have been suggested as initiating or perpetuating factors in certain sub-groups of TMD patients.14,68–75 Although the available research and clinical observations gen-erally support this contention, the exact role of parafunctional habits in TMDs remains unclear because few studies have directly assessed these behaviors. Attrition severity secondary to bruxism cannot distinguish TMD patients from asymptomatic individuals, and muscle hyper-activity has not been shown to be associated with arthrogenous TMJ disorders.76–78 Further-more, clenching does not cause neuromuscu-lar fatigue because muscles compensate for sustained muscle activity by derecruitment of motor neurons or through slower ring rates.79Despite the lack of evidence that nonex-perimentally induced parafunction or clenching can cause TMDs, some studies have shown that experimentally induced parafunction can result in transient pain similar to that reported by patients with TMDs.72,80–82 The impact of these studies is limited by their small sam-ple size. The intensity and frequency of oral parafunctional activity may be exacerbated by stress and anxiety, sleep disorders, and medications (eg, neuroleptics, alcohol, and other substances), although the relationship between sleep bruxism and psychologic fac-tors has been questioned.14,83,84 Some forms of masticatory muscle hyperactivity have been associated with emotional behavior and may be mediated via the cortex through the hypo-thalamus.85 Intense and persistent parafunc-tion can also occur in patients with neurologic disorders (eg, cerebral palsy) and extrapyra-midal disorders (eg, orofacial dyskinesia and epilepsy).86 Conversely, sleep bruxism has not been related to facial type or head form.87The most commonly believed indication of past sleep bruxism severity is dental attrition.88 However, dental attrition can also be partly ex-plained by overbite and overjet changes that correlate with age and sex, protrusive guid-ance schemes, dentofacial morphology, ero-sive diets, the bite force ability, and environ-mental factors.89–97 In addition, it is not clear whether sleep bruxism is a pathogenic disor-der or a normal physiologic process. Recent evidence suggests that sleep bruxism may be associated with increasing salivation during sleep, resulting in lubrication of oropharyngeal structures, or with increasing the space of the upper airways to aid with airway patency, or both.98–101 Furthermore, it has been suggested that sleep bruxism plays a protective role as a compensatory mechanism to protect the airway during sleep-related breathing disor-ders.102 Therefore, the issue of whether or not sleep bruxism requires management without the presentation of signicant problems is de-batable. A more pragmatic approach may be to view this as an issue regarding “consequence management,” taking into account risk or side effect/benet ratio.103 Another problem arises when attrition is used to suggest current brux-ism levels.71 Attrition appears to be episodic in nature and occurs in bursts caused by as yet unspecied factors, and thus any noted attrition may not necessarily represent ongo-ing habits.25,104 Continued research with more direct measurements of parafunction (eg, por-table electromyography, sleep laboratory, and direct observation) will be necessary to clarify the specic role of current parafunction.105–107 150Dierential Diagnosis and Management of TMDs8Anatomical factorsSkeletal factorsSkeletal factors include adverse biomechanical relationships that can be genetic, developmen-tal, or iatrogenic in origin. Severe skeletal malfor-mations, interarch and intraarch discrepancies, and past injuries to the teeth may play a role in TMDs, but this role may be less strong than pre-viously believed. For example, while it is known that disc displacement is common in children with facial skeletal abnormalities such as ret-rognathia, it cannot be said that these anatomi-cal anomalies are etiologic.108 In addition, TMD patients with a disc displacement as well as other TMD patients generally do not have an in-creased prevalence of forward head posture.109A steep articular eminence has also been proposed as an etiologic factor in internal de-rangement of the TMJ. In asymptomatic indi-viduals, a steeper eminence was associated with an increased posterior rotation of the disc, posing a potential anatomical risk fac-tor.110 However, several studies have shown that in TMJs with disc displacement without reduction and TMJs with osseous changes, the eminence was less steep than in TMJs with disc displacement with reduction or TMJs without osseous changes, indicating adaptive remodeling.111– 113 In addition, unilateral joint sounds were associated with the side with the less steep condylar movement path.114Occlusal relationshipsThe dental profession has historically viewed occlusal variation as a primary etiologic factor for TMDs. Occlusal features such as work-ing and nonworking posterior contacts and discrepancies between the retruded contact position (RCP) and intercuspal position (ICP) have been commonly identied as predispos-ing, initiating, and perpetuating factors. The current available evidence suggests that the inuence of the occlusion on the onset and development of TMDs is low.115, 116 Among the occlusal factors evaluated, loss of posterior support and unilateral crossbite show some association across studies.115Several occlusal factors (eg, large overjet, minimal anterior overlap and anterior skeletal open bite, unilateral posterior crossbite, oc-clusal slides greater than 2 mm, and lack of rm posterior tooth contact) were found to be more prevalent in patients than in convenience samples. However, this is possibly due to con-dylar positional changes following intracapsu-lar alterations associated with the disease pro-cess itself. Therefore, these occlusal factors may be the result rather than the cause of the disease.115, 117, 118 Previous studies have lacked reliable occlusal measurement techniques and data collection methods, which may explain the diversity of some ndings. Nevertheless, whether considered individually or simultane-ously, little evidence is available to implicate occlusal factors in TMD etiology despite the historic views.118Pathophysiologic factorsSystemic factorsSystemic pathophysiologic conditions may inuence local TMDs and should generally be managed in cooperation with the patient’s primary care physician or other medical spe-cialists. These conditions can include degen-erative, endocrine, infectious, metabolic, neoplastic, neurologic, rheumatologic, and vascular disorders. Systemic factors can act simultaneously at a central and local (ie, pe-ripheral) level.119,120Generalized joint laxity (ie, hypermobility) has been cited as a possible contributing fac-tor to TMDs and has proven to be signicantly more prevalent in patients with internal de-rangements than with other types of TMDs or in normal controls.25,121–125 Altered collagen me-tabolism may also play a role in joint laxity, and the collagen composition in TMJs with pain-ful disc displacement compared with asymp-tomatic joints has been found to differ.123,126 151Etiology of TMDsNevertheless, there is only a weak correlation between the mobility of peripheral joints or the trunk and mandibular mobility, and research has yet to demonstrate that joint laxity can predict the potential for developing TMDs.127Local (peripheral) factorsLocal pathophysiologic factors of TMDs such as masticatory efciency appear to be multi-factorial and involve such a large span of indi-vidual variation that it is difcult to establish norms.128 In addition, chewing force is also inuenced by sex, age, and pain levels.129–135Masticatory muscle tenderness is not al-ways related to variation in muscle activity or the site or side of reported tenderness.120,136–138 While the masseter muscle may react to proximal muscle pain, the anterior temporalis muscle does not, and any associations may be parallel developments rather than etiologic. Muscle tenderness does not appear to be the result of inammation but is probably related to prolonged central hyperexcitability and al-tered CNS processing following peripheral tis-sue injury.138 Cervical muscle activity has been shown to inuence masticatory muscle activ-ity, probably involving a primary afferent reex response.139–141 Thus, a primary cervical or TMJ disorder may precipitate a secondary mastica-tory muscle condition. Muscle hyperalgesia can also result from TMJ inammation.142Of great concern to the clinician is the distinction between pathologic and adaptive responses to disease in the TMJ. Histologic studies suggest that cartilage thickness and composition adapt to shearing stresses during functional loading.143,144 Maintenance of an in-tact articular surface is to be expected, even in the face of osteoarthritic changes, allowing for both stable morphologic relationships and his-tologic compatibility between the articulating components.118,145,146 Therefore, even though morphologic change is mostly irreversible, it usually achieves and maintains stability and should be considered adaptive.147 The goal of treating osteoarthritic changes in this light should not be to restore earlier morphology but to encourage the body’s adaptive response to pathophysiologic processes.In early disc derangements, signs of osteo-arthritis are not apparent. Disc derangements with reduction may persist for many years without development of radiographically visible changes or symptoms.148 Disc derangements in later stages with osteoarthritic changes occur possibly parallel but may also represent independent processes, and 50% will show some active cellular osteoblastic or osteoclas-tic activity.149,150 Osteoarthritic changes, altera-tions in synovial uid viscosity, and inadequate or altered lubrication may initiate derangement of the TMJ articular disc.151,152 Synovial uid analyses attempting to correlate biochemi-cal signs of inammation with pain reveal abnormal concentrations of plasma proteins or neurotransmitters and inammatory cyto-kines.153–158 While still controversial, cytokine proles of patients with intracapsular TMDs do appear to be different from controls.159 With these as well as animal model studies, additional research in this area could have the potential for targeted therapeutic treatments in a subset of individuals with TMDs.Frictional “sticking” of the disc has been proposed to cause internal derangement of the TMJ with the forces dependent on the type of clenching task, with the greater impact at ICP and during a unilateral molar clench.73,160,161 According to experimental models and animal studies, the forces are also increased by re-duced congruity between the opposing sur-faces and by at unrounded surfaces.161–165 The forces are affected by disc thickness and area and by mandibular deformation during clench-ing.164,166 Interestingly, nonworking tooth con-tacts have been hypothesized to reduce loads within the joint and act as a stress breaker for the clenching forces.161 Intracapsular pressure may also affect TMDs.167,168 With joint move-ment, the alternating pressure acts as a pump for joint lubrication, nutrition, blood supply, drug delivery, waste removal, and even con- 152Dierential Diagnosis and Management of TMDs8dylar growth. Thus, any interruption through immobilization or prolonged clenching might have the potential to initiate or advance TMD signs and symptoms.Female hormones might play a role in TMJ disc disease, but this has not been proven be-cause the presence of both estrogen and pro-gesterone receptors within the articular disc has been both conrmed and denied.169,170 Clinical randomized controlled trials (RCTs) indicate that estrogen does not play a role in the etiology of TMDs, whereas cohort stud-ies and case-control studies show contrast-ing results.171–174 The etiologic explanations for progression from disc displacement to osteo-arthritis and osteoarthritic changes are multi-factorial and include failure of the reparative ar-ticular chondrocyte response due to metabolic dysfunction and relative or absolute overload-ing due to excessive mechanical forces leading to articular cartilage biochemical failure.45,175 Remodeling, in contrast, is a physiologic re-sponse to accommodate an altered disc posi-tion.118 Thus, it is probable that a mechanical breakdown in the articular disc (eg, a perfora-tion) rather than an unusual disc position leads to osteoarthritis and/or osteoarthritic changes following disc displacement.176 It is not certain, however, that all gross abnormalities of disc morphology will lead to osteoarthritis because one experimental animal study suggests that the TMJ may be capable of healing disc perforations within a relatively short time.177 Mechanical stress may also lead to the accu-mulation of damaging free radicals in affected articular tissues of susceptible individuals. This condition is called oxidative stress.178 Dijkgraaf et al179 have proposed that free radicals may be responsible for the formation of adhesions in the TMJ by cross-linking of proteins.Genetic factorsWhile the body of literature available with regard to genetic susceptibility for TMDs is an expanding eld, genetic association stud-ies have been limited. The relationship be-tween catechol-O-methyltransferase (COMT) polymorphism, pain sensitivity, and the risk of TMD development has been evaluated, and three genetic variants (haplotypes) of the gene encoding COMT were identied and des-ignated as “low pain sensitivity,” “average pain sensitivity,” and “high pain sensitivity.”180 The haplotypes were associated with experimen-tal pain sensitivity, and the presence of even a single “low pain sensitivity” haplotype was shown to reduce the risk of developing myog-enous TMDs. Furthermore, the gene–environ-ment interaction was illustrated by the signi-cant role of stress, which doubles the rate of TMDs among those with low-activity COMT haplotypes.22 The most current data from the Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) trial did not demon-strate signicant variation in TMD incidence by genetic polymorphisms from a panel of candi-dates’ putative genes but found evidence for genetic associations in several pronociceptive intermediate phenotypes and their contribut-ing role.181 Single-nucleotide polymorphisms (SNPs) representing 358 genes involved in biologic systems associated with pain percep-tion were identied. Specically, SNPs had stronger associations with nonspecic orofa-cial symptoms, global psychologic symptoms, stress and negative affect, and heat and tem-poral summation. These included the following:• The glucocorticoid receptor gene, which suggests a role of the hypothalamic- pituitary-adrenal system in chronic TMDs• The serotonin receptor gene, indicating the inuence in nociceptive and affective pathways• The gene encoding the α subunit of the voltage-gated sodium channel NaV 1.1, which is involved in the generation and propagation of action potentials in sen-sory nerves• A variation in a gene encoding angioten-sin I-converting enzyme implicated in hypertension 153Etiology of TMDs• The prostaglandin-endoperoxide syn-thase 1 gene, a regulator of nociception and inammatory response• A variation in the gene encoding amyloid β (A4) precursor protein, which inuences synapse formation and neuronal plasticity• Multiple PDZ domain protein gene, in-uencing G-protein-coupled receptors involved in nociception and analgesiaThese most extensive panel-related candi-date genes support the strong indication that multiple genetic and biologic pathways contrib-ute to the risk for TMDs.181Psychosocial factorsPsychosocial factors include individual, inter-personal, and situational variables that impact the patient’s capacity to function adaptively. General distress is the most salient single fac-tor across most individuals with chronic TMD pain.182 General distress is readily assessed (see chapters 2 and 12), and certainly other factors may contribute actively to the mea-sured distress, such as personality character-istics, enduring stressors, a physical response style to stress, or limited coping skills.183–188There is evidence that some patients with TMDs experience more anxiety than healthy control groups and that some TMDs and oro-facial pain symptoms may be only one of sev-eral somatic manifestations of emotional dis-tress.189–192 Some muscle pain may in fact be caused by excessive sympathetic nervous sys-tem activity as an overresponse to life stress-ors, and the attention focused on the pain can adversely affect the intensity of the pain.193–196 Patients with such complaints often have a history of other stress-related disorders.192 Depression and anxiety related to other major life events may alter the patient’s perception of and tolerance of physical symptoms, caus-ing them to seek more care for what is pre-sented as a problem of the body.197 Patients with chronic TMDs have been found to have psychosocial and behavioral characteristics similar to patients with lower back pain and headache.198,199 In general, TMD patients are not signicantly different from healthy individu-als in personality type, and they do not differ from other pain patients in response to illness, attitudes toward health care, or ways of coping with stress.69,188,200–202 Any psychologic impair-ment may be merely associated with the pres-ence of pain persistence.131,197,203Environmental contingencies can greatly complicate treatment by affecting an indi-vidual’s perception of and responses to pain and disease. Some patients may experience a lessening of distress to the extent that psycho-genic symptoms decrease or resolve preexist-ing psychologic and interpersonal conicts. This primary gain of symptom formation is distinguished from the secondary gain of so-cial benets experienced by patients once a disorder is established.204–206 Secondary gain includes being exempt from ordinary daily re-sponsibilities; being compensated monetarily from insurance or litigation; using the rational-ization of “being ill” to avoid unpleasant tasks; and gaining attention from family, friends, or health care workers.206,207 What the clinician interprets as pain (eg, in response to a clini-cal examination procedure designed to evoke pain) may be less related to any local nocicep-tive mechanisms and more a function of pain behavior: how the individual presents his or her distress as motivated by factors beyond the stated complaint.From the psychosocial domain, the OPPERA study group evaluated 26 psychosocial mea-sures; among them, the frequency of somatic symptoms was the strongest predictor for TMD onset. Other contributors to a lesser degree were psychologic stress, anxiety, obsessive-compulsive feelings, and pain cop-ing strategies.208 Using a case-control analyti-cal approach as a foundation for their research, the OPPERA group reported that TMD cases are different than controls across multiple phe-notypic domains including sociodemographic 154Dierential Diagnosis and Management of TMDs8factors, clinical variables, psychologic function-ing, pain sensitivity, autonomic responses, and genetic associations. All of these elements are providing leading-edge information to the biologic pathways that may elucidate TMD pathophysiology.209Diagnostic Classication of TMDsThe classication of TMDs is hampered by lim-ited knowledge of the etiology and the natu-ral progression of these disorders, and yet advancement in our knowledge is dependent on an accepted taxonomy and corresponding diagnostic criteria.17 Diagnostic criteria allow comparisons of patient populations in different studies and provide a common language for developing a conceptual framework to use in the clinic.210 Any classication scheme or tax-onomy must be considered an evolving frame-work that will be modied by new ndings and with increased level of understanding. The fol-lowing outlines are based on the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD; a revision of the RDC/TMD), which in-clude the most common TMDs with sensitivity and specicity values, and the expanded tax-onomy, which includes less common TMDs without validity estimates (Box 8-1).211,212TMJ disordersJoint pain (ICD-10 M26.62)Previously described as synovitis, capsulitis, and retrodiscitis, joint pain has been explained in the biomedical model as an inammatory process of the synovial lining of the TMJ that can be due to infection, an immunologic con-dition secondary to cartilage degeneration, or trauma. Joint pain is characterized by localized pain that is exacerbated by function and para-function. On occasion, there may be a uctu-ating swelling that decreases the ability to oc-clude on the ipsilateral posterior teeth.Arthralgia (ICD-10 M26.62)This is pain of joint origin affected by jaw move-ment, function, or parafunction and replication of this pain with provocation testing, either during mandibular movement or palpation of the TMJs. Sensitivity is 0.89, and specicity is 0.98.History is positive for both of the following:• In the past 30 days, pain in the jaw, tem-ple, in front of the ear, or in the ear with examiner conrmation of pain location in a masticatory structure• Pain altered with jaw movement, func-tion, or parafunctionConrmation of the pain location in the TMJ area includes at least one of the follow-ing tests:• Palpation of the lateral pole (0.5 kg pres-sure) or around the lateral pole (1.0 kg pressure)• Maximum unassisted or assisted open-ing, right or left lateral movements, or protrusive movementsExamination of the TMJ elicits a report of familiar pain (dened as similar or like the pain the patient has experienced in the masticatory area palpated during the last 30 days).ArthritisThis is pain of joint origin with clinical charac-teristics of inammation or infection: edema, erythema, and/or increased temperature. It may arise in association with trauma. As-sociated symptoms can include occlusal changes such as ipsilateral posterior open bite if intra-articular swelling is present unilater-ally. This disorder has also been referred to as synovitis or capsulitis; however, these terms limit the sites of nociception. With this local-ized condition, there should be no history of systemic inammatory disease. Sensitivity and specicity have not been established. 155Diagnostic Classification of TMDsNote: This box was adapted from work performed by the International RDC-TMD Consortium sponsored by the International Association for Dental Research and the Special Interest Group on Orofacial Pain of the International Association for the Study of Pain.Temporomandibular joint disorders1. Joint pain (ICD-10 M26.62)A. ArthralgiaB. Arthritis2. Joint disordersA. Disc-condyle complex disorders (ICD-10 M26.62)i. Disc displacement with reductionii. Disc displacement with reduction with intermittent lockingiii. Disc displacement without reduction with limited openingiv. Disc displacement without reduction without limited openingB. Other hypomobility disorders (ICD-10 M26.61)i. Adhesions/adherenceii. Ankylosis a. Fibrous ankylosis b. Osseous ankylosisC. Hypermobility disordersi. Subluxation (ICD-10 S03.0XXA)ii. Luxation (ICD-10 S03.0XXA)a. Closed dislocation (ICD-10 S03.0XXA)b. Recurrent dislocation (ICD-10 M26.69)c. Ligamentous laxity (ICD-10 M24.20)3. Joint diseasesA. Degenerative joint diseases (ICD-10 M19.91)i. Osteoarthrosisii. OsteoarthritisB. Condylysis (ICD-10 M26.69)C. Osteochondritis dissecans (ICD-10 M93.20)D. Osteonecrosis (ICD-10 M87.08)E. Systemic arthritides (rheumatoid arthritis: ICD-10 M06.9)F. Neoplasm (benign: ICD-10 D16.5; malignant: ICD-10 C41.1)G. Synovial chondromatosis (ICD-10 D48.0)4. FracturesA. Closed fracture of condylar process (ICD-10 S02.61XA)B. Closed fracture of subcondylar process (ICD-10 S02.62XA)C. Open fracture of condylar process (ICD-10 S02.61XB)D. Open fracture of subcondylar process (ICD-10 S02.62XB)5. Congenital/developmental disordersA. Aplasia (ICD-10 Q67.4)B. Hypoplasia (ICD-10 M27.8)C. Hyperplasia (ICD-10 M27.8)Masticatory muscle disorders1. Muscle pain limited to the orofacial regionA. Myalgia (ICD-10 M79.1)i. Local myalgiaii. Myofascial painiii. Myofascial pain with referralB. Tendonitis (ICD-10 M67.90)C. Myositisi. Noninfective (ICD-10 M60.9)ii. Infective (ICD-10 M60.009)C. Spasm (ICD-10 M62.838)2. ContractureA. Muscle (ICD-10 M62.40)B. Tendon3. Hypertrophy (ICD-10 M62.9)4. NeoplasmsA. Jawi. Malignant (ICD-10 C41.1)ii. Benign (ICD-10 D16.5)B. Soft tissues of head, face, and necki. Malignant (ICD-10 C49.0)ii. Benign (ICD-10 D21.0)5. Movement disordersA. Orafacial dyskinesiai. Abnormal involuntary movements (ICD-10 R25.1 [tremor unspecied]; R25.2 [cramp and spasm]; R25.3 [fasciculations])ii. Ataxia, unspecied (ICD-10 R27.0); muscular incoordination (ICD-10 R27.9)iii. Subacute, due to drugs; oral tardive dyskinesia (ICD-10 G24.01)B. Oromandibular dystoniai. Acute, due to drugs (ICD-10 G24.02)ii. Deformans, familial, idiopathic, and torsion dystonia (ICD-10 G24.1)6. Masticatory muscle pain attributed to systemic/central disordersA. Fibromyalgia (ICD-10 M79.7)B. Centrally mediated myalgia (ICD-10 M79.1)Masticatory muscle disorders1. Headache attributed to TMDs (ICD-10 G44.89 or ICD-10 R51)Associated structures1. Coronoid hyperplasia (ICD-10 M27.8)Box 8-1 Expanded TMD taxonomy 156Dierential Diagnosis and Management of TMDs8History is positive for arthralgia as dened above as well as one of the following:• Swelling, redness, and/or increased tem-perature in front of the ear• Dental occlusal changes resulting from articular inammatory exudate (eg, pos-terior open bite)Examination is positive for arthralgia as de-ned above as well as one of the following:• Presence of edema, erythema, and/or in-creased temperature over the TMJs• Reduction in dental occlusal con-tacts noted between two consecutive measurementsUnilateral or bilateral posterior open bite must not be attributable to other causes. The patient is negative for rheumatologic disease, including those in systemic arthritides. The pain is not better accounted for by another pain diagnosis.Joint disordersArticular disc displacement is the most com-mon TMJ arthropathy and is characterized by several stages of clinical dysfunction that involve the condyle-disc relationship. It is characterized by an abnormal relation or mis-alignment of the articular disc relative to the condyle. Although posterior and mediolateral displacements of the articular disc have been described, the usual direction for displacement is in an anterior or anteromedial direction.213–220 Nevertheless, pain or mandibular movement symptoms are not specic for disc derange-ment disorders, and the disc position is not related to any presenting symptoms.221,222The causes of disc displacement are not agreed upon; however, it is postulated that in the majority of cases, elongated or torn liga-ments binding the disc to the condyle permit the disc to displace.223 Lubrication impairment is also suggested as a possible etiologic factor of disc displacement.73,152 Disc displacement is subdivided into disc displacement with reduc-tion and disc displacement without reduction.Disc-condyle complex disordersDisc displacement with reduction (ICD-10 M26.63)This is an intracapsular biomechanical disor-der involving the condyle-disc complex: In the closed mouth position, the disc is in an anterior position relative to the condyle, and the disc re-duces upon opening of the mouth. Medial and lateral displacement of the disc may also be present. Clicking, popping, or snapping noises may occur with disc reduction. Using MRI as the reference standard, sensitivity is 0.34, and specicity is 0.92. Although not required for this diagnosis and without diagnostic validity, elimination of the opening and closing noise, if present, with protrusion can help corroborate this diagnosis.History is positive for the following:• In the last 30 days, any noise(s) pres-ent with jaw movement or function, or patient report of joint sounds during the examinationExamination is positive for at least one of the following:• Both an opening and closing clicking, popping, or snapping noise detected with palpation during at least one of three rep-etitions of jaw opening and closing• Either an opening or closing clicking, pop-ping, or snapping noise detected with palpation during at least one of three repetitions of opening and closing and a clicking, popping, and/or snapping noise detected with palpation during at least one of three repetitions of left lateral, right lateral, or protrusive movements 157Diagnostic Classification of TMDsWhen this diagnosis needs to be conrmed, then imaging analyses criteria, using TMJ MRI, are positive for both of the following:• In the maximum intercuspal position, the posterior band of the disc is located an-terior to the 11:30 position, and the inter-mediate zone of the disc is anterior to the condyle and the articular eminence.• On full opening, the intermediate zone of the disc is positioned between the con-dyle and the articular eminence.Disc displacement with reduction with intermittent locking (ICD-10 M26.63)This is an intracapsular biomechanical disor-der involving the condyle-disc complex: In the closed mouth position, the disc is in an anterior position relative to the condyle, and the disc in-termittently reduces with opening of the mouth. When the disc does not reduce with opening of the mouth, intermittent limited mandibular opening occurs. When the limited opening oc-curs, a maneuver may be needed to unlock the TMJ. Medial and lateral displacement of the disc may also be present. Clicking, popping, or snapping noises may occur with disc reduction. Although not required for this diagnosis, occur-rence of intermittent closed lock during the clinical examination can help corroborate this diagnosis. Using MRI as the reference stan-dard, sensitivity is 0.38, and specicity is 0.98.History is positive for both of the following:• In the last 30 days or during the examina-tion itself, any noises present with jaw movement or function• In the last 30 days, report of intermittent locking with limited opening or evidence of intermittent locking during clinical examinationExamination is positive for the following:• Disc displacement with reduction as de-ned aboveWhen this diagnosis needs to be conrmed, the imaging analysis criteria are the same as for disc displacement with reduction. If locking occurs during imaging, then an imaging-based diagnosis of disc displacement without reduc-tion will be rendered, and clinical conrmation of reversion to intermittent locking is needed.Disc displacement without reduction with limited opening (ICD-10 M26.63)This is an intracapsular biomechanical disor-der involving the condyle-disc complex: In the closed mouth position, the disc is in an anterior position relative to the condyle and the disc does not reduce with opening of the mouth. Medial and lateral displacement of the disc may also be present. This disorder is as-sociated with limited mandibular opening that does not reduce with the clinician or patient performing a manipulative maneuver. This is also referred to as closed lock. Using MRI as the reference standard, sensitivity is 0.80, and specicity is 0.97.History is positive for both of the following:• Jaw lock or catch so that it will not open all the way• Limitation in jaw opening severe enough to interfere with the ability to eatExamination is positive for the following:• Maximum assisted opening (passive stretch) < 40 mm including vertical inci-sal overlapWhen this diagnosis needs to be conrmed, then imaging analysis criteria, using TMJ MRI, are positive for both of the following:• In the maximum intercuspal position, the posterior band of the disc is located an-terior to the 11:30 position, and the inter-mediate zone of the disc is anterior to the condyle and the articular eminence. 158Dierential Diagnosis and Management of TMDs8• On full opening, the intermediate zone of the disc is positioned anterior to the condyle.Disc displacement without reduction without limited opening (ICD-10 M26.63)This is an intracapsular biomechanical disor-der involving the condyle-disc complex: In the closed mouth position, the disc is anterior relative to the condyle, and the disc does not reduce with opening of the mouth. Medial and lateral displacement of the disc may also be present. This disorder is not associated with limited mandibular opening. Using MRI as the reference standard, sensitivity is 0.54, and specicity is 0.79.History is the same as dened for disc displacement without reduction with limited opening.Examination is positive for the following:• Maximum assisted opening (passive stretch) > 40 mm including vertical inci-sal overlapWhen this diagnosis needs to be con-rmed, then imaging analysis criteria are the same as for disc displacement without reduc-tion with limited opening.Other hypomobility disorders (ICD-10 M26.61)Intra-articular brous adhesions and ankyloses are characterized by a restricted mandibular movement with deection to the affected side on opening that may occur as a long-term se-quela of trauma, including mandibular fracture. In case of bilateral involvement, asymmetries in mandibular movements during clinical exam-ination will be less pronounced or absent. The diagnostic criteria of mandibular movement asymmetries are for unilateral causes of hypo-mobility. Hypomobility is rm and unyielding because of intra-articular brous adhesions, more widespread brotic changes in the cap-sular ligaments (brous ankylosis), and/or, less frequently, the formation of a bony mass that results in fusion of the joint components (bony ankylosis). The condition is usually not asso-ciated with pain. The most frequent cause of TMJ ankylosis is macrotrauma; less frequent causes are infection of the mastoid or middle ear, systemic disease, and inadequate surgical treatment of the condylar area.Adhesions and adherenceFibrous adhesions within the TMJ are thought to occur mainly in the superior compartment of the TMJ. They produce decreased move-ment of the disc-condyle complex. Adhesions may occur secondary to joint inammation that results from direct trauma, excessive loading, or systemic conditions such as a poly-arthritic disease. They are typically associated with disc-condyle complex disorders.History is positive for both of the following:• No history of TMJ clicking (historically to differentiate from disc displacement without reduction with limited opening)• History of loss of jaw mobilityExamination is positive for all of the following:• Limited range of motion on opening• Uncorrected deviation of the jaw to the affected side on opening if present unilaterally• Marked limited laterotrusion to the con-tralateral side if unilateralWhen this diagnosis needs to be con-rmed, arthrography, MRI, or arthroscopy may show the presence of adhesions. Sensitivity and specicity have not been established.AnkylosisTMJ ankyloses are differentiated by the type of tissues that are causing them: brous or bony. In brous ankylosis, there are no gross bony changes and no radiographic ndings other 159than absence of ipsilateral condylar translation on opening. Bony ankylosis is characterized by the union of the bones of the TMJ as a result of bone cell proliferation; this may cause com-plete immobility of that joint. It is characterized by radiographic evidence of bone proliferation with marked deection to the affected side and marked limited laterotrusion to the contra-lateral side. Sensitivity and specicity have not been established for these disorders.Fibrous ankylosisHistory is positive for the following:• History of progressive loss of jaw mobilityExamination is positive for all of the following:• Severe limited range of motion on opening• Uncorrected jaw deviation to the affected side• Marked limited laterotrusion to the con-tralateral sideComputed tomography (CT) or cone beam CT (CBCT) is positive for both of the following:• Imaging ndings of decreased ipsilateral condylar translation on opening• Imaging ndings of a joint space be-tween ipsilateral condyle and eminenceBony ankylosisHistory is positive for the following:• History of progressive loss of jaw mobilityExamination is positive for the following:• Absence of or severely limited jaw mobil-ity with all movementsCT/CBCT is positive for the following:• Imaging-based evidence of bone prolif-eration with obliteration of part or all of the joint spaceHypermobility disorders (closed dislocation: ICD-10 S03.0XXA; recurrent dislocation: ICD-10 M26.69; ligamentous laxity: ICD-10 M24.20)Hypermobility disorders include two types of TMJ dislocations in which the disc-condyle complex is positioned anterior to the articular eminence and is unable to return to a closed position without a specic maneuver by the patient (ie, subluxation or partial dislocation) or by the clinician (ie, luxation or dislocation). The latter disorder is also referred to as open lock. Note that the condyle is frequently anterior to the eminence at full mouth opening and thus by itself is not a predictor of hypermobility dis-orders. The duration of dislocation may be mo-mentary or prolonged. Pain may occur at the time of dislocation with residual pain following the episode.Subluxation (ICD-10 S03.0XXA)This is a condition involving the disc-condyle complex and the articular eminence. In the open mouth position, the disc-condyle com-plex is positioned anterior to the articular emi-nence and is unable to return to normal closed mouth position without a manipulative ma-neuver by the patient. When the patient needs the assistance of the clinician to reduce the dislocation and normalize the jaw position, it is called luxation or open lock. Using history only, sensitivity is 0.98, and specicity is 1.00.History is positive for both of the following:• In the last 30 days, jaw locking or catch-ing in a wide open mouth position, even for a moment, so the patient could not close from the wide open positionDiagnostic Classification of TMDs 160Dierential Diagnosis and Management of TMDs8• Inability to close the mouth from wide opening without a self-maneuverNo examination ndings are required. If the patient presents with this disorder, he or she is then found clinically positive for inability to return to a normal closed mouth position with-out manipulative patient maneuver. Luxation (ICD-10 S03.0XXA)This is a condition in which the disc-condyle complex is positioned anterior to the articular eminence and is unable to return to the fossa without a specic manipulative maneuver by a clinician. This is also referred to as open lock. Sensitivity and specicity have not been established.History is positive for both of the following:• Report of inability to close from wide opening• Report that mouth closing can be achieved only with a specic mandibular maneuver by the clinicianExamination is positive for one of the fol-lowing persistent presentations:• Wide open mouth• Protruded jaw position• Lateral position to the contralateral side if unilateralWhen this diagnosis needs to be con-rmed, CT/CBCT or MRI scans are positive for the following:• The condyle is anterior to the articular eminence with the patient attempting to close the mouth.Joint diseasesOsteoarthritis (ie, osteoarthrosis or DJD) is de-ned as a degenerative condition of the joint characterized by deterioration and abrasion of articular tissue and concomitant remodel-ing of the underlying subchondral bone due to overload of the remodeling mechanism. The progressive loss of articular cartilage in the os-teoarthritic TMJ results from an imbalance be-tween predominantly chondrocyte-controlled reparative and degradative processes.224 The process accelerates as proteoglycan deple-tion, collagen ber network disintegration, and fatty degeneration weaken the functional capacity of the articular cartilage. Different kinds of biochemical markers have been de-termined in the synovial uid of TMJs with osteoarthritis. These include interleukin-6 (IL-6), tissue inhibitor metalloproteinase-1 (TIMP-1), matrix metalloproteinases, heat shock protein (HSP), transforming growth factor β 1 (TGF-β1), bone morphogenetic pro-tein 2 (BMP-2), chondroitin-4-sulfate (C4S) and chondroitin-6-sulfate (C6S), keratan sulfate (KS), and human leucocyte antigen D related (HLA-DR).225–235 The clinical and diagnostic value of these markers remains to be evalu-ated because similar markers have also been present in other joint diseases. Radiographic evidence typically lags behind articular tissue changes.236 The early changes in the synovial membrane, such as synovial intima hyperpla-sia, cell hypertrophy with subsequent loss of brous material in the intima matrix, and ar-ticular cartilage are only detectable with biopsy and arthroscopy.175,237,238 Thus, osteoarthrosis frequently escapes early clinical detection.239DJD (ICD-10 M19.91; localized/primary)Degenerative disorders involving the joint are characterized by deterioration of articular tis-sue with concomitant osseous changes in the condyle and articular eminence. Using CT/CBCT as the reference standard, sensitivity is 0.55, and specicity is 0.61.History is positive for one of the following:• In the past month, any joint noises pres-ent with jaw movement or function• Patient report of any noises during the examination 161Diagnostic Classification of TMDsExamination is positive for the following:• Crepitus detected with palpation during at least one of the following: maximum unassisted opening, maximum assisted opening, right or left lateral movements, or protrusive movementsCT/CBCT is positive for at least one of the following:• Subchondral cyst• Erosion• Generalized sclerosis• OsteophyteFlattening and/or cortical sclerosis are con-sidered indeterminate ndings for DJD and may represent normal variation, aging, remod-eling, or a precursor to frank DJD.Condylysis/idiopathic condylar resorption (ICD-10 M26.69)This is an idiopathic degenerative condition leading to the loss of condylar height and a progressive anterior open bite. The condi-tion occurs spontaneously, is mainly bilateral, and occurs primarily in adolescent and young adult females.212 The presence of pain or joint sounds is variable. In early stages, dental oc-clusal changes may not be evident, but imag-ing ndings would be positive. It has been suggested that it may be a severe form of DJD and that low estrogen levels may be im-plicated.240 Sensitivity and specicity have not been established.History is positive for the following:• Progressive dental occlusal changesExamination is positive for both of the following:• Anterior open bite• Evidence of progressive dental occlusal changes with either occlusal facets that cannot be approximated or change in se-quential occlusal measurement over time based on overbite, overjet, or intercuspal contactsImaging includes CT/CBCT evidence of partial or total condylar resorption or change with sequential imaging over time from lat-eral cephalometric images, which may include clockwise mandibular rotation, increase in mandibular plane angle, or increased A point–nasion–B point. Serologic tests for rheumato-logic disease, including systemic arthritides, must be negative.Osteochondritis dissecans (ICD-10 M93.20)This is a joint condition in which a piece of car-tilage and a small bone fragment break loose from the end of the bone and result in loose osteochondral fragments within the joint. The pathophysiology is unclear. It usually occurs in the knee and elbow and is often related to sports. Case reports describe the condition in the TMJ, but little is known about signs and symptoms. Sensitivity and specicity have not been established.History is positive for any of the following:• Arthralgia as previously dened• Joint noises with mandibular movement or swellingExamination is positive for one of the following:• Same clinical ndings as operationalized for arthralgia• Crepitus detected by the examiner dur-ing palpation or reported by patient dur-ing mandibular movements• Maximum assisted opening plus vertical overlap < 40 mm• Swelling around the affected jointCT/CBCT will provide positive ndings for loose osteochondral fragments within the 162Dierential Diagnosis and Management of TMDs8joint. Serologic tests for rheumatologic dis-ease, including systemic arthritides, must be negative.Osteonecrosis (ICD-10 M87.08)Osteonecrosis is a painful condition most commonly affecting the ends of long bones such as the femur. Other common sites in-clude the humerus and the knees. The condi-tion is found in the mandibular condyle on MRI as decreased signal in T1-weighted or proton density images and on T2-weighted images (sclerosis pattern) and can be combined with increased signal on T2 images (edema). The cause, clinical signicance, and the need for treatment are unknown.To diagnose osteonecrosis, the patient must fulll criteria for arthralgia as previously dened, and imaging must show a decreased signal in T1-weighted or proton density MR im-ages and can be combined with an increased signal on T2-weighted images. In addition, lab-oratory testing will conrm negative serologic results for rheumatologic disease. Sensitivity and specicity have not been established.Systemic arthritides (rheumatoid arthritis: ICD-10 M06.9)This is joint inammation resulting in pain or structural changes caused by a generalized systemic inflammatory disease, including rheumatoid arthritis, juvenile idiopathic ar-thritis, spondyloarthropathies (eg, ankylosing spondylitis, psoriatic arthritis, infectious ar-thritis, Reiter syndrome), and crystal-induced disease (eg, gout, chondrocalcinosis). Other rheumatologically related diseases that may affect the TMJ include autoimmune disorders and other mixed connective tissue diseases (eg, scleroderma, Sjögren syndrome, lupus erythematosus).241 This group of arthritides therefore comprises multiple diagnostic cat-egories that are best diagnosed and managed by rheumatologists regarding the general or systemic therapy. Clinical signs and symp-toms of an ongoing chronic TMJ inammation are variable between patients and within a pa-tient over time. They can vary from no signs or symptoms to only pain to only swelling and exudate to only tissue degradation to only growth disturbance. Resorption of condylar structures may be associated with malocclu-sion such as a progressive anterior open bite. A diagnostic instrument should aim to identify patients with chronic inammation early and accurately, should not exclude patients with chronic arthritis of long duration, and should not only cover rheumatoid arthritis but the whole range of chronic inammatory states. Imaging in early stages may not demonstrate osseous ndings. Sensitivity and specicity have not been established.History is positive for both of the following:• Rheumatologic diagnosis of a systemic inammatory joint disease• TMJ pain or noises present in the past month or TMJ pain that worsens with the episodes and exacerbations of the sys-temic inammatory joint diseaseExamination is positive for both of the following:• Rheumatologic diagnosis of a systemic joint disease• Arthritis signs and symptoms as dened previously or crepitus detected with pal-pation during maximum unassisted and assisted opening, lateral, and protrusive movementsImaging criteria are the same as for DJD; CT/CBCT is positive for at least one of the following:• Subchondral cyst• Erosion• Generalized sclerosis• Osteophyte 163Diagnostic Classification of TMDsNeoplasm (TMJ) (benign: ICD-10 D16.5; malignant: ICD-10 C41.1)A neoplasm is new, often uncontrolled growth of abnormal tissue, in this case arising or in-volving the TMJ or supporting structures. Neo-plasms in this area may be benign, malignant, or metastatic. Although neoplasia as an un-derlying cause of TMJ dysfunction is rare, it is well known in the literature.242 Approximately 3% of malignant neoplasia metastasizes to the jaws.243,244 Neoplasia most frequently extend-ing to the TMJ region causing pain and dys-function are squamous cell carcinomas of the maxillofacial region and primary nasopharyn-geal tumors.16,245–253 Neoplasia arising in the pa-rotid gland, such as adenoid cystic carcinomas and mucoepidermoid carcinomas, may pro-duce TMJ pain and dysfunction.254–256 The most common signs and symptoms are reduced opening, crepitation, occlusal changes, pain with function, and swelling.257 If the condyle is involved, there is frequently development of a facial asymmetry with a midline shift as that seen in condylar hyperplasia.258 The most com-mon treatment is surgery. Diagnostic imaging and biopsy are essential when a neoplasm is suspected. Sensitivity and specicity have not been established.Synovial chondromatosis (ICD-10 D48.0)Synovial chondromatosis is a cartilaginous metaplasia of the mesenchymal remnants of the synovial tissue of the joint. Its main characteristic is the formation of cartilaginous nodules that may be pedunculated and/or detached from the synovial membrane, be-coming loose bodies within the joint space. Calcication of the cartilage can occur (ie, os-teochondromatosis). The disease may be as-sociated with malocclusion, such as a progres-sive ipsilateral posterior open bite. Imaging is needed to establish the diagnosis. Sensitivity and specicity have not been established.History must be positive for at least one of the following:• Report of preauricular swelling• Arthralgia as previously dened• Progressive limitation in mouth opening• Presence of joint noises in the last monthExamination must conrm at least one of the following:• Preauricular swelling• Arthralgia as previously dened• Maximum assisted opening (passive stretch) < 40 mm, including the vertical incisal overlap• Crepitus as per DJDMRI or CT/CBCT of the TMJ must be posi-tive for at least one of the following:• MRI: multiple chondroid nodules, joint effusion, and amorphous iso-intensity signal tissues within the joint space and capsule• CT/CBCT: loose calcied bodies in the soft tissues of the TMJHistologic examination conrms cartilagi-nous metaplasia.FracturesDirect traumatic force can injure all related bony components of the masticatory system (ie, temporal bone, maxilla, zygoma, sphenoid bone, and mandible). This trauma can be re-lated to the following conditions: fracture, dis-location, contusion, or laceration of articular surfaces, ligaments, and disc, with or without intraarticular hemarthrosis. Sequelae could include adhesions, ankylosis, occlusal abnor-malities, or joint degeneration.167,259 Patients with nonsurgically treated dislocated fractures may be prone to symptoms of TMDs, func-tional disorders, and occlusal disorders.259 Fractures of the condylar process may result in facial asymmetry; in general, there are greater skeletal changes when the fracture occurs earlier in life. Closed treatments have report- 164Dierential Diagnosis and Management of TMDs8edly also resulted in facial asymmetries, even in adults.260 Sensitivity and specicity have not been established.Examples of fractures are the following:• Closed fracture of condylar process (ICD-10 S02.61XA)• Closed fracture of subcondylar process (ICD-10 S02.62XA)• Open fracture of condylar process (ICD-10 S02.61XB)• Open fracture of subcondylar process (ICD-10 S02.62XB)History must be positive for both of the following:• Trauma to the orofacial region• A preauricular swelling, arthralgia as pre-viously dened, or limited mouth openingExamination is positive for at least one of the following:• Preauricular swelling• Arthralgia as previously dened• Maximum assisted opening (passive stretch) < 40 mm including vertical inci-sal overlapImaging is positive for evidence of fracture.Congenital/developmental disordersAplasia (ICD-10 Q67.4)Aplasia is dened as a typically unilateral ab-sence of the condyle and incomplete devel-opment of the articular fossa and eminence, resulting in facial asymmetries. It is commonly associated with other congenital anomalies (eg, oculo-auriculo-vertebral spectrum [Gold-enhar syndrome], hemifacial microsomia, and mandibulofacial dysostosis [Treacher Collins syndrome]). It is occasionally bilateral, and in such cases asymmetry is not present, but micrognathia is the dominant clinical mani-festation. The condition may be associated with malocclusion, which may include open bite. Sensitivity and specicity have not been established.History must be positive for both of the following:• Progressive development of mandibular asymmetry or micrognathia from birth or early childhood• Development of malocclusion, which may include posterior open biteExamination is positive for both of the following:• Conrmation of mandibular asymmetry, with deviation of the chin to the affected side or micrognathia• Inability to detect the condyle upon pal-pation during mandibular movements.Imaging will show both of the following:• Severe hypoplasia of the fossa and eminence• Aplasia of the condyleHypoplasia (ICD-10 M27.8)Hypoplasia is dened as incomplete devel-opment or underdevelopment of the cranial bones or the mandible. Growth is proportion-ately reduced and less severe than in aplasia. This condition bridges the continuum from aplasia to normal condylar size. Condylar hy-poplasia can be secondary to facial trauma. The condition may be associated with maloc-clusion, which may include open bite. Sensitiv-ity and specicity have not been established.History must be positive for both of the following:• Progressive development of mandibular asymmetry or micrognathia from birth or early childhood• Development of malocclusion, which may include posterior open bite 165Diagnostic Classification of TMDsExamination must conrm this history.Imaging using CT/CBCT will show at least one of the following:• Hypoplasia of the fossa• Hypoplasia of the condyle• Shortened mandibular ramus heightHyperplasia (ICD-10 M27.8)Hyperplasia is an overdevelopment of the cra-nial bones or mandible. It is a nonneoplastic increase in the number of normal cells. It can occur unilaterally or bilaterally as a localized enlargement such as condylar hyperplasia, or as an overdevelopment of the entire mandible or side of the face. Sensitivity and specicity have not been established.To diagnose hyperplasia, the history must be positive for progressive development of mandibular or facial asymmetry, and the ex-amination must conrm this history. Imaging using panoramic radiography and/or CT/CBCT and single-photon emission CT are positive for the following:• Asymmetry in mandibular ramus height• Increased uptake of technetium-99m hy-droxyl diphosphonate on bone scintigra-phy scan (nuclear imaging)Masticatory muscle disordersThe mechanisms that produce pain in skeletal muscles are still not well understood. Overuse of a normally perfused muscle or ischemia of a normally working muscle may cause pain.261–264 Sympathetic and fusimotor reexes can pro-duce changes in the blood supply and muscle tone.265,266 Furthermore, different psychologic or emotional states can alter muscle tone.267,268 Neurons that mediate pain from skeletal mus-cles are subject to strong modulatory inu-ences. Endogenous substances (eg, bradyki-nin, serotonin, prostaglandins, neuropeptides, and substance P) can sensitize the nociceptive endings very easily. Painful muscle conditions not only lead to increased sensitivity of periph-eral nociceptors but also produce hyperexcit-ability in the central nervous system, resulting in central sensitization presenting with local-ized hyperalgesia and allodynia.34,261,269–271Some systemic conditions that produce muscle pain are polymyalgia rheumatica, poly-myositis, dermatomyositis, lupus erythemato-sus, and bromyalgia (ie, chronic widespread pain). Fibromyalgia is of particular interest because it may easily be confused with a regional masticatory muscle disorder. When bromyalgia is suspected, a referral to a rheu-matologist is necessary.Muscle pain limited to the orofacial regionMyalgia (ICD-10 M79.1)Pain of muscle origin is modied by jaw move-ment, function, or parafunction, and replication of this pain is elicited with provocation testing of the temporalis or masseter muscles, which are the muscles involved with highest preva-lence. Although not required in the criteria, a positive nding with the specied provocation tests when examining the other masticatory muscles can help to corroborate this diagno-sis if the location of the pain associated with the chief complaint is in these muscles; lim-ited mandibular range of motion may also be present. Hypothetically, based on the work by the validation research group and later on by the DC/TMD international community, three subtypes of myalgia can be identied, but only myalgia and myofascial pain with referral are the clinical diagnoses with diagnostic validity values; the other two diagnoses—local myal-gia and myofascial pain with spreading—do not have sensitivity and specicity estimates.History must be positive for both of the following:• Pain in the jaw, temple, ear, or in front of the ear in the last 30 days.• Pain is modified by jaw function or para function. 166Dierential Diagnosis and Management of TMDs8In addition, the clinical examination will reveal conrmation of the localization of the pain in the masticatory muscle structure, con-rmed by the examiner, and report of familiar pain during vertical mandibular movements or palpation of the masticatory muscles. The sen-sitivity and specicity estimates are 0.90 and 0.99, respectively.Local myalgiaThis involves pain of muscle origin plus a re-port of pain localized only to the site of palpa-tion (immediate site to stimulation). Limitation of mandibular movements secondary to pain may be present. Sensitivity and specicity have not been established. The criterion for this diagnostic group limits the familiar pain to be provoked only with palpation and not with mandibular movement.Myofascial pain with spreadingThis involves pain of muscle origin plus a re-port of pain spreading beyond the location of the palpating ngers but within the boundary of the masticatory muscle being examined. Limitation of mandibular movements second-ary to pain may be present. Sensitivity and specicity have not been established.To diagnose myofascial pain with spread-ing, the patient must have local myalgia, and the examination of the temporalis or masseter muscle must conrm both of the following:• Familiar muscle pain with palpation• Pain with muscle palpation with spread-ing of the pain beyond the location of palpation but within the boundary of the palpated muscleNote: Other masticatory muscles may be examined as required.Myofascial pain with referralThis involves pain of muscle origin as dened for myalgia plus a referral of pain beyond the boundary of the masticatory muscles being palpated, for example, to the ear, tooth, or eye; spreading may be present. The sensitiv-ity and specicity values are 0.86 and 0.98, respectively.To diagnose myofascial pain with referral, the patient must have myalgia, and the exami-nation of the temporalis or masseter muscle must conrm both of the following:• Familiar muscle pain with palpation• Pain with muscle palpation beyond the boundary of the muscleOther masticatory muscles may be exam-ined as required.Tendonitis (ICD-10 M67.90)Tendonitis involves pain of tendon origin af-fected by jaw movement, function, or parafunc-tion and replication of this pain with provocation testing of the masticatory tendon. Limitation of mandibular movements secondary to pain may be present. The temporalis tendon is a com-mon site of tendonitis with referred pain to the teeth or other structures. Sensitivity and speci-city have not been established.To diagnose tendonitis, the patient must have myalgia as previously dened, and the examination must conrm the diagnosis of myalgia but restricted to the temporalis ten-don. This condition could also apply to other masticatory muscle tendons.Myositis (noninfective: ICD-10 M60.9; infective: ICD-10 M60.009)This involves pain of muscle origin with clini-cal characteristics of inammation or infec-tion: edema, erythema, and/or increased tem-perature. It generally arises acutely following direct trauma of the muscle or from infection or chronically with autoimmune disease. Limi-tation of unassisted mandibular movements secondary to pain is often present. Calcica-tion of the muscle can occur (ie, myositis os-sicans). Sensitivity and specicity have not been established. 167Diagnostic Classification of TMDsTo diagnose myositis, the patient must have local myalgia, and the examination of the tem-poralis or masseter muscle must conrm both of the following:• Local myalgia• Presence of edema, erythema, and/or increased temperature over the muscleIn addition, serologic tests may reveal el-evated enzyme levels (eg, creatine kinase), markers of inammation, and the presence of autoimmune diseases. Other masticatory muscles may be examined as required.Spasm (ICD-10 M62.838)This is a sudden, involuntary, reversible tonic contraction of a muscle. Acute malocclusion may be present. Sensitivity and specicity have not been established.To diagnose a spasm, the patient must re-port the following:• Immediate onset of muscle pain modi-ed by function and parafunction as op-erationalized in myalgia• Immediate report of limited range of jaw motionIn addition, the examination must conrm both of the following:• Myalgia that may include all masticatory muscles• Limited range of jaw motion in the direc-tion that elongates the affected muscle (eg, for jaw closers, opening will be lim-ited to < 40 mm; for the lateral pterygoid muscle, ipsilateral movement will be lim-ited to < 7 mm)When this diagnosis needs to be con-rmed, laboratory testing will conrm elevated electromyographic activity compared with the contralateral unaffected muscle. Sensitivity and specicity have not been established.Contracture (ICD -10 M62.40)Contracture is the shortening of a muscle due to brosis of tendons, ligaments, or muscle -bers. It is usually not painful unless the muscle is overextended. A history of radiation therapy, trauma, or infection is often present. Sensitiv-ity and specicity have not been established. To diagnose contracture, the patient must have progressive loss of range of motion, and the examination must conrm that unassisted and assisted jaw movements are limited such that maximum assisted opening is < 40 mm. It must also be associated with a hard end feel that has been operationalized as having un-yielding resistance to assisted movements as felt by the clinician.Hypertrophy (ICD-10 M62.9)Hypertrophy is enlargement of one or more masticatory muscles. It is usually not associ-ated with pain and can be secondary to over-use and/or chronic tensing of the muscle(s). Some cases are familial or genetic in origin. Sensitivity and specicity have not been es-tablished. To diagnose hypertrophy, the pa-tient must have enlargement of one or more masticatory muscles as evidenced from pho-tographs or previous records, and the exami-nation must conrm this enlargement. Diag-nosis is based on the clinician’s assessment of muscle size and requires consideration of craniofacial morphology and ethnicity.Neoplasm (soft tissues of head, face, and neck) (benign: ICD-10 D21.0; malignant: ICD-10 C49.0)Neoplasms of the masticatory muscles result from tissue proliferation with histologic char-acteristics and may be benign (eg, myoma), malignant (eg, rhabdomyosarcoma), or meta-static. They are uncommon. They may present with swelling, spasm, pain during function, limited mouth opening, and/or sensory-motor changes (eg, paresthesias). Diagnostic imag-ing (typically using CT/CBCT and/or MRI) and biopsy are essential when a neoplasm is sus- 168Dierential Diagnosis and Management of TMDs8pected. Sensitivity and specicity have not been established.Movement disordersOrofacial dyskinesiaThe ICD-10 codes for the different types of orofacial dyskinesia are as follows:• Tremor unspecied: ICD-10 R25.1• Cramp and spasm: ICD-10 R25.2• Fasciculations: ICD-10 R25.3• Ataxia, unspecied: ICD-10 R27.0• Muscular incoordination: ICD-10 R27.9• Subacute, due to drugs; oral tardive dys-kinesia: ICD-10 G24.01Orofacial dyskinesia involves involuntary, mainly choreatic (dancelike) movements that may involve the face, lips, tongue, and/or jaw. The disorder may result in traumatic injury to the oral mucosa or tongue. It is more common with advancing age and in patients with a his-tory of using neuroleptic medications and/or associated with traumatic brain injury, psychi-atric conditions, or other neurologic disorders (eg, Wilson disease). Reduction or discontinu-ation of the movement pattern could occur when the mouth or face receives sensory stimulation (sensory trick). Sensitivity and specicity have not been established.To allocate these diagnoses, the patient must provide a positive history of neurologic diagnosis of dyskinesia in the orofacial re-gion and history components of myalgia and/or arthralgia (diagnostic criteria as previously described) that worsens with episodes of dyskinesia.Examination will be positive for all of the following:• Sensory and/or motor nerve conduction decit• Central and/or peripheral myopathic disease• Muscular hyperactivity conrmed by in-tramuscular electromyography (EMG)• Myalgia and/or arthralgiaOromandibular dystoniaThe ICD-10 codes for the different types of orofacial dyskinesia are as follows:• Acute, due to drugs: ICD-10 G24.02• Deformans, familial, idiopathic, and tor-sion dystonia: ICD-10 G24.1This involves excessive, involuntary, and sustained muscle contractions that may in-volve the face, lips, tongue, and/or jaw. They could be components of a number of central nervous systems disorders, including Parkin-son disease and Meige syndrome, and could be an adverse event related to medication usage, notably neuroleptics. Trauma to the brain, head, and neck can trigger the onset of transient or permanent dystonia of the masti-catory muscles. The disorder can also be ge-netically determined. Normally, the dystonia disappears during sleep. The affected muscles are often painful. The condition can make open-ing and closing the mouth difcult and impair speech, swallowing, and chewing. Sensitivity and specicity have not been established.To allocate these diagnoses, the patient must provide a positive history of neurologic diagnosis of dystonia in the orofacial region and history components of myalgia and/or arthral-gia (diagnostic criteria as previously described) that worsens with episodes of dystonia.Examination will be positive for all of the following:• Sensory and/or motor nerve conduction decit• Central and/or peripheral myopathic disease• Dystonia confirmed by intramuscular EMG• Myalgia and/or arthralgia 169Diagnostic Classification of TMDsMasticatory muscle pain attributed to systemic/central disordersFibromyalgia (ICD-10 M79.7)Fibromyalgia involves widespread pain with concurrent masticatory muscle pain (see chap-ter 10). History and examination are positive for both a rheumatologic-based diagnosis of -bromyalgia and myalgia as previously dened. Sensitivity and specicity have not been estab-lished. Historically, in diagnosing bromyalgia, there needed to be tenderness in at least 11 of 18 specied sites and the presence of wide-spread pain denoted as axial pain, right and left pain, and upper and lower segment pain. Cur-rent criteria eliminate the tender points and focus on a widespread pain index and symp-tom severity scale.272,273Centrally mediated myalgia (ICD-10 M79.1)Centrally mediated myalgia is defined as chronic, continuous muscle pain that is ag-gravated by function. Intermittent muscle pain conditions may not produce centrally medi-ated myalgia, while a prolonged and constant period of muscle pain is likely to lead to the condition. Sensitivity and specicity have not been established.History must be positive for all of the following:• Prolonged and continuous pain in the jaw, temple, in front of the ear, or in the ear in the past 30 days• Regional dull, aching pain at rest• Pain is aggravated by function of the af-fected muscles• Presence of at least three nonspecic somatic symptoms, such as sensation of muscle stiffness, weakness, and/or fatigue• Sensation of acute dental occlusal changes not veried clinically• Ear symptoms (eg, tinnitus, feeling of fullness, blocked ear), vertigo, dental pain symptoms not attributed to another diag-nosis, or headache symptoms not oth-erwise classiable by the International Classication of Headache Disorders, third edition (beta version) (ICHD)• Limited mouth opening (due to pain or myobrotic contracture)In addition, the examination must conrm at least two of the following:• Myalgia• Evidence of sensory dysfunction (eg, allodynia, paresthesia, dental occlusal awareness)• Muscular atrophy• Maximum unassisted opening < 40 mm including vertical incisal overlapHeadache disordersHeadache attributed to TMDs (ICHD-3 11.7; ICD-10 G44.89)If the headache is caused by a disorder in-volving structures in the temporomandibular region, it can be considered a headache attrib-uted to TMDs. According to the International Headache Society, this headache is considered present when there is evidence of a pathologic process affecting the TMJ, muscles of masti-cation, and/or associated structures, together with evidence of a causal relationship with the headache. Causation is demonstrated when at least two of the following symptoms are present274:• Headache has developed in a temporal relationship to the onset of the TMDs.• Headache has signicantly worsened in parallel with progression of the TMDs, and/or headache has signicantly im-proved or resolved in parallel with im-provement in or resolution of the TMDs.• Headache is produced or exacerbated by active jaw movements, passive jaw movements, and/or provocative maneu- 170Dierential Diagnosis and Management of TMDs8vers applied to temporomandibular struc-tures such as palpation pressure.• When unilateral, headache is ipsilateral to the side of the TMDs.In the DC/TMD, headache attributed to TMD is included as one of the new diagnostic sub-types.211 In general, the DC/TMD criteria for this headache closely follow those of the ICHD. An important difference, however, relates to the denition of the TMD subtype that should be present: the DC/TMD specically links the headache to a pain-related TMD diagnosis like myalgia or arthralgia. Sensitivity and specicity values are 0.89 and 0.98, respectively.To allocate this diagnosis, both of the fol-lowing criteria must be met:• History of headaches of any type local-ized in the temple region during the last 30 days that are modied by jaw move-ment in function or parafunction• During clinical examination, conrma-tion of the location of the headaches in the temporalis muscle area and report of familiar headache upon palpation of the temporalis muscle or during mandibular movementsAssociated structuresCoronoid hyperplasia (ICD-10 M27.8)Coronoid hyperplasia is progressive enlarge-ment of the coronoid process that impedes mandibular opening when it is obstructed by the zygomatic process of the maxilla. Sensitiv-ity and specicity have not been established.To diagnose coronoid hyperplasia, the pa-tient must complain of progressive limitation of jaw opening, the examination must conrm the reduction of active and passive maximum jaw opening, and imaging must show an elon-gated coronoid process that approximates the posterior aspect of the zygomatic process of the maxilla on opening.Management of TMDsManagement goals for patients with TMDs are similar to those for other orthopedic or rheu-matologic disorders. They include decreased pain, decreased adverse loading, restoration of function, and resumption of normal daily activities. These management goals are best achieved by a well-dened program designed to treat the physical disorder(s) and to reduce or eliminate the effects of all contributing fac-tors. The treatment options and sequences for TMDs outlined here are consistent with treat-ment of other musculoskeletal disorders.As in many musculoskeletal conditions, the signs and symptoms of TMDs over time may be transient and self-limiting, resolving without serious long-term effects.15,275 Little is known about which signs and symptoms will progress to more serious conditions in the natural course of TMDs. Therefore, special ef-forts should be made to avoid early use of ag-gressive, irreversible treatments such as com-plex occlusal therapy or surgery. Conservative (ie, reversible), noninvasive treatment such as self-management instructions, behavioral modication, physical therapy, medications, and orthopedic appliances are endorsed for the initial care of nearly all TMDs.15Principles of managementMost patients with TMDs achieve good symptom relief with conservative ther-apy.23,276,277 Long-term follow-up of TMD pa-tients shows that 50% to over 90% of the patients have few or no symptoms after con-servative treatment; from a retrospective study of 154 patients, it was concluded that most TMD patients have minimal recurrent symp-toms 7 years after treatment.278 More than 85% to 90% of the patients in three longitu-dinal studies lasting 2 to 10 years had relief of symptoms after conservative treatment.279–281 Stability was achieved in most cases between 6 and 12 months after the start of treatment.281 171Management of TMDsIn many patients with disc displacement (reducing and nonreducing), painless jaw func-tion is possible with a displaced disc.276,282,283 Patients with pain-free clicking TMJs generally do not need treatment except for reassurance and explanation of the condition, whereas pa-tients with nonreducing discs typically respond well to conservative treatment.282–285 Internal derangement of the TMJ often exhibits a natu-ral progression of compensatory adaptation and remodeling.286–288 Even with progression or with osteoarthritic changes, the outcome is typically benign with adequate masticatory function.289,290 Myogenous disorders more fre-quently require recurrent treatment as com-pared with TMJ articular disorders.70,291Relevant precipitating and perpetuat-ing contributing factors should be identied through the history and clinical examination. Factors such as bruxism and other parafunc-tional habits, trauma, adverse anatomical re-lationships, and pathophysiologic and psycho-social conditions may all impact TMDs, but as the majority of these factors are highly preva-lent in the general population, their presence in an individual case may be coincidental and not contribute to the TMDs. Therefore, in addi-tion to the physical diagnosis, the goal of each evaluation should be the development of a pri-oritized problem list of the relevant contribut-ing factors. This has direct implications for the treatment plan and strategic sequencing.Treatment prognosis can be affected by a number of considerations. Early treatment of acute musculoskeletal pain results in greater patient satisfaction, fewer work days lost, and reduced chance of development of a chronic pain condition.292 In cases of chronic TMDs where pain is less frequent and patients en-gage in greater daily activity, the prognosis is better.293 The power of nonspecic effects in healing (eg, placebo effect) in the treatment of psychosocial and biologic conditions has been well documented.294 These effects cer-tainly play a role in the successful treatment of TMDs, and the value of a good doctor–patient relationship should be recognized and used.295 Despite the documented success of the vari-ous forms of conservative care, some patients with TMDs do not improve. Reasons for this vary, but these patients typically fall into two groups: patients with an incomplete or incor-rect diagnosis or patients with unsuccessfully addressed or even unrecognized contributing factors.276 When multiple contributing factors are present, and especially if the condition is chronic, a pain management program with a multidisciplinary team of clinicians may be needed. It is difcult for an individual clinician to address the multiple contributing factors that may be present in complex chronic pain patients.296 Treatment options include patient education and self-management, cognitive behavioral therapy (CBT), pharmacotherapy, physical therapy, orthopedic appliances, oc-clusal therapy, and possibly surgery. It is im-portant to also remember that Axis II (psy-chologic) factors need to be considered in the management of all TMDs. These factors are reviewed in chapter 12.Patient education and self-managementThe success of a self-management program depends on patient acceptance, motivation, cooperation, and compliance. The time spent on patient reassurance and education is a sig-nicant factor in developing a high level of rap-port and treatment compliance. The clinician’s explanation of the problem and treatment recommendations should use terminology the patient can understand.A successful self-management program allows healing and prevents further injury to the musculoskeletal system. This may be enough to control the problem.23,297,298 A self-management routine should include the following: rest of the masticatory system through voluntary limitation of mandibular function, habit awareness and modication, and a home physiotherapy program. An expla-nation of the advantages of resting the affected 172Dierential Diagnosis and Management of TMDs8muscular and articular structures and function-ing only within pain-free limits, much the same as an athlete must rest an injured joint, is often helpful. Modication of function (eg, avoidance of heavy mastication, gum chewing, wide yawning, singing, and playing certain musical instruments) and parafunctional habit rever-sal (eg, clenching, bruxing, tongue thrusting, cheek biting, poor sleeping posture, or object biting) should be emphasized.Offending habits can be modied with habit awareness, motivation to change, and knowledge in how to change. Commitment to conscientious monitoring for the habits can lead to successful habit modication. A simple feedback mechanism, such as visual or audio reminders adapted to the patient’s daily activities, should be discussed and im-plemented (eg, small stickers strategically placed at home, in the patient’s vehicle, and at work; alarms sounding from electronic sources; phone apps). Keeping a diary aimed at identifying circumstances and activities that foster the offending habits may also be help-ful so that the patient can titrate the need for more or less monitoring during any given day. Progress with habit modication should be discussed at each follow-up appointment with the patient.A home physiotherapy program has also been proposed for the treatment of TMD pain and dysfunction because it is simple and non-invasive, is cost-effective, allows an easy self- management approach, cultivates good doctor- patient communication, and can be managed by the general practitioner.299 Emphasis should be placed on patient self-control. A program of heat and/or ice to the affected areas, massage of the affected muscles, and gentle range-of- motion exercises can decrease tenderness and pain and increase range of motion. Heat stimu-lates muscle relaxation and vascular perfusion. Heat should not be used following an acute in-jury (ie, less than 72 hours) or for acute inam-mation or infection. Ice packs are used primarily for local analgesic and anti-inammatory ef-fects in muscle and joint tissues. Because the temperature differential is greater with cold, a shorter application may produce a greater re-sponse. Cold should not be used over areas with poor circulation (eg, as a result of diabetes or radiation) or over open wounds.Recently, efforts were taken to construct an expert-based standardized denition of self-management. The core components iden-tied for self-management include education; self-exercises; self-massage; thermal therapy; dietary advice and nutrition; and parafunctional behavior identication, monitoring, and avoid-ance. Self-management components can be provided to the patient rst as essential inter-ventional steps and continued as fundamental for the continuous management with the in-tent that these elements will be used through-out the patient’s life.300Biobehavioral therapyBehavioral modication for overuse or para-functional behaviors remains a central part of the overall treatment program for individuals with TMDs despite the as-yet unclear evidence for their overall role in etiology or in contribut-ing to persistence of the disorder.301 In general, the clinician should err toward overemphasis on this part of treatment based on the extent by which higher levels of parafunction are ob-served in individuals with chronic TMDs, the difculty in reliably identifying the true extent of such behaviors if present except through repeated assessments over time, and the suc-cess of such treatment for those who have been refractive to conservative dental/physical medicine treatment approaches.52,302The success in reducing the frequency of parafunctional behaviors depends on several patient factors and clinical factors. Patient fac-tors include the level and continuity of aware-ness of the putative behaviors, long-term mo-tivation and commitment to treatment, and extent to which other factors (eg, life stress) are uncontrollable triggers for the behaviors. 173Management of TMDsClinical factors include curiosity in exploring possible symptom-behavior relationships, per-sistence in monitoring behavioral patterns and level of patient skills, and skill in effecting be-havioral change. Patients whose parafunctional behaviors may seem severe, chronic, and under the control of extensive environmen-tal factors may nevertheless respond quickly to the clinician’s initial intervention, while pa-tients whose parafunctional behaviors seem simple may require extensive treatment from a behavioral specialist.301,303 Consequently, initiating intervention of parafunctional behav-iors is a pragmatic decision for every patient, recognizing that signicant modication of their lifestyle is often necessary to alter the contributing factors in the interest of long-term prevention of recurrent TMD pain. If a more structured approach is indicated, strategies for behavior modication such as a habit-reversal program, lifestyle counseling, CBT for stress management, progressive relaxation, hypno-sis, and biofeedback should be considered. Treatment should be individualized based on the patient’s problems, preferences, and life-style. Several manuals and texts more fully describe this information.304–306Biofeedback is a structured therapy based on the theory that when an individual receives information about a desired change and is supported in making the change, the change is more likely to occur.307,308 In general, bio-feedback training uses equipment to measure biologic activity (eg, surface EMG to measure muscle activity). The equipment is designed with a feedback loop so that a patient can receive immediate feedback regarding perfor-mance. A number of controlled studies have demonstrated that relaxation training, with or without the use of surface EMG biofeed-back, can decrease awake tonic muscle activ-ity.303,309,310 Most trials evaluating biofeedback for the treatment of TMDs have been under-taken with small sample sizes, and although there is cumulative evidence of effectiveness when biofeedback was compared with con-trols, there remains a need for large-sample, controlled-outcome trials.311Biofeedback may be less effective in the treatment of sleep bruxism.312 EMG biofeed-back during sleep without a more comprehen-sive stress management program appears to decrease sleep bruxism only temporarily, and therefore its use may be limited to short-term management of acute conditions.313,314 Com-prehensive stress management and counsel-ing programs that involve a combination of EMG biofeedback, progressive relaxation, and self-directed changes in lifestyle appear to be more effective when used together than any single behavioral treatment. Use of behavioral therapies in conjunction with usual physi-cal medicine and medication therapies also appears to enhance the overall therapeutic effects.315,316A recent systematic review evaluating noninvasive interventions for persistent TMD concluded that CBT in addition to standard care yielded better results than standard care alone with regard to life interference and de-pression as well as pain intensity; however, the latter difference was not deemed to reach clinical importance.317 Another recent sys-tematic review on the effect of counseling and self-management for TMDs revealed that these strategies yielded similar positive results in pain reduction and increase in mouth open-ing compared with the use of interocclusal appliances with no additive effect when used together. The studies included mostly patients with myofascial pain.318Pharmacologic managementPharmacologic agents may promote patient comfort and rehabilitation when used as part of a comprehensive program. Clinicians who decide to prescribe medications should be fa-miliar with a variety of drugs to realize maximal treatment effect and benet, avoid unexpected complications, and act in response to adverse drug interactions. 174Dierential Diagnosis and Management of TMDs8Drug misuse and abuse are of concern in the pharmacologic management of TMDs. Opioid narcotics produce tolerance and dependence and therefore are most useful in short-term, acute pain conditions. Long-term narcotic an-algesic use in patients with chronic TMDs re-quires careful consideration.319–321 Prescribing drugs on a pain-contingent basis to be taken “as needed” in chronic noncancer pain has long been associated with concern that it may lead to abuse for some patients. Recent evi-dence, however, indicated that time-contingent prescribing of opioids may lead to use of higher amounts and may be associated with more patient concerns regarding their opioid use.322 Given the continuing controversies and risks associated with long-term opioid use for non-cancer pain, all other avenues of treatment should be pursued before relying on narcotic medication for TMD patients.The most widely used pharmacologic agents for the management of TMDs include analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and low-dose antidepressants.323 Pharmacologic agents less often used include gabapentinoids, benzodiaz-epines, and muscle relaxants. The analgesics, corticosteroids, and benzodiazepines are indi-cated for acute TMD pain; NSAIDs and muscle relaxants may be used for both acute and chronic conditions; and the tricyclic antidepres-sants (TCAs) are primarily indicated for chronic orofacial pain management.AnalgesicsMild analgesics (nonopiate preparations) are usually the pharmacologic agents of choice to reduce pain associated with TMDs. The non-opioid analgesics are a heterogenous group of compounds that share certain therapeutic actions and side effects. They may be used for mild to moderate pain associated with TMDs. Aspirin, which inhibits prostaglandin synthe-sis, is the prototype for these compounds. All salicylate drugs are antipyretic, analgesic, and anti-inammatory, but there are impor-tant differences in their effects. If the patient is sensitive to aspirin, a nonacetylated aspirin, choline magnesium trisalicylate, or salsalate may be effective.324 Opioid narcotics act on specic opioid receptor sites in the central and peripheral nervous systems. Opioids have central nervous system depression qualities and addiction liabilities. They may be consid-ered for short-term use for moderate to severe acute pain.320Nonsteroidal anti-inammatory drugsNSAIDs have been reported as effective for mild to moderate inammatory conditions and acute postoperative pain.320 A recent Coch-rane review did not provide any support for or against the use of NSAIDs in TMDs.325 There are several chemically dissimilar groups of NSAIDs, which each differ in their antipyretic, analgesic, and anti-inammatory efcacy.326 Therefore, if one NSAID fails, another agent may succeed. NSAIDs may have serious side effects, and patients on NSAIDs should there-fore be carefully monitored.327 Gastrointestinal complications form the greatest risk associ-ated with the use of NSAIDs. If gastroprotec-tion is needed, a proton pump inhibitor should be used in conjunction with NSAID therapy. Patients who do not have cardiovascular risk and are not on aspirin therapy also may use a cyclooxygenase-2 inhibitor, if indicated, in conjunction with a proton pump inhibitor.328 Renal effects from the NSAIDs can also cause or increase hypertension as well as lead to acute renal injury.329 All NSAIDs contain the same box warning regarding cardiovascular and gastrointestinal toxicity regardless of the route of administration. NSAIDs increase risk of serious and potentially fatal cardiovascular thrombotic events including myocardial infarc-tion and stroke; risk may occur early in treat-ment and may increase with the duration of use. NSAIDs are contraindicated for coronary artery bypass graft pain management.330 175Management of TMDsCorticosteroids and sodium hyaluronateCorticosteroids are potent anti-inammatory drugs not commonly prescribed for systemic use in the treatment of TMDs due to their side effects. The exception is for acute severely painful joint inammation, or joint inamma-tion associated with the polyarthritides. Intra-capsular TMJ injection of corticosteroids (ie, methylprednisolone) has been recommended on a limited basis in cases of acute are-up of severe joint pain where conservative treat-ment has been unsuccessful. Although there have been some concerns regarding long-term effects (ie, progression of joint destruction), the 6-month follow-up appears good for alle-viating TMJ pain and dysfunction with no or minimal increase of radiographically visible de-generative changes.331,332Sodium hyaluronate is the sodium salt of puried natural sodium hyaluronic acid. Hyal-uronic acid is a naturally occurring polysaccha-ride belonging to the glycosaminoglycan fam-ily. In healthy synovial joints, hyaluronic acid maintains viscosity of the synovial uid and supports the lubricating and shock-absorbing properties of the articular cartilage. Currently, hyaluronate has not demonstrated a superior result to other treatments, and a review on the use of hyaluronate for TMDs could not support or refute its use.333,334 RCTs are needed to pro-vide evidence of efcacy of hyaluronate over standard treatments for TMDs.There are limited studies on injecting platelet-rich plasma (PRP) in intra-articular TMDs. One study comparing PRP to arthro-centesis in patients with anterior displaced discs with reduction demonstrated a bet-ter response with PRP.335 Larger controlled studies are needed to demonstrate effec-tiveness, along with long-term follow-up and cost-analysis comparisons.BenzodiazepinesBenzodiazepines are antianxiety agents that have been administered to patients with chronic pain. These drugs are potentially habit forming, and there is a concern that they may worsen depression in chronic pain patients.323 A review of studies could not support or refute their use.325,336Muscle relaxantsMuscle relaxants that are used to reduce skel-etal muscle tone are prescribed in an effort to reduce the supposed increased muscle activ-ity associated with TMDs.337 Experimentally, muscle relaxants depress spinal polysynaptic reexes preferentially over monosynaptic re-exes. Muscle relaxants affect neuronal activity associated with muscle stretch reexes, primar-ily in the lateral reticular area of the brainstem. The oral doses of all of these drugs are well below the levels required to elicit experimen-tal muscle relaxant activity. Therefore, some investigators conclude that their muscle relax-ant activity is related only to their sedative ef-fect.323 Some central skeletal muscle relaxants are available in combination with analgesics.In TMD patients, cyclobenzaprine was found to be statistically superior to either pla-cebo or clonazepam in reducing jaw pain upon awakening, but neither drug had any effect on sleep improvement.338 Another study reported no difference in efcacy between short-term treatment of TMD patients with a splint or with orphenadrine.339 Recently, a combined proto-col utilizing splint therapy with either a placebo or combined muscle relaxant and benzodiaze-pine demonstrated better pain control with the active medications.340 As with other pharmaco-logic treatments, additional RCTs are needed prior to determining if muscle relaxants are of benet in treating TMDs. Because there is lim-ited evidence of efcacy of muscle relaxants in the treatment of TMDs, their use should prob-ably be limited to a brief trial in conjunction with conservative TMD therapy. 176Dierential Diagnosis and Management of TMDs8AntidepressantsAntidepressants have been used in chronic pain and have demonstrated pain relief that is not associated with depression relief.341 The TCAs, particularly amitriptyline, have an-algesic properties independent of antidepres-sant effect and are prescribed for chronic pain patients with depression and sleep distur-bance.342 The therapeutic effect of these drugs is thought to be related to their ability to in-crease the availability of the biogenic amines serotonin and norepinephrine at the synaptic junction in the central nervous system. The TCAs are benecial in dosages as low as 10 mg in the treatment of tension-type headache and musculoskeletal pain.343 They decrease the number of awakenings, increase slow-wave sleep (δ sleep), and markedly decrease time in rapid eye movement (REM) sleep. For these reasons, it was thought that TCAs might have potential in the treatment of certain types of sleep bruxism; however, three double-blind crossover studies reported that amitriptyline did not signicantly decrease EMG activity or pain levels but did decrease stress levels as-sociated with sleep bruxism.344,345 Similarly, a systematic review on the use of TCAs in the treatment of TMDs indicated inconsistent or limited quality patient-oriented evidence for the use of this intervention.346 Amitriptyline has been reported, however, to signicantly reduce pain associated with both chronic muscular and TMJ dysfunction, and in combination with CBT showed signicant improvement over placebo.347,348 The therapeutic doses required to achieve an antidepressant action are signi-cantly larger than those needed to achieve pain control and sleep improvement, and treatment of depression with these medications should only be performed by clinicians who are trained in the diagnosis and treatment of depression.Most recently, the effect of selective serotonin reuptake inhibitors (SSRIs), se-lective serotonin-noradrenaline reuptake inhibitors (SSNRIs), and TCAs on pain was evaluated.349 In this meta-analysis, limited to placebo-controlled trials with an interven-tion period up to 6 months on a primary de-pressive disorder population, pain relief was signicantly superior in the SSRI and SSNRI groups compared with placebo, but there was no difference between these two drugs. Using a limited number of trials, no signicant results were observed with the use of TCAs compared with placebo. Secondary analysis included non-placebo-controlled trials with TCAs showing a trend of improvement but not better than SSRIs and SSNRIs; both analyses with TCAs should be interpreted with caution and are not conclusive. More so, it is important to keep in mind that the transfer of these re-sults to a primary pain population is limited. In a qualitative analysis on the effect of SSRIs in various chronic pain conditions (not specic to TMD), the authors concluded that SSRIs seem to have a positive effect in 70% of the trials.350 In a Cochrane systematic review, no benecial effect was found with the use of SSRIs and SNRIs on the prevention of tension type head-aches.351 Patients with TMDs are more likely to already be on an antidepressive agent and thus may not be candidates for treatment with these agents.352GabapentinoidsA well-designed RCT evaluated the effective-ness of gabapentin on the treatment of chronic pain in the masticatory muscles.353 The au-thors concluded that this agent was clinically and statistically superior to placebo in reduc-ing pain and hyperalgesia and improving daily function. As of this printing, however, this re-sult has not been replicated by other investiga-tors. Most of the trials using this agent focus on neuropathic pain conditions (postherpetic or diabetic) for which pregabalin is cleared by the US Food and Drug Administration (FDA). Gabapentin is FDA-cleared for postherpetic neuralgia. 177Management of TMDsGlucosamine and chondroitinThese nutritional supplements have gained widespread use in the treatment of osteoar-thritis with the potential theory that they act as disease-modifying agents not only to re-duce the symptoms but also to modify the natural history of osteoarthritis. Although a positive effect with their use has been shown, there are few high-quality trials, specically in the progression of the disease.354 In a recent report from a multicenter RCT using these supplements in a knee osteoarthritis model, it was demonstrated that the combination has comparable efcacy to celecoxib in reducing pain and stiffness and increasing function after 3 months, but such effects do not increase at the 6-month follow-up.355The effects of glucosamine hydrochloride (GH) and chondroitin sulfate (CS) have been evaluated in specic TMD populations, rst in a pilot study using 1,200 mg of chondroitin and 1,500 mg of glucosamine for 12 weeks. It was reported that participants using GH-CS had im-provement in pain, TMJ tenderness, and joint sounds compared with over-the-counter medi-cation use.356 In one study, glucosamine sul-fate (GS) had a signicantly greater decrease in TMJ pain with function compared with ibu-profen, while in another study comparing it with a placebo, GS seemed to have no supe-rior effect in reducing signs and symptoms of osteoarthritis in the TMJ.357,358Topical medicationsTopical NSAIDs are approved to treat os-teoarthritis pain (diclofenac formulations), and it is suggested that this formulation has similar effectiveness to oral formulations but with a greater safety prole due to lower serum concentrations.330 Other formulations have been investigated (eg, ibuprofen, keto-profen, piroxicam, and indomethacin), and it has been strongly suggested to consider the use of topical diclofenac and ibuprofen in the treatment of acute soft tissue injuries or chronic joint-pain-related conditions.359 A 2012 systematic review failed to show suf-cient evidence to support the use of topically applied NSAIDs in painful DJD of the TMJ.360 Topical capsaicin has not been shown to be effective when compared with placebo in the TMD patient.361 Transdermal patches could be evaluated for TMD, but the practicality would be limited.Other considerationsIn a Cochrane systematic review in which only trials comparing the active intervention versus placebo were included, there was insufcient evidence to either support or refute the use of NSAIDs, benzodiazepines, anticonvulsants, muscle relaxants, propanol, oral GH-CS, and topical capsaicin in the treatment of chronic TMDs.325 All presented pharmacologic agents have in theory a biologic plausibility, but in general, in the eld of TMD as a chronic pain condition, the efcacy and safety of most of them lack evidence due to methodologically compromised data.Several other supplements used in pain management have also been suggested for the treatment of primary headaches and osteo-arthritis. However, there is a lack of evidence to support their use as primary therapies; and therefore, they are mainly suggested as adju-vants. It has been suggested that magnesium provides an analgesic effect in postoperative pain and chronic neuropathic pain as well as in-creased opioid analgesia, but most of the avail-able data were based on animal studies.362,363 However, clinical studies have indicated that magnesium supplementation reduces opioid consumption. Vitamins C, D, and E have also been evaluated in the management of pain. Vitamin C exhibits analgesic properties, which may reduce pain and increase quality of life, and has been studied mainly in orthopedic pop-ulations.364 Existing literature does not support vitamin D supplementation as an efcacious in-dependent treatment for pain management.365 However, it has been suggested that vitamin E 178Dierential Diagnosis and Management of TMDs8plays a role in decreasing the reactive remodel-ing in osteoarthritis.366 Nevertheless, no data are specically available for the management of TMDs with these supplements.Physical therapyPhysical therapy helps to relieve musculo-skeletal pain and to restore normal function by altering sensory input; increasing range of motion; reducing inammation; decreasing, coordinating, and strengthening muscle activ-ity; and promoting the repair and regeneration of tissues. In most cases, physical therapy is used as an adjunct to other treatments. Sys-tematic reviews have demonstrated that some physical therapy modalities have support in de-creasing pain and increasing range of motion of the jaw.367,368 However, more recent RCTs report that the long-term decrease in pain and improvement in function in patients with masticatory muscle pain or disc displacement without reduction could not be attributed to physical therapy.369,370 Particularly, the effect of manual therapy, dened as “any hands-on therapy,” seems to improve pain, mandibular motion, and pressure pain threshold.371 This is further evidenced by meta-analysis methodol-ogy, which demonstrated that physiotherapy leads to pain reduction and may improve range of motion.372Posture trainingThe goal of posture training involves the pre-vention of untoward muscle activity of the head, neck, and shoulder musculature, as well as the masticatory and tongue muscles. The aim should be to maintain orthostatic posture to prevent increased cervical and shoulder muscle activity and possible protrusion of the mandible. The more anterior the head is relative to the spinal column, the greater is its effective weight. Except during function (ie, chewing, swallowing, and speaking), the man-dible should be in a relaxed rest position with the teeth separated.373RCTs of posture training are supportive of utilizing this technique in patients with TMDs.368 Although posture training is a com-mon physical therapeutic approach, its rela-tionship to TMDs is not well understood and needs further study.374 A common reversible treatment approach aiming to modify awake parafunctional activity is to monitor and control tongue position, mimicking rest position and reducing muscle activity in principle; never-theless, available information is controversial because position of the tongue on the oor of the mouth minimizes muscle activity or has no effect.373,375,376ExerciseClinical experience suggests that an active exercise program is important to the devel-opment and maintenance of normal muscle and joint comfort, function, and stability. One of the objectives of an exercise program is to teach the patient how to avoid activities that are injurious to the involved synovial joints. In addition, exercise has been recommended to stretch and relax the cervical and masticatory muscles, mobilize and stabilize the TMJs, in-crease muscle strength, and develop normal coordination arthrokinematics (reduce joint clicking).368 Three types of exercise are gen-erally recommended: repetitive exercises to establish coordinated, rhythmic muscle func-tion; isotonic exercises to increase range of motion; and isometric exercises to increase muscular strength. These exercises are pre-scribed to achieve specic goals and are modi-ed as the patient progresses. Most patients will not exercise if it increases pain. Therefore, the therapist must initially help the patient achieve some symptom relief with physical agents or modalities. A maintenance level of exercise is recommended to ensure long-term resolution once the patient has reached the goals of treatment. A recent systematic review and meta-analysis showed that most of the ef-fect sizes for this type of intervention were low to moderate with no clear discrimination 179Management of TMDsof exercises in comparison to other conserva-tive treatments.377MobilizationMobilization techniques are indicated for im-proving decreased range of motion and pain due to muscle contracture, disc displacement without reduction, and brous adhesions in the joint. In some cases, repeated manipu-lation by the therapist can restore a more physiologic resting muscle length or improve joint function to allow a normal range of jaw motion.220 Muscle relaxation and pain reduc-tion are often required to enhance the effect of mobilization. Thus, a combination of heat, cold, ultrasound, and electric stimulation is often employed before or in conjunction with mobilization. Acute disc displacement without reduction can at times be effectively reduced by manipulation of the mandible.378 The mobili-zation may be accomplished through gripping the mandible rmly with the thumbs on the oc-clusal surfaces of the posterior teeth. The un-affected side is securely braced, and rm but controlled force is applied to the mandible in a downward, forward, and inward direction.1,379 Another technique incorporates the patient’s voluntary maximal lateral excursive jaw move-ment to the unaffected side followed by open-ing through the lateral border path.379,380 Fol-lowing mobilization, therapy to maintain joint mobility should be considered, such as ortho-pedic appliance therapy, relaxation therapy, and exercises.Physical agents or modalitiesPhysical agents or modalities used for TMD management include electrotherapy, ultra-sound, iontophoresis, anesthetic agents, dry needling (ie, botulinum toxin), acupuncture, and low-level laser therapy.ElectrotherapyElectrotherapy devices can produce thermal, histochemical, and physiologic changes in the muscles and joints. These devices include electrogalvanic stimulation (EGS), transcu-taneous electrical nerve stimulation (TENS), and microvoltage stimulation. EGS uses a high-voltage, low-amperage, monophasic current of varied frequency. This modality has been applied clinically in an effort to aid in muscle relaxation, reduce inammation, and increase blood ow to tissues.368 TENS uses a low-voltage, low-amperage, biphasic current of varied frequency and is designed primarily for sensory counterstimulation in painful dis-orders.381 Like EGS, this modality decreases muscle pain and hyperactivity and can aid in muscle reeducation. If signicant motor stimu-lation occurs concurrently, this may impair the analgesic effect and exacerbate acute muscle pain.382 Although TENS has more traditionally been used outside of the temporomandibular area, application techniques for temporoman-dibular and cervical pain have been described. A review of TENS in 1997 gave equivocal re-sults with a possible short-term benet but no difference in outcomes over time.383UltrasoundUltrasound is a frequently used physical treat-ment modality for musculoskeletal problems. The high-frequency oscillations of the trans-ducer head are converted to heat when trans-mitted though the tissue. This can heat the tissues to a depth of 5 cm.384 It has been pro-posed that ultrasound may be used to produce deep heat in the joints; treat joint contracture by increasing the stretch of the extracapsular soft tissue; decrease chronic pain, muscle con-traction, and tendonitis; and facilitate resorp-tion of the calcium deposits of bursitis.384–386 Ultrasound is also commonly used to carry medication into the tissue through phonopho-resis, although the mechanism and efcacy of drug delivery are unknown.387 A systematic review on the efcacy of ultrasound on the musculoskeletal system revealed that only 2 of 18 placebo-controlled trials showed a statis-tically and clinically signicant benet of ultra-sound. The four trials related to TMDs did not 180Dierential Diagnosis and Management of TMDs8reach the quality standard used in the review. In addition, they did not show any signicant benet of ultrasound.388IontophoresisIontophoresis is a technique to enhance the transport of drug ions across a tissue barrier. A weak current is used to enhance the transport of drug ions—usually corticosteroids—through the skin into the deeper tissues, where the drug is purported to exert its effect.389 How-ever, RCTs have not supported the efcacy of this modality to provide pain relief.390,391Anesthetic agentsAnesthetic agents have been proposed to be benecial to TMD therapy. Application of va-pocoolant sprays followed by muscle stretch-ing decreases muscle soreness and tightness and is thought to inactivate myofascial trigger points (TPs).66,392 To date, there are no RCTs showing efcacy of such therapy.Local anesthetic injection of myofascial TPs, alone or in conjunction with muscle stretching or mobilization, has been shown to be useful for the management of myofas-cial pain. Although the anesthetic is useful in pain reduction, it is not the most critical fac-tor in eliminating pain.393–395 Rather, it appears that the mechanical disruption of the TP by the needle provides the therapeutic effect. TP injections should be used adjunctively with other modalities such as pharmacother-apy, physical therapy, and—in many cases— behavioral medicine techniques.396 TP injec-tions are usually performed in a series of three to ve treatments to an individual muscle group, initially at weekly intervals. Long-acting local anesthetics such as bupivacaine should not be used for muscle injections because of increased myotoxicity, and there is no need to incorporate a vasoconstrictor because the integrated TP physiologic model suggests a localized hypoxic energy associated with sen-sory and autonomic reexes.397,398 In a recent RCT, the effect of TP injections inltrating with either saline or anesthetic showed no differ-ences in pain intensity, headache frequency, or intensity between the two intervention groups. It is important to note that the inter-ventions were enhanced with muscle stretch-ing, anti-inammatory medications, and ther-mal therapy.399Botulinum toxinBotulinum toxin has been trialed in the treat-ment of myofascial TPs. In a recent review of the literature, it was concluded that there was insufcient evidence to determine whether or not this medication is effective due to the lack of an adequate number and poor quality of the clinical trials.400 An update of a Cochrane re-view did not nd new studies and concluded that there is insufcient evidence for botu-linum use, highlighting that there is a lot of heterogeneity between the studies, includ-ing lack of standardized outcome measure-ments, treatment modalities, and follow-up.401 Contrasting results in a more recent sys-tematic review and meta-analysis including only double-blind studies with placebo controls showed that pain intensity was signicantly reduced in the botulinum-A groups compared with placebo groups at a relatively long term of 6 months, although the cost-effectiveness is questioned.402AcupunctureAcupuncture has also been used for the treatment of chronic musculoskeletal pain, but the precise mechanism of action is un-known. Early studies of its application for TMDs suggest that the benets of acupunc-ture are comparable with conventional TMD treatments.293 However, a systematic review and meta-analysis of acupuncture demon-strated only limited evidence that acupunc-ture treatment in TMDs is more effective than sham acupuncture, while others support that conventional acupuncture is effective.403,404 These contrasting ndings suggest that there is a need for rigorous clinical trials evaluating 181Management of TMDsacupuncture as an adjunctive therapy before denitive recommendations regarding its ap-plication can be made.Low-level laser therapyLow-level laser therapy has been used for the treatment of TMDs and is suggested to have biostimulating and analgesic effects through direct irradiation without causing a thermal response.405 Consistent findings support the claim that low-level laser therapy was no better than placebo in reducing chronic TMD pain.406,407 Because of the poor methodologic design of the studies and the utilization of dif-ferent types, frequencies, and duration of laser radiation in various patients groups, treatment parameters have not been standardized, and effectiveness cannot be evaluated. Two RCTs published just subsequently to the systematic review time period demonstrated positive ef-fects of the laser therapy compared with con-trols and positive but equal effects to splint therapy.408,409 Because of the small sample size of these studies, further research is needed to support the use of low-level laser therapy in TMD treatment.Orthopedic appliance therapyOrthopedic appliances, including interocclusal splints, orthotics, orthoses, bite guards, bite planes, night guards, or bruxism appliances, are routinely used in the treatment of TMDs. Based on current theory, removable acrylic resin appliances that cover the teeth have traditionally been used to alter occlusal rela-tionships and to redistribute occlusal forces, to prevent wear and mobility of the teeth, to reduce bruxism and parafunction, to treat masticatory muscle pain and dysfunction, to treat painful TMJs, and to alter structural rela-tionships in the TMJ.410 Researchers have not agreed, however, on the mechanism of action, what the most effective occlusal design is, or even whether the appliances are more effec-tive than placebos or other treatments.411–415Generally, studies focusing on appliance therapy have reported a reduction in orofacial pain and other symptoms associated with TMDs.315,411,416–418 However, most studies have been limited by small sample size, short-term outcome, inadequate control groups, and fail-ure to compare appliance therapy with other forms of treatment. Furthermore, several review papers have concluded that when these appliances were compared with an in-active placebo, they were mildly favorable, performing no better than nonoccluding appli-ances or other types of TMD therapies such as behavioral modication or self-regulation strategies.415,419–424 The most recent system-atic reviews and meta-analysis, however, did conclude that there is a moderate effect for reduction of pain with the use of splint therapy in TMDs.407,425 The three types of or-thopedic appliances that are described here include full-coverage stabilizing appliances, partial-coverage appliances, and anterior posi-tioning appliances.The complications that can occur with the excessive or incorrect use of any appliance include caries, gingival inammation, mouth odors, speech difculties, occlusal changes, and psychologic dependence on the appli-ance. Serious complications can include major, irreversible changes in functional and morpho-logic occlusal features as a result of long-term, full-time use of these appliances.426,427 This is a signicant concern with partial-arch coverage appliances.Stabilization appliancesStabilization appliances cover all of the max-illary or mandibular teeth. Stabilization appli-ances are used as an adjunct for managing symptoms associated with myogenous as well as arthrogenous TMDs.315,428–431 Preferably, they are used during sleep only, whereas behavioral modication strategies may be used to in-crease the patient’s awareness and reduce the impact of parafunctional habits on TMDs while awake. Because acrylic is softer than enamel, 182Dierential Diagnosis and Management of TMDs8these appliances have been used to reduce the chance of further tooth attrition in patients with sleep bruxism. Stabilization appliances can also be used for the management of an unstable occlusion, such as missing multiple bilateral posterior tooth contacts. Occasionally, they are used to reduce clenching-induced ear-ache and tooth pain as well as some forms of temporal headache.432–436EMG monitoring of the masseter muscle has been used in an attempt to demonstrate a short-term decrease in the level of sleep brux-ism activity when an appliance is worn.437,438 However, studies demonstrated that the re-sponse is variable and that sleep bruxism is not eliminated with stabilization appliances.88,410,439 These studies emphasize the variability of the clinical response to these appliances and the need for careful follow-up. The occlusal surface of the appliance should be adjusted to provide a stable physiologic mandibular posture by cre-ating bilateral, even posterior occlusal contacts for the opposing teeth on closure.88 Appliances adjusted to a “neuromuscularly determined” jaw position seem to show no advantage over conventional stabilization appliances.193 Ante-rior guidance may be provided by acrylic guide ramps in the canine or anterior areas of the appliance to separate the opposing poste-rior teeth from the appliance in all excursive movements of the mandible. Clinical experi-ence suggests that the occlusal surface of the appliance should be adjusted initially and periodically to compensate for changes in the maxillomandibular relationship as pain, muscle activity, inammation, edema, or soft tissue structural relations change.In acute cases, the appliance may be worn full-time for a specied period of time. As symptom reduction occurs, use of the appli-ance only during sleep is preferred. This is es-pecially true with ongoing sleep bruxism and related morning pain. Patients not showing a positive response within 3 to 4 weeks should be reevaluated. Failure to show an initial posi-tive response does not necessarily indicate a need for more aggressive or prolonged ther-apy; other factors should be considered such as chronic pain behavior, noncompliance, mis-diagnosis, or degree of TMJ pathology.Use of a stabilization appliance with ad-junctive therapy for pain relief and improved function is also a viable treatment option for TMJ internal derangement.440–442 Asymptom-atic clicks by themselves do not warrant treat-ment, and studies using TMJ imaging throw doubt on the need for a “correct” or “perfect” disc position.443 In the treatment of internal de-rangement, if improvement is not realized with orthopedic appliance therapy and adjunctive measures, and if signicant pain and mechani-cal symptoms persist, minimally invasive pro-cedures such as arthrocentesis and/or arthros-copy or open joint surgery may be necessary.Past research regarding the use of stabiliza-tion appliances fabricated with a soft resilient material have provided mixed results regard-ing the effect of these appliances in reducing sleep bruxism and signs and symptoms of TMDs.437,444–447 Concern regarding the effect of using unadjusted appliances on occlusal con-tacts has been raised.448 One study suggested that the efcacy of these appliances may be re-lated to the stability of the appliance occlusion, and with stable contacts, occlusal changes do not occur.298 Studies comparing soft appli-ances with hard acrylic appliances have found both to be equally effective in reducing painful symptoms, but they were no more effective than self-management treatment without ap-pliance therapy.446,447 Techniques for adjusting soft resilient appliances are available.379,449 These appliances currently seem best suited for treatment of children with a mixed denti-tion as the soft appliance seems to have mini-mal effect on dental development.444Partial-coverage appliancesOne type of partial-coverage appliance only covers the maxillary central incisors and con-tacts with only one or two opposing mandibu-lar teeth.450 The claimed mechanism of action 183Management of TMDswas that occlusal forces applied to a few ante-rior teeth would be less than forces applied to a full occlusion, resulting in a decrease in mus-cle activity and/or diminished loading of the TMJ. Whereas in a 3-month follow-up study, no differences in improvement were observed between TMD patients wearing this appliance and patients wearing a stabilization appliance, a 6-month follow-up study reported that more patients in the stabilization appliance group im-proved.451,452 A systematic review of this type of appliance indicated that they can be used successfully, but they should only be used in cases where patients will be compliant with their follow-up appointments.453 Due to its compact size, a less than well-retained appli-ance at night has the potential risk for aspi-ration. Recently, it was reported that the use of this type of device as initial therapy did not provide any additional benet in reducing pain or improving jaw function.454Another partial-coverage oral appliance is one that covers only the posterior teeth. The posterior bite plane is usually fabricated for the mandibular teeth and consists of areas of hard acrylic located over the posterior teeth and con-nected by a cast metal lingual bar. It has been advocated in cases of loss of vertical dimension or when there is a need to make major changes in anterior positioning of the mandible.455 The efcacy of this type of appliance has been stud-ied in only one small controlled trial.456Studies supporting the efcacy of partial- coverage appliances in reducing TMD symp-toms are limited by number and sample size. In addition, they have the potential to produce a malocclusion and possible internal TMJ changes.452 There is no evidence to state that they reduce TMD symptoms more effectively than full-arch appliances.Anterior positioning appliancesAnterior positioning appliances, also called anterior repositioning appliances, are usually fabricated for the maxillary arch to guide the mandible into a protrusive position. All teeth in the arch are covered, and the opposing teeth are provided with minimal posterior occlusal indentations and a reverse guidance incline in the anterior segment of the appliance.457 This design is aimed at providing guidance to a more comfortable therapeutic condyle-disc-fossa re-lationship. Anterior positioning appliances are used to decrease joint pain, joint noise (click-ing), and associated secondary muscle symp-toms in TMDs.458,459 The primary indication for anterior positioning appliance therapy is acute joint pain associated with disc displacement with reduction.315,460,461 Originally, full-time use of the appliance was suggested with the in-tent to establish a new jaw position with the disc “recaptured.”462 Although short-term suc-cess with full-time wear of anterior positioning appliances was good, long-term success at es-tablishing a new occlusal position with the disc recaptured has not been realized.26,459,460,463–465 Therefore, attempts to achieve a new thera-peutic mandibular position aimed at restoring the disc-condyle relationship with anterior po-sitioning appliances should be restricted to a few select cases of articular pain that can only be managed by maintained jaw positioning. In these cases, the patient needs to understand in advance the involved nature of the treatment in terms of time and expense. Whether the ap-pliance will be used full-time or part-time, the potential occlusal consequences need to be discussed with the patient prior to treatment since mandibular repositioning can result in ir-reversible changes in the occlusion (ie, a pos-terior open bite).466An anterior positioning appliance may be ef-fective in reducing symptoms associated with disc displacement with reduction. Use of the appliance during sleep is also often effective for preventing intermittent disc displacement without reduction on awakening and reducing joint pain. By using the appliance only dur-ing sleep, the potential for occlusal changes is greatly reduced. Full-time short-term wear of the anterior repositioning appliance should be limited to cases with acute disc displace- 184Dierential Diagnosis and Management of TMDs8ment without reduction (ie, acute closed lock), only if the clinician is able to reduce the disc (ie, unlock the jaw). In such cases, restoring the disc-condyle relationship full-time for 5 to 7 days may reduce or prevent additional lock-ing episodes and encourage adaptation. Once joint pain and dysfunction are decreased, the appliance use may be gradually reduced to sleep-time wear only, and, if needed, eventu-ally replaced with a stabilization appliance.The goal of this treatment is to allow the mandible to approximate the pretreatment occlusal position, as ample evidence has de-termined that permanent mandibular reposi-tioning as a treatment goal for TMDs does not fall within the standard of medically necessary treatment.467 This approach is strongly recom-mended to avoid or minimize the need for unnecessary restorative or orthodontic treat-ment. The treatment is not intended to correct the disc-condyle relationship but to facilitate control of symptoms similar to other treat-ments.282 Clicking is not usually eliminated but may be decreased in intensity. In some instances, returning the patient to the preex-isting occlusal condition reinitiates the painful joint symptoms. This is likely due to the lack of adaptation of the retrodiscal tissues. In most instances, immediately returning the patient to the anterior positioning appliance therapy will once again reduce the symptoms. When this occurs, more time should be allowed for tissue adaptation. Allowing more time will minimize the need for any permanent occlusal changes. Only after repeated unsuccessful attempts to return the joint to an orthopedically stable po-sition in the fossa should permanent occlusal changes be considered. The need for perma-nent occlusal therapy is very rare and should not be considered a goal of therapy, but rather necessary due to the potential risks associated with long-term use of repositioning appliances.Occlusal therapyThose interested in studying TMD pathophysi-ology and therapeutic concepts related to oc-clusal discrepancies may struggle with the role of occlusion in TMD treatment. It is difcult to establish any signicant cause and effect rela-tionships due to the many variables involved with these multifactorial problems.115,468,469 Many of these variables are difcult if not im-possible to exclude clinically. There are valid reasons for occlusal treatment for many dental conditions: lack of inter/intra–arch tooth stabil-ity; tooth mobility; fremitus; occlusal-related fracture of a tooth or restoration; tooth sen-sitivity; altered or compromised masticatory function, swallowing, or speech; and compro-mised supporting tissues due to adverse load-ing. Although occlusal-related dental treatment may be necessary for patients with TMDs, it is believed to be unnecessary for the purpose of treating TMDs.336The use of anterior positioning appliances in the treatment of TMJ disc displacement to establish a mandibular position with a cor-rected disc-condyle relationship has led to the concept of two-phase treatment. This treat-ment approach was especially popular in the late 1970s and the 1980s. Phase 1 involved the use of the anterior positioning appliance and any adjunctive therapies. Phase 2 involved rearticulation of the teeth in the newly ac-quired therapeutic jaw position through deni-tive, irreversible occlusal treatment: occlusal adjustment, restorative or prosthodontic den-tal treatment, or orthodontic or orthognathic treatment. Given that permanent mandibular repositioning as a treatment goal does not ful-ll all of the criteria for medical necessity, it is strongly suggested that the use of the terms phase 1 and phase 2 treatment of TMDs be discontinued.467 The problem with this termi-nology is that it implies that phase 2 treatment inevitably follows phase 1 treatment. The sci-entic literature does not support the need for a two-phase treatment because denitive 185Management of TMDsocclusal therapy is not required for the effec-tive treatment of most TMDs.470,471 In spite of the lack of scientic support, the two-phase philosophy continues to be promoted by many continuing education courses and concepts of occlusal etiology for TMDs and is adhered to by many dental professionals.472Primary occlusal therapy should be used with caution because there is no evidence that natural occlusal morphologic variation is a common cause of TMDs.115,184,470,473,474 Based on current evidence, the routine emphasis of treatment of chronic malocclusions to treat TMDs is unsupported. TMDs, especially involv-ing TMJ pathology, may affect the dental oc-clusion. In other words, the malocclusion may be a consequence of the TMDs rather than a cause.475,476 The clinician should not proceed with occlusal treatment to correct the resul-tant malocclusion until he or she is reason-ably assured that the TMJ pathology is stable and no further changes are likely. Evidence of stability may be obtained through longitu-dinal monitoring of pain symptoms, occlusal relationships, TMJ imaging, and cephalometric measurements. The risk of recurrence or pro-gression should be clearly communicated to the patient before initiating the denitive oc-clusal treatment.The clinician is advised to proceed cau-tiously, using the least invasive procedures possible, when treating occlusal changes in the TMD patient.477 The pretreatment in-tercuspal relationship should be preserved whenever possible. There is no evidence that anterior guidance is superior to other forms of guidance for treating TMD symptoms related to sleep bruxism.478,479 Also, anterior guidance may not provide optimal joint loading for all TMD articular conditions.161,480 Thus, altering the occlusion to provide anterior guidance for patients with TMDs is questionable. In gen-eral, there is a lack of evidence that complex occlusal therapy to provide an idealized dental occlusion is necessary for routine TMD man-agement. 470,474,481Occlusal adjustmentOcclusal adjustment was at one time consid-ered benecial for TMDs, and occlusal interfer-ences were implicated in the etiology of TMDs. However, there is no evidence for which type of occlusal interference, if any, might impede jaw function or play an etiologic role in the development of TMDs.470 A review of studies adding articial occlusal interferences failed to induce TMD symptoms and in fact showed reduced masseter activity after application of the occlusal interference.470,482 A Cochrane Da-tabase review and several other systematic reviews of RCTs showed that there was not enough evidence that occlusal adjustments are useful to prevent or treat TMDs.423,470,483,484 For these reasons and because occlusal ad-justment is an irreversible and invasive treat-ment modality, it should not be considered as initial therapy for TMDs. The reviews agree that occlusal adjustment may be considered as a treatment option to improve mandibular stabil-ity in cases where specic TMD disturbances have resulted in an unstable occlusal relation-ship, or when an occlusal interference related to a recently placed restoration precipitates symptoms.Restorative and prosthodontic therapyRestorative or prosthodontic dental care should never be a primary treatment option for TMDs.470 Once stability and symptom res-olution are achieved, restorative therapy has been suggested for patients who might likely benet from reduction of adverse loading and redistribution of occlusal forces, as suggested by earlier studies.485–487 However, as with other irreversible and invasive occlusal therapies like occlusal adjustment, the efcacy of this treat-ment for TMDs is not predictable, and further research is needed on the inuence of dental occlusion on TMJ loading. There are a few in-stances when the occlusal condition is associ-ated with TMD symptoms by way of functional mandibular instability. In these instances, the 186Dierential Diagnosis and Management of TMDs8occlusal condition must be addressed, but any extensive restorative therapy in TMD patients should be undertaken with caution. Sudden, radical changes in occlusion in these patients carry some risk, though the occlusal altera-tions are usually well tolerated according to human and animal studies.488–490Orthodontic-orthognathic therapyOrthodontic treatment is often the treatment of choice when major occlusal alterations are considered to be dentally advantageous. Fixed, removable, functional, and extraoral orthodon-tic appliances are all capable of improving oc-clusal and mandibular stability.491 Orthodontics has been suggested subsequent to anterior positioning appliance therapy to correct a TMJ disc displacement. This has not proven to be as successful on a longitudinal basis as ante-rior positioning appliance therapy alone.492,493 Orthodontic therapy does present some risk of destabilizing the masticatory system during treatment.494 Therefore, the orthodontic diag-nosis and treatment plan must consider pos-sible inuences of resulting occlusal instability during treatment on preexisting TMDs.495,496Many retrospective clinical studies have ex-amined the relationship between orthodontic treatment and TMDs and have found no sig-nicant correlation on a population basis.497 Additionally, several recent prospective long-term studies also conrm no correlation between orthodontic treatment in childhood and increased risk of developing TMDs later in life.433,498–500 Orthodontic treatment with premolar extraction has been specically im-plicated in the development of TMDs through incisor retraction and subsequent distalization of the mandible.501 However, studies compar-ing orthodontic treatments with and without premolar extraction have found no difference in posttreatment condylar position, overbite, discrepancy between ICP and RCP, or symp-toms of TMDs.502–507 In a prospective study of posttreatment changes in the TMJ, no statisti-cally signicant correlation between changes in the condyle/fossa relationship based on age, sex, skeletal or dental variables, signs or symp-toms of a TMD, headgear use, type of elastics, or nonextraction vs extraction treatment were identied.508 Additionally, there are some lon-gitudinal studies that suggest patients with a history of orthodontics tend to have a lower prevalence of signs and symptoms than those with no history of orthodontic treatment.433,509 A review of the literature concluded that, based on the available evidence, orthodontic treatment “neither causes nor cures TMDs.”510Although there is little evidence that orthodontically treated patients as a group have a greater prevalence of TMD symptoms, the individual patient response to the dental insta-bilities associated with orthodontic treatment may be quite different.511 Thus, the orthodontic clinician must be alert for, and be prepared to deal with, the onset or exacerbation of signs and symptoms that may occur during orthodon-tic tooth movement. The potential for problems clearly mandates a pretreatment TMD screen-ing examination for all orthodontic patients.511,512Orthognathic surgery may be considered in conjunction with orthodontic or restorative or prosthodontic treatment for correction of skel-etal malocclusions. However, when orthogna-thic surgery is considered in TMD patients, it should always follow careful evaluation con-rming reasonable symptom resolution and stability of the maxillomandibular relationship. Surgical treatment for skeletal asymmetries and growth anomalies with the specic intent of alleviating pain associated with TMDs is rarely indicated and should only follow care-ful evaluation and management of any other contributing factors. However, in those TMD patients with severe skeletal malocclusion who desire greater occlusal stability or im-proved esthetics, orthognathic treatment is often the method of choice.513–515 Two retro-spective studies showed no increase in TMD signs and symptoms in patients with juvenile rheumatoid arthritis or patients with anterior open bites who underwent orthognathic sur- 187Management of TMDsgery.516,517 Another study showed that in pa-tients who underwent orthognathic surgery with rigid xation, symptoms of clicking and muscle pain improved, whereas these symp-toms increased in patients with nonrigid xa-tion.518 A systematic review from 2010 pointed out that the studies up to that date gener-ally had small groups, no controls, and other methodologic aws.519 A systematic review and meta-analysis from 2017 could not predict which patients might improve or worsen in TMD symptoms after orthognathic surgery.520 The more recent prospective studies indicate that orthognathic surgery in patients with TMDs may improve the condition; however, there are also reports of exacerbation of TMD signs and symptoms. For TMD patients who desire correction of skeletal malocclusions, or-thognathic surgery is an option, but informed consent should emphasize the correction of the malocclusion, not the potential improve-ment in TMD.SurgeryTMJ surgery is an effective treatment for spe-cic articular disorders. However, the complex-ity of available techniques, potential complica-tions, prevalence of behavioral and psychosocial contributing factors, and the availability of non-surgical approaches suggest that TMJ surgery should only be used in select cases.The decision to treat the patient surgically depends on the degree of pathology or ana-tomic derangement present within the joint, the potential for repair of the condition, the outcome of appropriate nonsurgical treatment, and the degree of impairment the problem cre-ates for the patient. The appropriate duration and complexity of nonsurgical treatment prior to considering surgery are determined by a combination of factors. Factors to be consid-ered include expected prognosis compared with actual improvement realized, the degree of impairment, and the patient’s compliance with the program. Patients with complicating factors such as pending litigation, psychologic issues, uncontrolled sleep bruxism, or prior joint surgeries may have a poor surgical prog-nosis. The clinician must have a full knowledge and appreciation of the potential for surgical failure and potential complications including neuropathic pain disorders (ie, deafferentation pain). Once this information is available, a real-istic discussion of the prognosis, the patient’s expectations, and the complicating factors can provide the patient with the information neces-sary to make an informed decision.Preoperative and postoperative nonsurgi-cal management must be integrated into the overall surgical treatment plan. This therapy is directed at decreasing the functional load placed on the joint, eliminating or modifying contributing factors such as oral parafunctional habits, and providing appropriate psychologic and medical support. The clinical practice guidelines for TMJ surgery of the American Association of Oral and Maxillofacial Sur-geons state that TMJ surgery is only indicated when nonsurgical therapy has been ineffec-tive and is not indicated for asymptomatic or minimally symptomatic cases.521 In addition, surgery should not be performed for preven-tive reasons. Indications for surgery include moderate to severe pain or dysfunction that is disabling.521 Radiographic evidence of in-ternal derangement may be indicated. Sur-gical management may include joint lavage (arthrocentesis), closed surgical procedures (arthroscopy), and open surgical procedures (arthrotomy or arthroplasty), as well as total joint replacement.ArthrocentesisArthrocentesis involves simple intra-articular irrigation or lavage of TMJ with or without cor-ticosteroids or hyaluronic acid. It has been sug-gested this method may be as effective as ar-throscopy when used with joint mobilization in the treatment of intra-articular joint restrictions of mandibular movement such as internal de-rangement without reduction.522,523 However, it 188Dierential Diagnosis and Management of TMDs8also can be used as a palliative procedure for patients with acute episodes of degenerative or rheumatoid arthritis and to relieve the pain in patients who have painful clicking in the TMJ that does not respond to medical manage-ment.524,525 Two reviews evaluating outcomes of arthrocentesis performed on patients with different types of internal derangement indi-cated successful treatment outcomes in about 80% of the cases but noted that most studies could be criticized because of methodologic aws.526,527 Before the efcacy of this proce-dure can be conrmed, more clinical RCTs are needed.ArthroscopyArthroscopy allows direct observation and sampling of the joint tissues and holds prom-ise as a modality for treating painful joints and joints with hypomobility secondary to a per-sistent nonreducing displaced disc.528,529 Ar-throscopic revision of previous open surgery has been suggested as helpful in alleviating postoperative pain and intracapsular brosis.530 At this time, arthroscopy is primarily performed in the upper joint space and is used for minor debridement and lavage, removal of minor ad-hesions, and biopsies. Reduction of symptoms following arthroscopic surgery is not caused by improved disc position; postarthroscopy MRI scans reveal that a vast majority of pa-tients have persistent anterior disc displace-ment but increased disc mobility.531–538 The prognosis of arthroscopy appears comparable to that of discectomy and discoplasty.539–542 Be-cause arthroscopy is less invasive than open joint surgeries, it should have preference over them whenever possible. A meta-analysis performed in 2003 showed the most robust evidence for efcacy of arthrocentesis and arthroscopy for treatment of disc displace-ment without reduction that was refractory to nonsurgical modalities.543 While a systematic review published in 2015 reported better pain control and increased maximum opening with arthroscopy over arthrocentesis, the differ-ences may not be clinically relevant.520ArthrotomyOpen surgical intervention of the TMJ (arthrot-omy) is usually required for bony or brous an-kylosis, neoplasia, severe chronic dislocations, persistent painful disc derangement, and se-vere osteoarthritis refractory to conservative modalities of treatment.529 Surgery is less often indicated in displaced condylar fractures, agenesis of the condyle, and severe painful chronic arthritides. Surgery is seldom, if ever, indicated in inammatory joint disorders (eg, synovitis or capsulitis), condylysis, and non-painful degenerative arthritis. Arthrotomy is generally indicated for patients with advanced TMJ disease who meet the surgical criteria and have disease refractory to or not amena-ble to arthroscopic surgical techniques.Open joint surgical procedures may include discoplasty; disc repositioning or discectomy, with or without replacement; arthroplasty, which includes high condylectomy; and total joint reconstruction or replacements. Disco-plasty and disc repositioning with plication have been reported to have an 80% to 90% success rate in reducing joint pain and noise and increasing mouth opening (although mouth opening remains short of normal ranges).539,544–547 The discectomy procedure without replacement has the longest history and shows good long-term success (up to 30 years).548–551 Use of a dermis graft in discec-tomy does not appear to prevent remodeling, but it may be benecial in eliminating or pre-venting joint noises.552The success obtained with less invasive procedures has greatly reduced the need for arthroplasty. Condylectomy (subcondylar osteotomy) and condylotomy are performed infrequently. These procedures have been indicated for more complex diseases or trau-matic conditions.553,554 There can be more post-surgical complications with these procedures, 189189Referencesincluding marked occlusal changes. Modied condylotomy (using an intraoral vertical ramus osteotomy) in the treatment of TMJ internal derangement can reduce related pain and predictably correct disc position.555–557 Further controlled investigations are needed regarding these applications.ConclusionDespite increasing evidence that TMDs are best managed with conservative revers-ible treatments, some clinicians continue to choose treatments based on personal biases rather than controlled scientific investiga-tion.472,494 There continues to be a need for RCTs regarding nonsurgical and surgical TMD treatment. In addition, studies designed to elu-cidate the etiology of TMDs are much needed. Practicing clinicians involved in the treatment of TMDs on a daily basis should be knowledge-able in clinical trial methodology and be able to critically appraise the literature upon which they base their treatments. Discriminating readers and clinicians will result, and our pa-tients will benet.References 1. Okeson JP. 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