TMD 1

Classification and Diagnosis
o f Tem p o ro m a n d i b u l a r
D i s o rd e r s
a n d Te m p o ro m a n d i b u l a r D i s o rd e r
Pain
Gary D. Klasser, DMDa,*, Jean-Paul Goulet, DDS, MSD, FRCD
b
,
Isabel Moreno-Hay, DDS PhD ABOP ABDSMc
KEYWORDS
! Classification systems ! Diagnostic criteria ! Temporomandibular disorders (TMD)
! Orofacial pain
KEY POINTS
! Classification systems are essential because they provide a conceptual framework of in-
formation that stems from our understanding of the etiology, pathophysiology, and fea-
tures of diseases and disorders specific to a field of interest to improve the quality of
diagnosis and patient management.
! There is no consensus regarding a unique and universal classification of temporomandib-
ular disorders (TMD); however, the breadth of clinical entities under the umbrella term
“temporomandibular disorders” is best captured for now within the classification scheme
proposed by the American Academy of Orofacial Pain.
! To date, the Diagnostic Criteria for Temporomandibular Disorders remains universally
accepted as a reliable evidence-based diagnostic system for common TMD.
! The integration of ontology principles, relevant genetics/epigenetics vulnerability factors,
neurobiological processes, and biomarkers represent promising steps toward the future
development of a treatment-oriented classification system for TMD.
a
Department of Diagnostic Sciences, School of Dentistry, Louisiana State University Health
Sciences Center, 1100 Florida Avenue, Box #8, New Orleans, LA 70119, USA; b Pavillon de
Médecine Dentaire, Université Laval, 2420 Rue de La Terrasse, Québec, G1V 0A6, Canada;
c
Orofacial Pain, College of Dentistry, University of Kentucky, Kentucky Clinic, Room E214, 740 S
Limestone, Lexington, KY 40536, USA
* Corresponding author.
E-mail address: [email protected]
Dent Clin N Am - (2022) -–-

https://doi.org/10.1016/j.cden.2022.12.001 dental.theclinics.com
0011-8532/22/ª 2022 Elsevier Inc. All rights reserved.
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2 Klasser et al
INTRODUCTION
Currently, classification is broadly defined as a “systematic arrangement in groups or

categories according to established criteria.”1 More specifically, classification systems
can be viewed as a set of disease characteristics used to group individuals into a well-
defined relatively homogenous population with similar clinical disease features.2 These
systems are essential for understanding disease pathogenesis and assessing treatment
response. The allure of following a classification system is that it simplifies the definition
of specific entities according to specific characteristics. The basis to do so is derived
from an understanding and comprehension of the etiology, pathophysiology, diagnosis,
and/or management of a specific disease or disorder. It must be remembered that clas-
sification systems are not intended to capture the whole universe of possible patients,
but rather to capture most of the patients with key shared features of the condition. For a
classification system to be ideal,3 the following requirements would have to be met: it
should be exhaustive (comprising all clinical diseases or disorders belonging to the field
of interest), biologically plausible (the symptoms and signs should match with known
biological processes), mutually exclusive (there should be no overlap between disease
entities because of common symptoms), clinically useful (so that it can be used to help
in treatment and prognosis), reliable (consistently applicable in a reproducible way be-
tween clinicians and over time) and simple for practical use.
Several organizations and individuals have developed classification systems for
temporomandibular disorders (TMD), which according to the American Association
for Orofacial Pain (AAOP) is defined as “A group of musculoskeletal and neuromus-
cular conditions that involve the TMJs, the masticatory muscles, and all associated tis-
sues”.4 Although TMDs represent a primary cause of nonodontogenic pain in the
orofacial region with pain being one of the most common and limiting clinical manifes-
tations of such disorders, it should be realized that to be labeled with having TMD does
not strictly imply this to be a painful condition. There are several conditions that may
simply be viewed as annoyances rather than being painful.5 Unfortunately, all TMD
classification systems, of past and present, share the commonality of having inherent
shortcomings in at least one of these qualifying requirements listed previously.
Diagnosis may be defined as the determination of the nature of an illness by evalu-
ation of the signs, symptoms, and supportive tests in an individual patient to identify a
specific disorder. Diagnostic criteria are a conglomeration of signs, symptoms, or sup-
portive tests used in routine clinical workup to aid in a clinical diagnosis of an individual
patient. Diagnostic criteria are generally broad and must reflect the different features
of a disease (heterogeneity), with a view to accurately identify as many people with the
condition as possible. During the care of the individual patient, diagnostic criteria may
be first used to guide medical/dental care and second to help the patient gain an un-
derstanding of the disease process with prognosis. Given this complexity, the devel-
opment and validation of diagnostic criteria can be quite challenging.6,7
Classification systems and diagnostic criteria for TMD have been developed, often
based on expert opinion and the best available knowledge with their focus most often
derived from particular organ systems or pathophysiological processes. Several orga-
nizations created task forces of experts to share their knowledge and experience and
develop a restricted set of criteria to denominate a set of particular diagnoses orga-
nized within a hierarchical approach. Validated diagnostic criteria were used if avail-
able and if absent, criteria were formulated and supplemented with commentary
explaining that data-driven criteria (validated through high-quality studies on diag-
nostic accuracy) are, to date, lacking. Unfortunately, this approach creates less-
than-ideal situations as selected signs and symptoms and criteria are used to
Classification and Diagnosis of TMD and TMD Pain 3
characterize an already selected group thus allowing for an overlapping of disease en-
tities and contributing to heterogeneity. Moreover, if a group of patients are selected
based on specific criteria, it is not known whether they all belong to a single disease or
that it is a sample of (partially) overlapping disease entities. Finally, the possibility of
circular reasoning exists when a criterion for selecting a group of symptomatic individ-
uals becomes part of the diagnostic criteria defining the presence or absence of a spe-
cific disease or disorder. These issues will be further elaborated upon as individual
classification systems and diagnostic criteria are discussed.
Classification systems and diagnostic criteria, although seem to be different, essen-
tially work by complementing each other. An analogy to this process would be that of a
filing system. This system includes a filing cabinet that represents the broader more
encompassing classification system. The folders and files within the filing cabinet
embody all diseases and disorders pertaining to a specific field according to specific
criteria that distinguish each individual condition contained therein from one to another.
Classification systems and diagnostic criteria allow the clinician to follow a struc-
tured and logical approach (similar to a roadmap) thereby facilitating the accurate
naming and classifying of a specific disease. This is the precursor to developing inter-
ventional approaches and strategies for patient management and thus providing a
platform for discussing a prognosis with the patient. From the patient perspective,
this approach results in the patient, receiving a clear and definitive diagnosis which ul-
timately allows for a better understanding and acceptance of aspects related to etiol-
ogy and pathophysiology, promotes inclusion to a specific group, and facilitates
acceptance of the various management strategies. Furthermore, it accommodates
the growth of the scientific process, as researchers are able to use homogenous sam-
ples when designing clinical studies. It promotes the ability for every patient entered
into a research project to be categorized according to specific and established
set(s) of diagnostic criteria. Lastly, it enables all stakeholders to use a common lan-
guage, thereby enhancing collaborative efforts using establishing clear terminology
that will allow communication and data sharing in an unambiguous manner.
CLASSIFICATION SYSTEMS FOR TEMPOROMANDIBULAR DISORDERS

International Classification of Diseases-11th Revision by the World Health
Organization
For over a century, the International Classification of Diseases (ICD) has been the
reference base for gathering health statistics information and understanding the cause
of death. The ICD 11th revision endorsed by the World Health Organization (WHO) in
2019 has recently come into effect.8 The ICD is a fully electronic database that enables
the assembly of large volumes of data for widespread use on the extent and conse-
quence of human diseases. Diseases and disorders in this conceptual framework
are spread across 28 top-level ICD chapters (categories) reflecting major aspects of
diseases and divided into subgroups. The ICD has categories for diseases, disorders,
syndromes, signs, symptoms, findings, injuries, external causes of morbidity and mor-
tality, factors influencing health status, reasons for encounter with the health system,
and traditional medicine. TMD are scattered across a large volume of anatomically,
etiologically, or phenotypically defined diseases and disorders and an entity may be
classified in more than one category. Entering "temporomandibular joint pain" in the
coding tool leads to "Temporomandibular joint disorders" in Chapter 15, Diseases
of the musculoskeletal system or connective tissue, and to "Headache or orofacial
pain associated with chronic secondary temporomandibular disorders" in Chapter
21, Symptoms, signs or clinical findings, not elsewhere classified.
4 Klasser et al
Among the significant improvements of the ICD 11 is the addition in Chapter 21 of a

systematic classification for chronic pain of any source which is then subdivided into
primary and secondary pain disorders as defined by the International Association for
the Study of Pain (IASP).9 Chronic primary TMD pain refers to pain without an estab-
lished cause, although substantial knowledge may exist regarding the pathophysio-
logical mechanisms, whereas chronic secondary TMD pain refers to pain with a
known etiology and pathophysiology.10,11 Therefore, ICD 11 allows the coding of indi-
vidual TMD entities. However, as they are not all regrouped into a single chapter, it is
not a classification system that enables clinicians to capture at a glance the scope of
TMD conditions.
ACTTION-APS Pain Taxonomy

The limitations with existing classification systems inspired the Analgesic, Anesthetic,
and Addiction Clinical Trial Translations, Innovations, Opportunities, and Networks
(ACTTION) to develop a new evidence-based classification scheme for chronic
pain, taking into account consequential biopsychosocial mechanisms. In partnership
with the American Pain Society (APS) and the US Food and Drug Administration, this
endeavor led to the 2014 publication of their collaborative taxonomy (AAPT), which is a
multidimensional classification framework for chronic pain disorders.3
To guide clinicians toward tailored pain management and better outcomes, the
AAPT categorizes chronic pain disorders into five organ systems/anatomic structures:
(1) Peripheral and central nervous systems, (2) Musculoskeletal pain system, (3) Oro-
facial and head pain system, (4) Visceral, pelvic, and urogenital pain, (5) Disease-
associated pains not classified elsewhere. Each is further divided into subcategories.
For instance, “Temporomandibular disorders,” “Headache disorders,” and “Other
orofacial pain” are specific subcategories in the “Orofacial and head pain system.”
The AAPT framework further characterized individual entities of chronic pain accord-
ing to five dimensions: (1) core diagnostic criteria; (2) common features; (3) common
medical and psychiatric comorbidities; (4) neurobiological, psychosocial, and func-
tional consequences; and (5) putative neurobiologic and psychosocial mechanisms,
risk factors, and protective factors.
Since its inception, the AAPT framework has been used for fibromyalgia and periph-
eral neuropathic pain conditions (ie, postherpetic neuralgia, persistent posttraumatic
neuropathic pain, complex regional pain disorder, and trigeminal neuralgia).12,13 A
recent initiative led to the development of a multidimensional framework adapted
for acute pain conditions (AAAPT). “Surgical/Procedural” and “Nonsurgical” are the
top-level categories with fourteen and seven subcategories based on organ systems
and anatomic location.14 The five-dimensional structures retained for characterizing
acute pain are (1) core criteria, (2) common features, (3) modulating factors, (4)
impact/functional consequences, and (5) putative pain pathophysiologic mechanisms.
The AAPT and AAAPT offer a sound blueprint framework for building a comprehen-
sive multiaxial classification that would complement, beyond the physical axis, the
diagnosis of pain-related TMD included in the International Classification of Orofacial
Pain (ICOP) and the AAOP taxonomy. Moreover, adapting the AAPT and AAAPT
framework dimensions for non-painful TMD could benefit researchers and clinicians
and help patient management. However, the full spectrum of TMD is still best captured
and outlined in the classification system proposed by the AAOP.
American Academy of Orofacial Pain

The AAOP classification system for TMD has gained widespread dissemination and
acceptance among clinicians through the AAOP Guidelines 6th edition (2018) manual.4
The current classification stemmed from the need for an agreed-upon TMD classifica-
tion for systematic use by clinicians and researchers. The work taking place under the
initiative of the International RDC/TMD Consortium of the IADR (renamed to INfORM –
International Network for Orofacial Pain and Related Disorders Methodology) in partner-
ship with the Orofacial and Head Pain Special Interest Group (OFHP SIG) of the IASP,
the AAOP, the National Institute of Dental and Craniofacial Research (NIDCR), and the
AAOP sister European and Australian Academies led to the consensus-based
expanded TMD taxonomy published in the AAOP Guidelines manual in 2013. An over-
view of the methods and process of this successful endeavor has been previously pre-
sented.15 Based on the AAOP 2008 classification scheme, TMD are sorted according to
the anatomic source of signs and symptoms into joint disorders and masticatory muscle
disorders. Before 2013, the AAOP classification for TMD included up to 21 individual en-
tities compared with 52 in the current edition. The AAOP classification regroups clinical
entities under joint and muscle disorders into empirically-derived categories tied to clin-
ical features or pathophysiologic processes (Table 1).
To foster exchange with medical communities, the AAOP provides the correspond-
ing ICD codes for each TMD (ICD 10th Revision). The AAOP classification allows going
further than the original expanded TMD taxonomy when an ICD code exists for sub-
typing a disorder based on etiology. For example, there are three subtypes for orofa-
cial dyskinesia and two for oromandibular dystonia. A retrospective look at the
iterations of the AAOP TMD taxonomy exemplified the evolving nature of a classifica-
tion system as new knowledge emerges. Although the AAOP classification does not
include all TMD and is unrelated to etiology, it remains the best available reference.
Besides capturing the scope and breadth of TMD, it also provides diagnostic criteria
based on history, clinical features, and specific tests for all TMD listed, for which val-
idity is established for the most frequent joint and muscle conditions.
American Academy of Craniofacial Pain

In 2009, the AACP published a guidelines manual for assessing, diagnosing, and man-
aging craniofacial pain. There are three chapters devoted to conditions attributed to
TMD. One chapter outlines extracapsular TMD, another deals with temporomandib-
ular joint disorders, and the third chapter discusses myofascial pain.16 For TMD, the
AACP uses the classification published by Pertes and Gross in 1995, which separates
TMD into three groups: (1) Temporomandibular joint disorders, (2) Masticatory muscle
disorders, and (3) Congenital and developmental disorders.17 The thirteen conditions
under temporomandibular joint disorders are regrouped into six subcategories ac-
cording to disease processes (ie, Inflammatory conditions, Degenerative diseases,
Ankylosis) and anatomic structures (ie, Deviation in form, Disk displacement,
Displacement of the disc-condyle complex). Seven masticatory muscle disorders
were subcategorized into acute and chronic with six conditions being outlined under
congenital and developmental disorders.17
While referring to the Pertes and Gross classification of TMD, the AACP Guidelines
manual sometimes uses a different terminology when designating individual disorders.
In addition, the AACP also describes a few conditions not listed by Pertes and Gross
(ie, myalgia, trismus, temporal tendinitis, Ernest syndrome) while ignoring others (ie,
muscle hypertrophy, myalgia secondary to systemic disease, and all the congenital
and developmental disorders).
The AACP classification of TMD has not been subjected to revision since its original
publication in 2009. Furthermore, the ICD codes provided are also dated as they orig-
inate from the ICD 9th edition. Alternatively, the AACP includes the most common
TMD seen in clinics, and the selected TMD categories have relevant labels. However,
6 Klasser et al
Table 1
American Academy of Orofacial Pain taxonomy for temporomandibular disorders4
Temporomandibular Joint Disorders 5.Congenital/developmental disorders

1. Joint pain A. Aplasia
A. Arthralgia a B. Hypoplasia
B. Arthritis a C. Hyperplasia
2. Joint disorders Masticatory Muscle Disorders
A. Disk-condyle complex disorders 1.Muscle pain
i. Disk displacement with reduction A. Myalgia a
ii. Disk displacement with reduction i. Local myalgia a
with intermittent locking ii. Myofascial pain a
iii. Disk displacement without iii. Myofascial pain with referral a
reduction with limited opening B. Tendonitis a
iv. Disk displacement without C. Myositis a
reduction without limited opening i. Noninfective
B. Other hypomobility disorders ii. Infective
i. Adhesions/adherence D. Spasm a
ii. Ankylosis 2. Contracture
a. Fibrous A. Muscle
b. Osseous B. Tendon
C. Hypermobility disorders 3. Hypertrophy
i. Subluxation 4. Neoplasms
ii. Luxation A. Jaw
a. Closed dislocation i. Malignant
b. Recurrent dislocation ii. Benign
c. Ligamentous laxity B. Soft tissues of head, face, and neck
3. Joint diseases i. Malignant
A. Degenerative joint disease ii. Benign
1. Osteoathrosis 5. Movement disorders
2. Osteoarthritis a A. Orofacial dyskinesia
B. Condylysis i. Abnormal involuntary movements
C. Osteochondritis dissecans ii. Ataxia unspecified, muscular
D. Osteonecrosis incoordination
E. Systemic arthritidis a iii. Subacute, due to drugs; oral
F. Neoplasms tardive dyskinesia
G. Synovial chondromatosis B. Oromandibular dystonia
4. Fracture i.Acute due to drugs
A. Closed fracture of condylar process ii. Deformans, familial, idiopathic, and
B. Closed fracture of subcondylar process torsion dystonia
C. Open fracture of condylar process 6. Masticatory muscle pain attributed to
D. Open fracture of subcondylar process systemic/central pain disorders
A. Fibromyalgiaa
B. Centrally mediated myalgiaa
Headache Disorders
1. Headache attributed to TMD a
Associated Structures
1. Coronoid hyperplasia
a
Pain-related TMDs.
the overall scope of TMD is narrower compared with more recent classification
schemes, which include subcategories such as joint diseases, neoplasms, and move-
ment disorders. In light of this, the AACP needs to address terminology issues since
muscle splinting, trismus, capsulitis, synovitis, and retrodiscitis are no longer used
to designate specific TMD as evident in more recent classification systems.
Despite providing expert-driven diagnostic criteria for individual TMD entities, the
scope makes the AACP classification less attractive to clinicians.
The International Classification of Orofacial Pain

In 2020 an international collaborative group consisting of members of the OFHP SIG of
the IASP, the INfORM group, the AAOP, and the International Headache Society (IHS)
published the first edition of the ICOP.18 This comprehensive hierarchical classifica-
tion incorporates all types of orofacial pain, including TMD-related pain, with the
exception of those not causing pain. Muscle and joint-related painful TMD are group-
ed into primary and secondary pain disorders under "Myofascial orofacial pain" and
"Temporomandibular joint pain." Primary muscle and joint-related pain are subcate-
gorized into acute and chronic using an onset cut-off of greater than 3 months for
the later. ICOP uses myofascial orofacial pain as an overarching label for any type
of masticatory muscle pain including localized myalgia. Myofascial orofacial pain
and temporomandibular joint pain diagnoses can be further subcategorized according
to the presence or absence of pain referral during palpation. As previously mentioned,
the ICOP (Table 2) uses the IASP definition for primary and secondary pain.10,11
Okeson Classification of Temporomandibular Disorders (8th Edition)

Okeson’s contribution to the classification, diagnosis, and management of TMD has
gained significant recognition worldwide through his textbook "Management of
Temporomandibular Disorders and Occlusion."19 Although no organization or associ-
ation has officially adopted Okeson’s classification scheme of TMD, it has neverthe-
less influenced the evolution and refinement of the current AAOP classification
scheme, and many clinicians follow it.
Okeson’s TMD classification includes four major groups: (I) Masticatory muscle dis-
orders, (II) temporomandibular joint (TMJ) disorders, (III) Chronic mandibular hypomo-
bility, and (IV) Growth disorders. Except for Group I Masticatory muscle disorders, the
other groups have one or more subcategories corresponding to the anatomic struc-
ture or underlying pathophysiological process. The proposed comprehensive classifi-
cation scheme includes 34 individual entities but excludes joint diseases that are not
trivial such as condylysis and movement disorders.
Table 2
Taxonomy of pain-related temporomandibular disorders from the International Classification
of Orofacial Pain18
2. Myofascial orofacial pain 3. Temporomandibular Joint (TMJ) pain

2.1. Primary myofascial orofacial pain 3.1. Primary temporomandibular joint
2.1.1. Acute primary myofascial pain
orofacial pain 3.1.1. Acute primary
2.1.2. Chronic primary myofascial temporomandibular joint pain
orofacial pain 3.1.2. Chronic primary
2.2. Secondary myofascial orofacial pain temporomandibular joint pain
2.2.1. Myofascial orofacial pain 3.2. Secondary temporomandibular joint
attributed to tendonitis pain
2.2.2. Myofascial orofacial pain 3.2.1. Temporomandibular joint pain
attributed to myositis attributed to arthritis
2.2.3. Myofascial orofacial pain 3.2.2. Temporomandibular joint pain
attributed to muscle spasm attributed to disk
displacement
3.2.3. Temporomandibular joint pain
attributed to degenerative
joint disease
3.2.4. Temporomandibular joint pain
attributed to subluxation
8 Klasser et al
DIAGNOSTIC SYSTEMS FOR TEMPOROMANDIBULAR DISORDERS

Research Diagnostic Criteria for Temporomandibular Disorders
In 1992, Dworkin and LeResche20 published the Research Diagnostic Criteria for
Temporomandibular Disorders (RDC/TMD). The aim of this diagnostic system was
to provide evidence-based standardized diagnostic criteria for clinical and epidemio-
logic research purposes. Taking into consideration the biopsychosocial model, the
RDC/TMD subdivided the diagnoses into two axes:
! Axis I encompassed clinical diagnoses identifying abnormalities of function and
structure of the masticatory muscles or temporomandibular joints.
! Axis II incorporated the assessment of global severity including pain intensity,
pain-related disability, depression, and nonspecific physical symptoms.
Over the following decades, these criteria were widely adopted by clinical re-
searchers worldwide and translated into 20 different languages. Research efforts
were also conducted to examine and revise the reliability, validity, and clinical utility
of the diagnostic system, particularly among the Axis I diagnoses which were based
solely on self-report and physical examination.21–27
As these diagnostic criteria were not originally intended for clinical practice, only a
limited number of subtypes of TMD were included in Axis I (Box 1). Hence, these diag-
nostic categories were broadly defined, for example, the term myofascial pain was
used for muscle pain but did not distinguish between local and referred pain. Similarly
in Axis II, certain relevant variables to the management of TMD were also omitted from
the original publication, such as the assessment of anxiety, sleep disorders, or post-
traumatic stress disorder.
Diagnostic Criteria for Temporomandibular Disorders

The International RDC/TMD Consortium of the IADR and the OFHP SIG of the IASP
joined forces in 2014 and presented the evidence-based DC/TMD appropriate for
both research and clinical settings.28
In Axis I, the diagnostic algorithms for the most common TMD were subdivided into
pain-related TMD and intra-articular TMD (Box 2). A total of 12 diagnoses were
included of which all, but myofascial pain and local myalgia, presented specificity
and sensitivity data. Less common TMD without demonstrated validity were added
to the expanded taxonomic classification (see below).15
Box 1
RDC/TMD axis I: clinical TMD conditions20
I. Muscle diagnoses
a. Myofascial pain
b. Myofascial pain with limited opening
II. Disk displacements
a. Disk displacement with reduction
b. Disk displacement without reduction, with limited opening
c. Disk displacement without reduction, without limited opening
III. Arthralgia, arthritis, arthrosis
a. Arthralgia
b. Osteoarthritis of the TMJ
c. Osteoarthrosis of the TMJ
Box 2
DC/TMD axis I: clinical TMD conditions20
Most Common Pain-Related Temporomandibular Disorders

1. Myalgia
a. Local myalgia
b. Myofascial pain
c. Myofascial pain with referral
2. Arthralgia
3. Headache attributed to TMD
Most Common Intra-articular Temporomandibular Disorders
1. Disk displacement with reduction
2. Disk displacement with reduction with intermittent locking
3. Disk displacement without reduction, with limited opening
4. Disk displacement without reduction, without limited opening
5. Degenerative joint disease
6. Subluxation
Axis II was also expanded with the inclusion of a range of assessment tools from
screening to a more comprehensive expert evaluation. These new recommendations
included a validated TMD pain screener for the identification of pain-related distur-
bances in any clinical setting.29 If a patient screen positively, further evaluation for
TMD is warranted (Box 3).
An important contribution of the DC/TMD was the introduction of criteria that
musculoskeletal pains, such as TMD, should be modified (increased or decreased)
by function, movement, or parafunction. Moreover, during the clinical examination,
provocation tests should reproduce the pain complaint as per the patient’s report.
The patient should confirm that the provoked pain is familiar to their chief complaint.
In addition, in the DC/TMD, the muscle diagnoses were reorganized, and the term
myofascial pain in RDC/TMD was replaced by myalgia, which was then subdivided
into local myalgia, myofascial pain, and myofascial pain with the referral. Thus, the
DC/TMD recognized myofascial pain with referral, as a distinct clinical disorder. For
the clinician, understanding pain referral to other anatomic sites, for example, dental
structures, is of great relevance in establishing a differential diagnosis and in the
consideration of various interventional strategies.
Another update to this diagnostic system was the addition of the diagnosis of
“headache attributed to TMD” following the International Classification of Headache
Disorders (ICHD). This diagnosis was included in reference to headaches located in
the temporalis area modified by jaw function, and the diagnostic criteria showed
excellent validity. However, as per ICHD-3 diagnostic classification, the diagnosis of
headache attributed to TMD can sometimes overlap the diagnosis of tension-type
headache, particularly in patients that present with pericranial tenderness.30 Although
it has some limitations, the DC/TMD remains universally accepted as a reliable diag-
nostic system for TMD.
Expanded Diagnostic Criteria for Temporomandibular Disorder taxonomy

The expanded taxonomy of the DC/TMD was developed to standardize the diagnosis
for the less common TMD that were not included in the DC/TMD structure due to a
lack of validated criteria. A total of 37 clinically significant conditions were included
by expert consensus. The aim of this expanded diagnostic system of Axis I was to pro-
vide a standardized framework for future research studies to investigate the validity of
the proposed diagnostic criteria.15
10 Klasser et al
Box 3
TMD pain screener29
1. In the last 30 days, how long did any pain last in your jaw or temple area on either side?
a. No pain (0 points)
b. Pain comes and goes (1 point)
c. Pain is always present (2 points)
2. In the last 30 days, have you had pain or stiffness in your jaw on awakening?
a. No (0 points)
b. Yes (1 point)
3. In the last 30 days, did the following activities change any pain (that is, make it better or
make it worse) in your jaw or temple area or on either side?
A. Chewing hard or tough food
a. No (0 points)
b. Yes (1 point)
B. Opening your mouth or moving your jaw forward or to the side
a.No (0 points)
b.Yes (1 point)
C. Jaw habits such as holding teeth together, clenching, grinding, or chewing gum
a.No (0 points)
b.Yes (1 point)
D. Other jaw activities such as talking, kissing, or yawning
a. No (0 points)
b. Yes (1 point)
The three-item version includes questions 1 through 3A, threshold value " 2.The six-item
version includes questions 1 through 3D, threshold value " 3.
International Classification for Orofacial Pain

As previously indicated, the first edition of the ICOP was published in January 2020.18
As with the DC/TMD, the ICOP classification was intended as a tool to be used for
both research and clinical settings. The diagnostic criteria developed for ICOP adopted
a similar structure to those present in the ICHD-3 to facilitate its use among different
medical specialties dedicated to the diagnosis and management of head and face
pain. One of the novel contributions of ICOP in the pain-related TMD category is the
consideration of pain frequency. Differentiating between acute and chronic pain is
important for the development of better therapeutic interventions as patients suffering
from chronic pain are managed differently than acute cases. Interestingly, the ICOP
adopted the term myofascial pain to refer to muscle pain, as in the original RDC/TMD
nomenclature. Nevertheless, the distinction between local and referred pain was main-
tained, and specific diagnostic criteria have been proposed for primary chronic myofas-
cial pain with and without a referral. Future research and validity studies will confirm the
relevance of the diagnostic subdivisions proposed by the ICOP.
FUTURE DIRECTIONS
Taxonomy Versus Ontology
For classification systems and diagnostic criteria to be relevant and operational, they
must follow certain principles and methodologies. Historically, nosologic methodology
with taxonomic principles has been implemented.31 However, this approach is limited
by a lack of sensitivity and specificity.32 An alternative approach following ontological
principles has been advocated.33 Taxonomy assigns a label to the pain condition
whereas ontology provides information regarding the pain. However, ontological metrics
have limitations as the criteria introduce new terminology that does not have widespread
acceptance, are only expert-derived and not evidence-based, and are yet to be tested.33
Genetics/Epigenetics
Genetic traits and epigenetic factors involving susceptibility and/or vulnerability to a
particular disease and/or treatment response are important factors to consider in
TMD patients. This is highlighted by an individual’s signs and symptoms as a manifes-
tation of their complex response trait with specific complaints being either amplified or
attenuated by their unique genetic makeup and/or prior life experiences.34 An example
of the influence of genetics occurs in relation to the endogenous mu-opioid system.35
Variations in genotype can result in differences in the synaptic availability of various
neurotransmitters such as catecholamines that influence pain perception and brain
activation.36 Past life experiences may alter an individual’s adaptive response by
modifying the state of the pain-stress response system.37,38 Furthermore, genetic fac-
tors play a role in the etiology of persistent pain conditions by modulating underlying
physiologic and psychological processes.39 Therefore, genetic variants that impact
pain sensitivity and psychological traits when combined with environmental factors
may interact to influence the risk for the development, initiation, and perpetuation of
TMD conditions.40
Neurobiological
The incorporation of neurobiological parameters into future classification systems and
diagnostic criteria would be beneficial as chronic pain patients experience significant
dynamic changes over time.41–44 This is evidenced by the processes of central neural
plasticity as imaging studies have shown alterations in gray-matter volume in chronic
pain45 or as a result of pain relief.46 The influence of central neural information pro-
cessing involving learning and memory are now invoked to better explain and describe
chronic pain’s capability for endurance47 and how these dimensions exert top-down
influences on the rest of physiology.48
Biomarkers
A biomarker is a characteristic that can be objectively measured and evaluated as an
indicator of a normal biological process, a pathologic process, or pharmacologic
(and nonpharmacological) response to a therapeutic intervention.49 In 2016, a joint
FDA-NIH working group (Biomarkers, Endpoints, and other Tools – BEST) identified
seven distinct biomarker categories that could be applied across the whole spectrum
of biological research.50 Candidate biomarkers and potential applicable tests that
should be considered can be categorized by physiologic tests, psychological or behav-
ioral characteristics, use of imaging, and molecular and protein assays.51 Each one of
these modalities has supporting evidence as being used either clinically and/or exper-
imentally for the diagnosis, measurement of burden of disease, or determination of the
prognosis or efficacy of treatment of pain conditions.51 Unfortunately, the current land-
scape for using the predictive value of available biomarkers in diagnosing pain is rather
low51 despite efforts of ongoing research.40,52 It is also unfortunate that other diagnostic
aids, be it laboratory and/or imaging studies, are also largely only research
based.39,53,54 Therefore, the current state of diagnosis remains heavily reliant on patient
self-report making diagnosis of pain conditions as much an art form as a pure science.32
Precision Medicine
Precision medicine, using a P4 approach, incorporates the following: prediction, pre-
vention, personalization, and participation.55 Prediction relates to identifying the
12 Klasser et al
genetic risks for diseases with signs of illness recognized before its manifestation. Pre-
vention involves in providing the individual with the tools to recognize the earliest signs
of the disease when it is most reversible. Personalization focuses on the individualiza-
tion and optimization of wellness by predicting disease and designing personalized in-
terventions for management. Participation facilitates that the individual should be well
informed about their health and better prepared to make their own health care deci-
sions. Incorporating the P4 approach into TMD classification systems and diagnostic
criteria will pave the way for enhanced patient care.
Artificial Intelligence
Artificial intelligence (AI) consists of developing computational systems that can
perform human intelligence tasks to assist with decision-making support.49 AI,
due to its ability to accumulate, analyze and draw inferences from vast amounts
of data is providing a paradigm shift toward precision medicine.56 Within AI is
the concept of machine learning (ML), the process of developing algorithms with
the ability to learn without being explicitly programmed. This approach removes
the “expert” brain from making an interpretation from the accumulated data.49 A
subset of ML is deep learning that involves artificial neural networks adapting
and learning from vast amounts of collected data. AI methods and ML algorithms
will allow for the phenotyping, endotyping, and the selection of management stra-
tegies for TMD. This process will transform the role of practitioners to be the trans-
lator of the technical data for the patient, act as a guide in assisting the patient in
understanding their digital health and be a counselor in navigating through health
care choices.57
In summary, the future is very bright for developing more precise and accurate clas-
sification and diagnostic systems. By incorporating ontological principles involving the
use of genetic traits/epigenetic factors and following neurobiological principles with
biomarkers in addition to the assistance afforded by AI, the potential for following pre-
cision medicine involving pain conditions is within our grasp.
CLINICS CARE POINTS
! Current classification systems for TMD are essential for providing a framework of
information that allow the provision of quality diagnosis and enhanced patient
management. It is important to recognize these systems need to evolve in order to provide
greater patient targeted care.
! Currently, there is a lack of a unique and universal classification of TMD, however, the
classification scheme proposed by the American Academy of Orofacial Pain (AAOP) can be
currently used as a best practices model.
! The current version of the Diagnostic Criteria for Temporomandibular Disorders (DC/TMD)
can be used both for clinical and research purposes as a universally accepted reliable
evidence-based diagnostic system for common temporomandibular disorders.
! The integration and incorporation of ontological principles, genetics /epigenetics
vulnerability factors, neurobiological processes and biomarkers, the concepts of precision
medicine and the application of artificial intelligence will ultimately coalesce and result in a
treatment oriented classification system for TMD.
DISCLOSURE
The authors have nothing to disclose.
Tem p o ro m a n d i b u l a r J o i n t
Review of Anatomy and Clinical Implications
Veronica Iturriaga, DDS, MSc, PhDa,*, Thomas Bornhardt, DDS, MSc

a
,
Nicol Velasquez, DDSb
KEYWORDS
! Temporomandibular joint ! Temporomandibular joint disorders ! Mandibular condyle
! Temporomandibular joint disk ! Synovial membrane ! Masticatory muscles
! Anatomy
KEY POINTS
! Temporomandibular joint (TMJ) is one of the most complex joints of the human being; it
allows the movement of the jaw and with it, the functions of the stomatognathic system.
! TMJ is composed of the mandibular fossa, joint tubercle, and the condylar process of the
mandible, separated by an articular disk.
! TMJ is a synovial joint and is covered by the synovial membrane, responsible for secreting
synovial fluid, which is responsible for joint nutrition, lubrication, and health.
! Both TMJs always work symmetrically supported by four pairs of muscles that create their
movements, known as muscles of mastication.
INTRODUCTION
The masticatory or stomatognathic system has to be understood as a physiologic,

functional, and perfectly defined entity composed of a heterogenous set of organs
and tissue, of which biology and physiopathology are absolutely interdependent.1
Its first sketches belong to chordate amphibians from around 550 million years
ago.2 Later, due to natural selection, the human masticatory system evolved following
a common plan with vertebrate gnathostomes, where we can find two distinct units,
one represented by the cranium and maxilla, and the other being the mandible.2
Both units were derived from the first pharyngeal arch and were composed of an
external osteoderm coating and a cartilaginous internal core.
a
Department of Integral Adult Care Dentistry, Universidad de La Frontera. Francisco Salazar
Avenue 01145, Temuco, Chile; b Temporomandibular Disorder, Orofacial Pain Program, Uni-
versidad de La Frontera. Francisco Salazar Avenue 01145, Temuco, Chile
* Corresponding author. Department of Integral Adult Care Dentistry, Universidad de La Fron-
tera. Francisco Salazar Avenue 01145, Temuco, Chile.

2 Iturriaga et al
In the evolution of the osseous components of the current temporomandibular joint

(TMJ), in the first instance, the primitive square-articular or Meckelian joint was found,
which evolved to become the joint of the incus and the malleus, hence its close
anatomic relationship with the current TMJ. This was followed by the first form of
TMJ called the squamosal dentary joint. This first form of TMJ was composed of two
bones: one called temporal squama, which presented membranous ossification; and
another called dentary bone, which presented endochondral ossification.2,3
Subsequently, a change is generated at the craniofacial level, where three important
events occur: (1) the adoption of an upright posture and bipedalism; (2) increased brain
volume; and (3) modification of the masticatory apparatus. The latter, mainly conceived
by changes in the function of the masticatory system, will generate an increase in the
height of the face and muscular development that will allow the richness of movements
that the system presents and gives way to one of the most complex joints of the organ-
ism.4 For his part, Baune1 postulated that the development of TMJs has a single
embryologic origin from two blastemas, separated in space and time: the condylar blas-
tema and the temporal or glenoid blastema. Unlike the other joints in the body, the TMJ
does not have the development of its two components at the same time. Initially, in the
seventh week of intrauterine life, the condylar component differentiates, while in the
ninth week of intrauterine life, the temporal component differentiates; the final process
culminates at the twenty-first week of gestation. Although the TMJ’s two components
begin their differentiation at different times, they develop in directions that approximate
them. The condylar component does it posteriorly, superiorly, and laterally; while the
temporal component, toward the bottom, anterior and medial.1,3
At the bone level, the TMJ is currently composed of the mandibular fossa (MF) and
the articular tubercle (AT), both belonging to the squamous portion of the temporal
bone; and the condylar process (CP) of the mandible, which includes the mandibular
condyle (MC)5,6 (Figs. 1 and 2). Both bones are separated by an articular disk (AD),
Fig. 1. Localization of the temporomandibular joint (human cadaveric specimen, sagittal

view). TMJ, temporomandibular joint; COP, coronoid process; CP, condylar process; MN,
mandibular notch; MR, mandibular ramus; TMT, temporalis muscle tendon; ZA, zygomatic
arch; Dotted circle, ANT, anterior; INF, inferior; POST, posterior; SUP, superior; TMJ
localization.
Review of Anatomy and Clinical Implications 3
Fig. 2. Temporomandibular joint anatomy components (human cadaveric specimen, sagittal

view). MF, mandibular fossa; AD, articular disk; ANT, anterior; AT, articular tubercle; COP, co-
ronoid process; CP, condylar process; INF, inferior; LPMIH, lateral pterygoid muscle, inferior
head; LPMSH, lateral pterygoid muscle, superior head; MC, mandibular condyle; MN,
mandibular notch; POST, posterior; SUP, superior; TM, temporalis muscle; TMT, temporalis
muscle tendon.
which is formed by fibrous connective tissue with islands of fibrocartilage devoid of

blood vessels or nerve fibers in its center.5 Various ligaments and muscle tissue are
attached to this structure, which will provide stability and movement, respectively.
According to the above, the objective of this article was to review the anatomy of the
TMJ and its adjoining structures from a clinical perspective. First, we review the gen-
eral characteristics of the TMJ, then its bony, cartilaginous, ligamentous, and synovial
components, and finally the muscles that are related to the TMJ.
GENERAL CHARACTERISTICS OF THE TEMPOROMANDIBULAR JOINT
On a sagittal plane, the TMJ is anatomically located in the middle region of the head,
being a union point for the temporal, cranial, and mandibular regions. This joint allows
the movement of the mandible and consequently gives way to all the functions of the
stomatognathic system. On a coronal plane, we can find two TMJs, one on the far right
of the face and one on the far left, sharing the mandibular bone. Because of this, both
TMJs function as a complex, where the movement of one joint will affect the contralat-
eral TMJ. The TMJ presents a mean depth from the skin to the lateral pole of the MC of
approximately 17 mm, with a high correlation between the depth of the right and left
sides. However, no correlation has been found between TMJ depth and age or sex.7
It is important to mention that the complex formed by both TMJ will confront the maxil-
lary bone with the mandibular bone and, therefore, will be related to the occlusion of the
teeth, being linked to the growth and development of these structures throughout life.
The TMJ is classified as a synovial joint, which is characterized by presenting a
space called the articular cavity, which is delimited by an articular capsule (AC). The
AC has a thin membrane that covers its internal portion, which is called synovium or
synovial membrane (SM) and is responsible for secreting synovial fluid (SF). The SF
is responsible for the nutrition, lubrication, and health of the joint.5,8
4 Iturriaga et al
OSSEOUS AND CARTILAGINOUS COMPONENTS OF THE TEMPOROMANDIBULAR

JOINT
Condylar Process and Mandibular Condyle
The TMJ comprises the CP of the mandibular bone and the AT and MF belonging to
the temporal bone. The CP of the mandibular bone belongs to the mandibular ramus
and is a prolongation that extends rostrally from the mandibular notch, passing
through the condylar neck and ending in the MC (see Figs. 1 and 2). The latter repre-
sents the portion that belongs to the TMJ and is defined as an eminence whose major
axis is oriented obliquely posteriorly and medially, approximately 20" to the coronal
plane6; it has a longer ellipsoidal convex shape lateromedially than anteroposteriorly,
approximately 15 to 20 mm and 8 to 10 mm, respectively.6,9 In a sagittal view, the MC
has a posterior and medial direction, and its functional surfaces are represented by its
superior and anterior zone. These features are responsible for the TMJ being classified
as a condylar or ellipsoidal joint.5
Four physiologic condylar shapes have been described which are flat, convex,
angled, and round. According to Yale and colleagues,6 97.1% of all condyles fall
into one of these four groups, with relative frequencies of 27.2% for flat, 43.3% for
convex, 13.4% for angled, and 12.1% for rounded. Alternatively, in a study by Oberg
and colleagues,10 where 102 TMJs of skulls between 20 and 93 years of age were
analyzed, it was observed that from a frontal plane, the most predominant shape
was rounded or slightly convex (55%), followed by the flat shape (20%) and an
inverted "V" shape or other shapes (25%). In clinical practice, we can also find
some alterations in the shape and condylar development, with the bifid shape or bifid
condyle being one of the most frequent anatomic variations. Two possible causes for
the bifid condyle are described; the first one was described by Blackwood (1957),
where it is postulated that the presence of a bifid condyle is associated with
the embryologic maintenance or preservation of a fibrovascular loop or septum in
the MC, which divides the growth of this in two; usually, these septa are present in
the condylar cartilage until week 20 of the embryonic development. The other theory
was presented by Thomason and Yusuf, which describes the appearance of the bifid
condyle occurring at a later stage of development associated with trauma and conse-
quent condylar fracture, which would cause a medial or lateral displacement of the
MC, generating growth and adaptation of the fracture trait, transforming into a
pseudo-condyle.11–13 Other alterations that can affect the CP, the temporal bone
components, and the AD are the agenesis, hypoplasia, and hyperplasia of these
tissues.
The MC has a lateral pole and a medial pole. The lateral pole is rough, with a blunt
tip,9 and is linked to the lateral collateral ligament and the lateral ligament (LL)
(formerly called temporomandibular ligament). Instead, the medial pole is smooth
and round and is where the medial collateral ligament is inserted. Also, the condylar
neck is part of the insertion of important ligamentous and muscular structures, and
the AC is inserted around it. On its anteromedial side is the pterygoid fovea, an
anatomic region of clinical importance since a large part of the upper portion of
the lateral pterygoid muscle and all of its lower portions are inserted6 (see Fig. 2).
Similarly, in the lateral area of the CP, fibers of the masseter muscle are inserted
in its deep superior portion, and in the medial area of the CP, fibers of the medial
pterygoid muscle are inserted. Therefore, from a clinical practice point of view,
the TMJ is a meeting point between the different muscles involved in mastication,
which, based on trigeminal motor control, will give way to complex mandibular
movements.
Mandibular Fossa and Articular Tubercule

In the cranial structure, the components of the TMJ correspond to the MF and the AT.
The MF is located in the squamous portion of the temporal bone. It is a concave struc-
ture that, when extended anteriorly, forms a convex structure, which corresponds to
the AT that belongs to the zygomatic process of the temporal bone6 (see Fig. 2). In
this way, the anterior slope of the MF corresponds to the same anatomic place as
the posterior slope of the AT. The MF presents a posterior and medial direction
from a sagittal cut, as does the MC. In the posterosuperior area, it is traversed by
the petrotympanic fissure and the tympanosquamous fissure, which delimit the func-
tional portion of the MF anteriorly. The functional portion of the AT extends up to 5 mm
anterior to its apex. Therefore, it is in these functional zones where the CM moves in
the different mandibular movements. The MF has no bony wall laterally, but this area is
reinforced by the AC and the LL. Unlike the lateral zone, the medial zone of the MF
does present a bony wall, which is related to the medial pole of the MC.
The functional surfaces of the MC, MF, and AT are covered by fibrocartilage, unlike the
other synovial joints, which are covered by hyaline cartilage. These functional surfaces
have thicknesses of approximately 1.5 to 2 mm in the MC and 0.5 to 1 mm in the MF
and AT9,14 (Fig. 3). Fibrocartilage is a tissue rich in collagen fibers associated with carti-
laginous tissue and gives the TMJ a greater capacity to withstand friction during joint
movements and a better repair capacity against adaptive conditions. Fibrocartilage pre-
sents three distinct histologic zones. The first one, often called the superficial, tangential,
or articular area, is the outermost layer and is covered by dense fibrous connective tissue
with type I and type III collagen, with little fibroblast-like cellularity. In this layer, the fibers
are parallel to the surface and are tightly bound to withstand the forces of movement. The
second layer, called the middle, transitional, proliferative or cellular zone, is composed of
undifferentiated cells and spherical chondrocytes in a matrix of proteoglycans, which
gives the articular cartilage the possibility of proliferation, allowing the TMJ to respond
to functional demands and loads. The third layer, called the deep, radial, or cartilaginous
zone, is the thickest of the three layers. It mainly presents lacunae of chondrocytes orga-
nized in isogenic groups with some intertwined type I and III collagen fibers and other fi-
bers in a radial manner; it also presents hypertrophic chondrocytes, although deeper. For
its part, below the fibrocartilage described above is calcified cartilage, which presents
necrotic hypertrophic chondrocytes surrounded by a calcified matrix, which gives way
to the subchondral bone with predominating blood elements in its bone marrow. Fig. 3
shows the different histologic layers and some of their main components.
Articular Disk
The AD is a fibrocartilage structure that lies between the surfaces of the MC, MF, and
AT. From a histologic point of view, the disk is a structure of avascular fibrous cartilage
with a predominance of type I collagen fibers arranged in parallel and chondrocytes
stacked in columns that follow the direction of the collagen fibers. These rows of chon-
drocytes become more abundant and denser toward the peripheral zone of the AD
(see Fig. 3). It has a concave-convex shape toward the upper and lower part, with a
thinner central zone, which thickens toward the periphery (see Fig. 2). Its thicknesses
are 3 mm in the posterior sector, 2 mm in the anterior, and 1 mm in the intermediate
area.9,14 From a sagittal view, the AD has a thick posterior zone that, at rest, will be
linked to the highest part of the MF and the top of the MC. It also presents a middle
zone, which, as mentioned, is the thinnest and, at rest, is linked to the anterior slope
of the MF and the anterosuperior zone of the MC. The anterior part is of intermediate
thickness and is linked, in a state of rest, to the anterior slope of the MF, the AT, and
6 Iturriaga et al
Fig. 3. Temporomandibular joint of rabbit (Oryctolagus cuniculus). (A). Sagittal section of a

general view of the joint, magnification 2.5x. (B). Sagittal section focused on the supradiscal
compartment, articular disk and mandibular fossa, 10x magnification. (C). Sagittal section
focused on the infradiscal compartment, articular disk and mandibular condyle, 10x magni-
fication. AD, articular disk; CC, calcified cartilage; DZ, deep zone; MC, mandibular condyle;
MF, Mandibular fossa; MZ, mid-zone; SM, synovial membrane; SZ, superficial zone; Oval
circle, chondrocytes arranged in clusters parallel to the collagen fibers; Asterisk, collagen
fibers in parallel with each other. Toluidine Blue stain.
the anterior area of the MC. When performing opening, lateral or protrusion move-
ments, the disk will change its location to place its thinner avascular and aneural
medial zone between the functional surfaces of the MF, AT and MC, accompanying
the condyle in its movements. It is important to mention that a large part of the superior
lateral pterygoid muscle head, as well as fibers of the inferior lateral pterygoid muscle
head, are inserted in the anterior area of the AD. From a clinical perspective, there are
some controversies regarding these insertions, suggesting that some disk displace-
ments could be related to this disk-muscular union. However, it has been determined
that the position of the AD depends mainly on its shape, inter-articular pressure, and
lubrication, so this relationship is still under study.
Regarding collateral ligaments, these attach the lateral and medial pole to the AD,
acting as an intermediate bridge, explaining why this structure is called disk and not
meniscus, allowing some movement of the AD during mandibular dynamics. This situa-
tion leads to two virtual spaces, a larger superior or supradiscal joint space, and a smaller
inferior or infradiscal joint space. The superior joint space is traditionally related to the
translation movements of the MC on the MF, and the inferior joint space is related to
condylar rotation movements.9,14 In any case, it is crucial to consider that joint movement
presents a constant roto-translation. In some disk-condylar pathologies, the articular
spaces may be compromised, for example, in disk perforations or displacements, in
which, as a consequence of joint inflammation, edema or effusion may occur. Currently,

with some minimally invasive procedures, treating these spaces more specifically is
possible, resulting in a more personalized therapeutic management of the condition.
LIGAMENTS AND SYNOVIAL MEMBRANE OF THE TEMPOROMANDIBULAR JOINT
The TMJ is surrounded by a connective tissue called AC, which is more fibrous later-
ally and looser medially. The AC is cone shaped. It originates from the zygomatic pro-
cess of the temporal bone, from the tympanosquamosal fissure to in front of the AT in a
superficial plane, and from the base of the spine of the sphenoid bone in a deep plane.
It extends inferiorly and posteriorly, covering the whole TMJ and inserting into the neck
of the MC.4,8,15 The AC acts by resisting forces that try to separate or dislocate the
joint surfaces. It is important to mention that the AC is directly related to the collateral
ligaments; it is even said that these would be an extension of this tissue. It is also
related to the AD, LL, and all muscle attachments found in the area. The inner area
of the AC is lined by a loose connective tissue membrane called SM, which confines
and produces the SF. This membrane has villi and extensions toward the articular cav-
ity, associating with the supradiscal and infradiscal spaces to deliver nutrition, lubrica-
tion, and health to the joint tissues. These folds increase in number with age, as well as
in pathologic processes, mainly inflammatory ones. The SM has two layers, the sub-
intimal, fibrovascular or subsynovial layer, which is attached to the fibrous connective
tissue of the AC and has a network of capillaries with some lymphatic vessels; and the
intimate synovial layer that is related to the articular space, presenting both phago-
cytic or type A synoviocytes, and secretory or type B synoviocytes. Secretory synovio-
cytes are responsible for producing SF, which is a yellowish viscous gel, similar to egg
white, that has regulatory, metabolic, and lubricating functions. The TMJ has two
forms of lubrication: limit lubrication which occurs during mandibular movements,
driving the SF from the margins or synovial recesses to the articular surface; and
exudative lubrication, which occurs in joint compression and decompression move-
ments, making the SF soak the surfaces like a sponge, favoring metabolic exchange.
The SF has a virtual volume of 1 mL and contains various plasma proteins, lipids,
sugars, cellular components, cytokines, growth factors, proteolytic enzymes, lubri-
cating molecules, and others. Of these components, the lubricating molecules stand
out, among which hyaluronic acid and lubricin are the main ones.16 Using these ele-
ments is how some currently used therapies seek to restore joint health in inflamma-
tory processes or osteoarthritis by supplementing exogenous hyaluronic acid,
promoting visco-induction, viscosupplementation and immunomodulation.
Similarly, if we continue with the ligamentous components, we find the LL, whose
function is to reinforce the lateral area of the TMJ. The LL is a fibrous connective tissue
structure that is traditionally divided into two portions: (1) a deep, short, horizontal
portion running from the AT to the lateral pole of the MC; and (2) a more extensive
and superficial oblique portion, which goes from the zygomatic arch downwards
and posteriorly to be inserted in the posterior part of the condylar neck and mandibular
ramus. Some authors also describe a medial or internal temporomandibular ligament,
which would extend obliquely from the spine of the sphenoid to the neck of the MC;
however, its description is scarce.15 Another intrinsic ligament of great importance
is the posterior ligament or bilaminar zone, previously called retrodiscal tissue. This
structure has elastic fibers in its upper part that join the AD with the posterior part
of the MF, and collagen fibers in its lower part that join the disk to the condylar
neck. Both fibers form something similar to a cushion, which is related to the posterior
part of the AC, which would be an entry point for vascular and neural tissues.
8 Iturriaga et al
MAIN MUSCLE COMPONENTS RELATED TO THE TEMPOROMANDIBULAR JOINT
Like any other type of joint, the TMJ itself cannot make movements; therefore, for the
TMJ to move, it needs the action of associated muscles. These muscles are called
masticatory muscles, one of the main muscle groups of the head. Masticatory mus-
cles are four pairs that work in a coordinated manner to produce mandibular move-
ment17 and correspond to the masseter, temporalis, medial pterygoid, and lateral
pterygoid muscles.
Embryologically, masticatory muscles develop from the first pharyngeal arch or
mandibular arch, together with the mandibular cartilage (or Meckel’s) and the trigem-
inal nerve. Therefore, masticatory muscles are motor innervated by one of the
branches of the trigeminal nerve, specifically the anterior trunk of the mandibular
nerve. Furthermore, they are mainly supplied by branches of the maxillary artery.
They are all paired muscles located on each side of the head, and from their origin,
they extend to be inserted into the rami of the mandible to produce all mandibular
movements in conjunction with the TMJ complex.9,17
The primary masticatory muscle is the masseter, and it is the most superficial and
palpable. It is rectangular and elongated from superior to inferior, occupying the thick-
ness of an anatomic region known as the masseteric region. Two portions form it; a su-
perficial fascicle, whose fibers have a descending and slightly oblique course toward the
back, and a deep fascicle, formed by vertical fibers (Fig. 4). Some authors describe the
presence of three fascicles: one superficial, another deep, and another intermediate.17 It
originates from the lower border and the anterior two-thirds of the zygomatic arch. Its
Fig. 4. Masticatory muscles (human cadaveric specimen, sagittal view). ANT, anterior; INF,
inferior; MMPF, masseter fasciculus profundus muscle; MMSF, masseter fasciculus superficialis
muscle; POST, posterior; SUP, superior; TM, temporalis muscle; TMT, temporalis muscle
tendon.
fibers converge inferiorly to insert on the outer face of the ramus of the mandible and the
mandibular angle. When this muscle contracts, it causes a robust elevation of the jaw,
and the teeth come into contact; In addition, the superficial fascicle, due to the direction
of its fibers, is related to the mandibular protrusive movements.9,17,18
Similarly, the temporalis muscle is a flat, radiated, fan-shaped muscle with anterior
fibers that are vertically oriented, middle fibers that are obliquely oriented, and poste-
rior fibers that are somewhat horizontally oriented. Its origin is in the temporal fossa of
the skull and the deep surface of the temporal fascia, at the level of the inferior tem-
poral line. The muscle fibers converge inferiorly, forming a tendon that emerges
from the temporal fossa, passes inferior to the zygomatic arch, and inserts into the
coronoid process, anterior border of the mandibular ramus, as well as the medial
and lateral borders of the retromolar fossa.17,19 (see Fig. 4). The anterior and middle
fibers of the temporalis muscle are used to elevate the mandible, and the posterior fi-
bers produce mandibular retrusion. In mandibular closure, this muscle is considered
an important stabilizer of movement.
The medial pterygoid muscle is a thick, rectangular muscle parallel to the masseter
muscle, but positioned on the inner face of the mandible. It originates at the pterygoid
fossa level located in the sphenoid bone’s pterygoid processes. Its muscular body is
oblique downwards, posteriorly, and laterally, inserting into the inner side of the mandib-
ular angle and ramus.17 This muscle and the masseter muscle form a muscular sling
around the inferior border and angle of the mandible, thus working together for mandib-
ular elevation and protrusion. This muscle also participates in lateral movements, where
unilateral contraction will produce a mandibular mediotrusion movement.
Lastly, the lateral pterygoid muscle is the primary muscle of the infratemporal fossa.
It comprises two portions: an upper head and a lower head. On the one hand, the su-
perior head is considerably smaller than the inferior head, originating from the infra-
temporal surface of the greater wing of the sphenoid bone; it extends almost
horizontally, posteriorly, and laterally until its insertion in the AC, AD, and condylar
neck.17 Regarding the percentage of fibers that are inserted into the AD, it has been
established mainly by histologic techniques and magnetic resonance imaging that
the percentages of insertion vary from 29.5% to 69.3%.20 On the other hand, the infe-
rior head of lateral pterygoid muscle originates on the outer face of the external wing of
the pterygoid process and extends posteriorly, superiorly, and laterally to insert into
the pterygoid fovea on the condylar neck. When the inferior bundles contract bilater-
ally, the MCs are tractioned by them, sliding anteriorly and inferiorly across the ATs,
producing protrusion of the mandible. If to this movement is added the effect of the
mandibular depressor muscles, mandibular descent or opening will be generated.
Unilateral contraction creates lateral movement of the mandible to the opposite
side. When the lower bundle acts during the opening, the upper head remains inactive,
only coming into action in conjunction with the levator muscles.
As described, the TMJs always work symmetrically, supported by these four pairs of
muscles that create their movements. When the TMJs work properly, the different
movements can be performed without pain or discomfort. However, the mandibular
movements can be affected when the TMJ presents some pathology. In the same
way, the muscles can perceive some joint alteration, producing a protective co-
contraction and even the maintenance of this and subsequent muscular pathology.
SUMMARY
The TMJ is one of the most important and complex joints in the human being. Each is
located at one end of the face: however, both work as morpho-functional sets. In this
10 Iturriaga et al
way, the anatomy of the TMJ and its associated structures will influence the mandi-
ble’s dynamics and function, so an alteration of its components can cause deteriora-
tion of the system and subsequent disease. Knowledge of the normal anatomy is
fundamental for the clinical approach, allowing differentiation between the healthy
and the sick.
CLINICS CARE POINTS
TMJ is anatomically located in the middle region of the head in sagittal view, being a union
point for the temporal, cranial, and mandibular regions. Is composed of the MF, AT, and CP of
the mandible, separated by an articular disk. TMJ allows the movement of the mandible and
consequently gives way to all the functions of the stomatognathic system.
Articular disk has a thick posterior zone that, at rest, is linked to the highest part of the MF and
the top of the MC. Also presents a middle zone, which is the thinnest and, at rest, is linked to
the anterior slope of the MF and the anterosuperior zone of the MC. During movements, the
disk will change its location to place its thinner avascular and aneural medial zone between the
functional surfaces of the MF, AT, and MC, accompanying the condyle in its movements.
The TMJ is classified as a synovial joint, composed of an AC and an SM that is responsible for
secreting SF. SF is synthesized by synoviocytes and is composed of various molecules among
which lubricating molecules such as hyaluronic acid and lubricin stand out. Thus, SF is
responsible for the nutrition, lubrication, and health of the joint.
TMJs always work symmetrically, supported by these four pairs of muscles that create their
movements. Because of this, both TMJs function as a complex, where the movement of one
joint will affect the contralateral TMJ. When the TMJs work properly, the different movements
can be performed without pain or discomfort, but the mandibular movements can be affected
when the TMJ presents some pathology.
DISCLOSURE
All authors contributed to the conception and design of the study, drafting the article,
critically revising the manuscript for important intellectual content, and giving final
approval and agreeing to be accountable for all aspects of this work.
Role of the funding source: The study was financed by Project DI20-0018 and the
Temporomandibular Disorder and Orofacial Pain Program, Universidad de La Fron-
tera, Chile.
Conflict of interest: The authors declare that they have no conflict of interest.
REFERENCES
1. Mejia C, Salazar L. Desarrollo ontogénico de la articulación temporomandibular

durante el perı́odo fetal. Rev Estomat 1996;72:15–26.
2. Gonzáles H. Origen y evolución del sistema estomatognático. In: Manns A, edi-
tor. Sistema Estomatognático. Bases biológicas y correlaciones clı́nicas. 1th Edi-
tion. Madrid: Ripano S.A.; 2011. p. 55–67.
3. Quijano Y. Anatomı́a clı́nica de la articulación temporomandibular. Morfolia 2011;
3:23–33.
4. Okeson J. Management of temporomandibular disorders and occlusion. 7th Edi-
tion. Barcelona: Elsevier; 2013. p. 7–14.
5. Vasconcellos H, Sousa E, Cavalcante M. Temporomandibular joint classification:
functional and anatomic aspects. Int J Odontostomat 2007;1:25–8.
D i s o rd e r C o m o r b i d i t i e s
Davis C. Thomas, BDS, DDS, MSD, MSc Med, MSca,b,*, Junad Khan, MSD, MPH, PhD
c
,
Daniele Manfredini, DDS, PhDd, Jessica Ailani, MD, FAHSe
KEYWORDS
! Temporomandibular joint disorder ! Temporomandibular joint ! Comorbidities
! Headaches
KEY POINTS
! The comorbidities that affect temporomandibular joint disorder (TMD) pain are crucial for
the treating physician to bring about effective management of TMD pain.
! In the absence of delineation of the comorbidities that may condition the patient’s expe-
rience of TMD pain, the clinician-patient team may most likely encounter the problem of
suboptimal management of pain.
! A complete discussion of the numerous comorbidities that affect TMD pain experience is
beyond the scope of any manuscript. It is up to pain education programs and individual
clinicians to educate the medical community regarding the significance of managing
TMD pain through effective management of the comorbidities.
! The discovery of comorbidities in a patient suffering from TMD and TMD pain may neces-
sitate a multidisciplinary approach of management involving more than 1 medical
specialty.
! Any clinician attempting to manage TMD and TMD pain must be familiar with the possibil-
ity of one or more comorbidities that may profoundly affect the patient’s experience of
pain.
INTRODUCTION
Comorbidity is largely defined in medical literature as a specific additional condition that

exists as temporally related to the condition being explored.1,2 Temporomandibular joint
disorders (TMDs) have been shown to have associations with several comorbidities,
a
Department of Diagnostic Sciences, Rutgers School of Dental Medicine, 110 Bergen Street,
Newark, NJ 07103, USA; b Eastman Institute of Oral Health, Rochester, NY, USA; c Department
of Orofacial Pain and TMJ Disorders, Eastman Institute for Oral Health, 2400 South Clinton
Avenue, Building H, Suite #125, Rochester, NY 14618, USA; d Department of Biomedical
Technologies, School of Dentistry, University of Siena, Viale Bracci - 53100 Siena, Italy;
e
Georgetown Headache Center, Strategic Planning Neurology, Medstar Georgetown Univer-
sity Hospital 3800 Reservoir Road. NW, Washington, DC 20007, USA

0011-8532/22/ª 2022 Published by Elsevier Inc.
2 Thomas et al
including, but not limited to, headaches, hypermobility syndromes, fibromyalgia, anxi-
ety/depression, and sleep disorders. Some of the comorbidities, such as hypermobility
syndromes, may have a predisposition to many of the TMD symptoms. A sound knowl-
edge about these comorbidities may be crucial in executing the best management mo-
dalities for TMDs. For example, management of TMDs using an antidepressant drug
such as low-dose amitriptyline may inherently help in the management of comorbid anx-
iety, depression, and fibromyalgia (FM). Screening for possible comorbidities such as
anxiety/depression and sleep disorders may even prove to be a lifesaver for these pa-
tients. A TMD patient being screened for the possibility of a systemic factor such as ane-
mia, vitamin deficiencies, nutritional deficiencies, or lack of sleep, may be instrumental
in shedding light on the factors conditioning the experience of TMD pain. It must be
noted that, because of the multitude of comorbidities that can probably associate
with TMD, a comprehensive discussion of the topics is beyond the purview of a single
article. The authors encourage readers to refer to the cited articles for additional infor-
mation. A recent systematic review showed a significant association of comorbid other
chronic pain conditions among patients who were diagnosed with TMD.3 These
included chronic migraine, fibromyalgia, and myofascial syndrome.
HEADACHES
Patients who have been diagnosed with TMD are more likely to have associated
chronic pain disorders such as chronic migraine, inflammatory bowel syndrome
(IBS), FM, and myofascial pain.3–6 Chronic migraine appears to be 8 times more com-
mon in patients diagnosed with TMDs than in the general population.3,7,8 The Orofacial
Pain Prospective Evaluation and Risk Assessment study found that headache was a
more common symptom in patients with a painful TMD compared with other chronic
overlapping pain conditions such as FM, IBS, and low back pain.3,5,9,10 Studies have
found a positive correlation between painful TMD and migraine, but not between TMD
and probable tension type headache (TTH) 30936004.7 However, other studies have
shown an association between TMD and TTH.11,12 Headaches in general, and
migraine in particular, have shown to indicate a higher likelihood of developing
TMD. The prevalence and frequency of headaches increase over time in patients
who develop TMD.11 Migraine is widespread in TMD patients with a prevalence/inci-
dence rate of approximately 25% to 50%,10,13–15 and it is linked to greater physical
and psychosocial distress.13,16–19
Migraine is common in women between the ages of 20 to 40, and involves activation
of the trigeminal nerve, which triggers pain, along with a host of associated symp-
toms.20 TMD is also a common disabling disorder seen more often in women between
the ages of 20 to 40, involving the activation of the trigeminal nerve and frequently co-
morbid with primary headache disorders.21 Migraine patients have approximately 8
times the risk of developing severe TMD as patients without migraine as a comorbid-
ity.13,14,22 Moreover, there is an association between headache frequency and the
duration and intensity of TMD pain.13,23 Migraine patients with TMDs show more cen-
tral sensitization symptoms than those without TMD.24 The central sensitization in
migraine can be explained by (among others) the action of calcitonin gene-related
peptide (CGRP).7,25
Headache secondary to TMD is not well described in the literature,21 and is consid-
ered a secondary headache disorder.26 The International Classification of Headache
Disorders (ICHD3) defines headache attributed to TMD as only rarely occurring as a
sole feature of TMD. The full criteria are listed in Box 1. The overall prevalence of head-
ache in the TMD population is approximately 60%, with migraine being the most
TMD Comorbidities 3
Box 1
International Classification of Headache Disorders Criteria for headache attributed to
temporomandibular joint disorders
A. Any headache fulfilling criteria

B. Clinical evidence of a painful pathologic process affecting elements of the
temporomandibular joint(s), muscles of mastication, and/or associated structures on one
or both sides
C. Evidence of causation demonstrated by at least 2 of the following:
1. The headache has developed in temporal relation to the onset of the
temporomandibular disorder, or led to its discovery
2. The headache is aggravated by jaw motion, jaw function (eg, chewing) and/or jaw
parafunction (eg, bruxism)
3. The headache is provoked on physical examination by temporalis muscle palpation
and/or passive movement of the jaw
4. Usually temporally located (one or both sides)
D. Not better accounted for by another ICHD-3 diagnosis
common, affecting approximately 40% of the people. The second most common
associated headache is tension-type headache (approximately 19%).27–30 The preva-
lence of TMD in the headache population based on a meta-analysis of published
studies was 59.42%.31 Those with painful-TMD had a higher prevalence of headache
at 82.80%, again with migraine being the more common headache. TMD is common in
those with primary headache disorders, especially migraine and TTH. People with
TMD are twice as likely to have chronic daily headaches with or without migraine.31
The more severe the TMD, the more severe the migraine31
Having both TMD and migraine leads to a significantly greater disability; therefore
effective treatment should focus on treating both disorders when they are present.20
Treating TMD and migraine simultaneously can also improve the therapeutic response
for each individual disorder.21 A multidisciplinary approach is often best in these pa-
tient groups. Treatment of TMD starts with patient education and conservative mea-
sures. Rest of the jaw and avoiding eating hard, chewy foods, or chewing gum are
important. Management of concomitant clenching and grinding should be discussed
with patients with TMD as well.20 Physical therapy is a simple, noninvasive option that
can be added to education as a first-line treatment for patients with TMD. Heat or ice
to the painful area, self-massage, and range-of-motion exercises can all reduce pain
and improve function.32 If this is only partially effective, a course of physical therapy for
active relaxation exercises, passive stretching, deep massage, ultrasound and
acupressure, electrical stimulation, transcutaneous electrical nerve stimulation, and
myofascial release have been shown to be effective.33 Jaw appliances, known as
splints, night guards, bite guards, or stabilization appliances, have shown some evi-
dence to be helpful when used appropriately in people with TMD. A systematic review
has shown good evidence for single-arch, hard, full-coverage stabilization appliances
for the treatment of TMD pain.34 When adjusted properly, these can have a modest
effect in the treatment of pain. When splints are used inappropriately, they can cause
complications such as misalignment of teeth and occlusal alterations.20 As stress and
anxiety can trigger or worsen TMD, addressing the psychological impact of pain can
improve outcomes.35 There are many ways this can be addressed. Cognitive behav-
ioral therapy can improve anxiety and can be done in person, via telehealth, or using
pain psychology-specific applications. If TMD pain continues despite conservative
measures, medications can be added to improve symptoms. Oral medications for
4 Thomas et al
TMD pain include nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxants,

and tricyclic antidepressants in cases of chronic disease and in those with associated
headache.20 Medications should be used for a prescribed interval of time and not
indefinitely to avoid adverse events.20 Medications employed to manage headaches
(including NSAIDs and beta blockers) are by default the same ones used to manage
TMD symptoms and other TMD-associated comorbidities. The TMD clinician may
want to consider ancillary diagnostic modalities including serologic testing in the
work-up of the comorbidities that may underlie TMD and TMD pain.
TMD and migraine share the same nociceptive system, the trigeminal nerve. Once
activated, the trigeminal nerve carries its signals through the trigeminocervical com-
plex, converging on the trigeminal nucleus caudalis, the central pathway of pain mod-
ulation to the thalamus.20 People with TMD and migraine are also more prone to
develop allodynia, a sign of central sensitization. This can be seen during attacks of
migraine and also between migraine attacks. Studies show allodynia is present in
86.9% of comorbid myofascial TMD and migraine, but only in 40% of those with
migraine alone.36 Both diseases may share a similar genetic basis.21 Headaches
that are comorbid with TMD significantly lower the quality of life for these patients.
Optimal management of TMD and TMD pain must include diagnosis and appropriate
management of the comorbid headache entities.
LOWER BACK PAIN
There is an abundance of literature showing significant association between LBP and

TMDs.37–41 Lower back pain (LBP) has been shown to have higher risk of association
with TMDs, and considered a contributing factor in the onset of TMD.37 Some recent
articles have placed a high association between TMD and LBP.9 Approximately two-
thirds of TMD patients reported LBP in a recent large cohort study.37,38 Other articles
have described LBP as a comorbidity with musculoskeletal disorders of the face and
jaw.37,41 Recent study also reported that when LBP became chronic, TMD symptoms
became more clinically positive.37 A prospective study found a greater prevalence of
TMD in patients with history of LBP (approximately 50%), compared to subjects with
no such history.42 Considerable overlap of symptoms were found with fibromyalgia,
TMD, and LBP.9 The TMD clinician must ask the patient about pain elsewhere in the
body, specifically LBP.
MYOFASCIAL PAIN
Association of pain outside the head and face with TMD and TMD-associated pain has
been shown in the early pain literature.43 Masticatory muscle disorders (MMDs) have
been found to be the most prevalent (approximately 45%) in the TMD population, as
opposed to much lesser prevalence of the same in the general population (approxi-
mately 10%).44,45 According to the Research Diagnostic Criteria for Temporomandib-
ular Disorders (RDC-TMD)/Diagnostic Criteria for Temporomandibular Disorders
(DC-TMD), myofascial pain with referral is subclassified under “myogenous
TMD.”46,47 Serologic testing has been suggested in an attempt to delineate the
comorbidities that exist with TMDs.44 A high prevalence of myofascial syndrome
was found in patients diagnosed with TMD.3
ANXIETY AND DEPRESSION
The association between TMD and such psychological comorbidities as anxiety and
depression is well documented in the recent literature.48–51 The National Institute of
TMD Comorbidities 5
Neurologic Disorders and Stroke (NINDS) has classified TMD under “chronic overlap-
ping pain conditions.”52 Another psychological entity that is comorbid with TMD is
post-traumatic stress disorder (PTSD).53 The recent literature of these associated
comorbidities is so robust that it prompted inclusion of psychosocial factors to predict
TMD incidence, and to identify TMD subgroups as per psychosocial and biological
characteristics.48,54 In musculoskeletal disorders such as TMD, there is an increased
level of proinflammatory cytokines, which, in turn, has correlation with depression and
stress.52,55 TMD and psychological factors as comorbid conditions in children and ad-
olescents have been a subject of discussion in the recent literature,56–60 with a trend
toward higher anxiety and depression in this population.61 A mechanistic explanation
of the association of depression and anxiety as comorbidities of TMDs is only evolving
in the current literature. The role of neurotransmitters common to pain and depression
has been proposed. Serotonin, and its role in TMDs, depression, and central and pe-
ripheral sensitizations, has been seen as one of the possible mechanisms of this as-
sociation.62,63 Another plausible explanation is genetic association between TMDs,
depression and anxiety. Systemic inflammation involving a higher level of proinflam-
matory cytokines has been proposed to have an effect on neurotransmitter systems,
thereby bringing about such behavioral changes as anhedonia, anxiety, and depres-
sion.64 The same literature has also shown that these proinflammatory agents
adversely affect the synthesis and function of monoamines such as serotonin, dopa-
mine, and norepinephrine. Consequently, a management program that may consis-
tently target and reduce systemic inflammation may in turn be more beneficial for
optimal pain management for TMD patients. This has led to the popular proposal of
using NSAIDs for the management of TMDs with concomitant depression and anxiety.
The clinician attempting to manage TMD pain must be aware of the strong association
of TMD with comorbid psychological conditions such as anxiety and depression, and
make the appropriate referrals for effective optimal pain management.
FIBROMYALGIA
Fibromyalgia (FM) has been traditionally seen in the literature as a poster child for cen-
tral sensitization pain syndromes. Orofacial pain in general, and TMD in particular,
have been known to be of high prevalence in FM subjects.9,65–68 The reported asso-
ciation of FM with TMDs was more with the younger group of patients; older age was
found to be more associated with LBP.9,37 Other recent studies have shown a strong
independent association of TMD with FM and other chronic pain syndromes.4 Studies
have shown an approximately 3 to 5 times greater prevalence of FM in TMD patients
compared with the general population.3,69–71 The pharmacologic therapy for FM is
similar to that of TMD-associated pain as to the drug classes used. Dysregulation of
adrenergic function has been shown in FM and TMD, with altered catecholamine
levels compared with normal controls.72 These findings have led to the use of beta
blockers such as propranolol in low doses for management of FM and TMDs. Also
to be noted is the use of low doses of antidepressants for the management of FM, co-
morbid depression, and TMDs.
IRRITABLE BOWEL SYNDROME
Chronic TMD is considered among functional pain syndromes including FM, IBS, and
chronic fatigue syndrome (CFS). This is even more true of myofascial TMD.73,74 There
have been several studies associating IBS with TMDs.75 In a large cohort of a wide age
range (18–65 years) of patients with IBS, the risk of having TMD was more than 3 times
that of a healthy control group.76 One study had reported a weak association between
6 Thomas et al
TMD and IBS.77 A greater risk of IBS has also been shown in TMD patients, and also
was observed a more severe form of IBS in TMD patients, compared with healthy con-
trols.75 Somatic and depressive symptoms were found to be more prevalent with TMD
and IBS.78 Reduced descending/endogenous pain modulation was found in IBS and
TMD patients.79 In view of the mounting evidence of association between IBS and
TMD, the treating physician should include a history and/or symptoms of IBS in
TMD patients with a higher suspicion of IBS.
CHRONIC FATIGUE SYNDROME
CFS has been shown to be associated with increased intensity and duration of TMD
pain.13 TMD patients presenting with myofascial pain have higher prevalence of self-
reported CFS, than those with nonmyofascial TMD.80 TMD has been shown to not only
coexist with CFS and FM, but to share symptomatology also. There is increasing ev-
idence that these three, and other entities, may have similar pathophysiologic mech-
anisms.74 A recent systematic review exploring TMD and CFS as comorbidities
suggested a potential high overlap between the 2 conditions, stressing the need for
rigorous studies for assessment of this relationship.81
STOMACH PAIN
One of the interesting TMD pain associations the authors found was stomach pain.
Multiple studies spanning across age, gender, and ethnicity showed an association
of TMD pain and stomach pain.82,83 However, some studies have shown negligible84
or weak85 association between the 2 entities. Frequent stomach pain was related to
long-term TMD, and it was the only comorbidity considerably more frequent in long-
term TMD patients compared with short-term TMD patients.86 An association of
TMD pain, preterm birth, and stomach pain was also shown.82 In a large cohort of
stomach pain patients with age ranges 25 to 75, approximately 60% reported occa-
sional TMD pain, and 57% reported having chronic TMD pain.87 The clinician manag-
ing TMD and TMD pain, once again, needs to enquire about other bodily pains
including stomach pain.
VULVODYNIA
Orofacial pain conditions including TMD was found to be common in women with vul-
vodynia and vestibulodynia,88 leading to the suggestion that there may be common
mechanisms mediating these conditions.89 Other studies on women with vulvodynia
showed moderate to strong association of TMD with this entity, as well as other co-
morbid conditions such as FM and IBS.90–92
SLEEP DISORDERS
Sleep disorders including insomnia, obstructive sleep apnea (OSA), and sleep-
related bruxism (SRB), have been explored for associations with TMD and TMD
pain. A long-term large cohort study recently showed that primary sleep disorders
are independent risk factors for both in the initiation and in the maintenance of
TMD and TMD pain.93 Approximately 90% of TMD patients have been shown to
have some comorbid sleep disorders.94–96 The prevalence of TMD has been pro-
posed to be higher in patients with OSA compared with the general population.97,98
This same literature also shows that TMD-related pain, craniofacial pain, and extrao-
ral pain, show higher prevalence in OSA patients. Further, OSA is considered a co-
morbidity for TMD and craniofacial pain.97 OSA has further been shown to be
TMD Comorbidities 7
associated with chronic pain disorders including TMD.99,100 OSA patients have been
shown to be more likely to present first-onset TMD.94,99 The spectrum of TMD as
associated with sleep disorders, CFS, and FM has also been proposed.74 Poor sleep
quality is reported in most TMD patients.93,96,101 There is mounting evidence of sleep
disturbances acting as an etiologic factor in the development and pathogenesis of
TMDs.80,93,102
Insomnia has shown to be of a high prevalence in chronic pain,103,104 and changes
in insomnia symptom and severity are associated with similar changes in the pain
experience of the TMD patient.103 Further, insomnia and related short sleep duration
have been shown to be associated with more severe clinical TMD pain profile.105
MANAGEMENT OF TEMPOROMANDIBULAR JOINT DISORDERS WITH

COMORBIDITIES
Comorbidities should be addressed in an attempt to manage TMD and TMD-

related pain. TMD patients should be evaluated for headaches in general, and
migraine and TTH in particular.106 A recently published randomized controlled trial
study showed the efficacy of propranolol in reducing TMD pain to be more in
migraine sufferers than in nonmigraine sufferers, and the mechanism of this was
reduction in the heart rate.107 The European Alliance of Associations for Rheuma-
tology (EULAR) guidelines recommend the use of nonpharmacological treatment
for central sensitization syndromes such as FM.108 There are also several manage-
ment modalities that have also shown efficacy in TMD and TMD pain.109 Biofeed-
back and cognitive behavioral therapies (CBT) have been shown to improve coping
skills in TMD pain and are well accepted by patients.110 Other studies have shown
that CBT and biofeedback employing surface electromyographic training of the
masticatory muscles are also efficacious in TMD pain management.111 On the con-
trary, a systematic review had shown that there is insufficient evidence to firmly
recommend the use of CBT in the management of TMD.112 However, when CBT
was combined with pharmacologic therapy, it yielded superior results in pain
reduction, improvement of depression, and improvement of quality of life in chronic
TMD patients.113 Pharmacologically, TMD and TMD pain are managed with several
classes of medications including, but not limited to NSAIDs, steroids, skeletal mus-
cle relaxants, antidepressants, and anticonvulsants.114 The comorbidities that are
discussed in this article should be managed using a multidisciplinary referral
method for optimal TMD pain management.115,116 Alternative health care modal-
ities such as acupuncture have shown modest to good efficacy in managing
TMD pain.115,117,118
CLINICAL PEARLS
Several comorbidities have been shown to exist with TMD and TMD pain. These
include, but are not limited to headaches, anxiety, depression, IBS, CFS and FM, sleep
disorders, vulvodynia, stomach pain, and LBP. The astute clinician attempting to
manage TMD and TMD pain must be well versed with the latest in the literature
regarding the association and correlation of comorbidities of TMD. Management phi-
losophies that do not take these into consideration may be narrow and insufficient in
achieving optimal pain control in TMD patients. It behooves the clinician to screen for
these known comorbidities, order succinct laboratory tests, and make prompt refer-
rals to appropriate specialists and pain management physicians, facilitating a holistic,
multidisciplinary management approach. This in turn results in efficient pain manage-
ment for the patient.
Imaging
a, b
Steven R. Singer, DDS *, Mel Mupparapu, DMD, MDS, Dipl ABOMR
KEYWORDS
! Imaging ! TMJ ! Panoramic ! Cone-beam computed tomography ! MRI
! Arthrography
KEY POINTS
! Radiographic examinations are individually prescribed.
! Imaging is selected based on complaint, anamnesis, and clinical findings.
! There is no single ideal imaging study for temporomandibular disorders (TMDs).
! Oral and maxillofacial radiologists can aid in reaching an accurate diagnosis of TMDs.
INTRODUCTION
The temporomandibular joints (TMJs) form the articulation between the cranium and
the mandible. The osseous components include the mandibular condyles and the
temporal bones. The articulation consists of 2 synovial joints, which enclose articular
discs of dense, fibrous, connective tissue. They are classified as a hinge joint with a
movable socket.
The first and foremost question that should be answered is “Why are we imaging
this anatomy?” In general, we image to confirm clinically suspected disorders, dis-
ease, and other pathologic entities. Further, properly selected imaging can yield infor-
mation such as the location and type of lesion, extent of change to the normal
structures, and ultimately lead to improved management of disease.
Basic rules of radiographic selection criteria apply to TMJ imaging. Radiographs, as
well as nonionizing radiation-based imaging examinations, are selected based on pa-
tient complaint and history, findings from clinical examination, and patient’s medical
history. Once this information is gathered, a clinical diagnosis is formulated, and an
imaging study may be prescribed. Because the TMJ is composed of both calcified
and noncalcified tissues, each type of tissue needs its own specialized imaging.
a
Department of Diagnostic Sciences, Rutgers School of Dental Medicine, 110 Bergen Street,
Room D885A, Newark, NJ 07103-2400, USA; b University of Pennsylvania School of Dental
Medicine, Philadelphia, PA, USA

2 Singer & Mupparapu
Further, radiation safety, including concepts such as ALARA (as low as reasonably
achievable) and ALADA-IP (as low as diagnostically acceptable being indication-
oriented and patient-specific)1,2 should be applied. In general, imaging studies should
be limited to region of interest (ROI) and use the lowest dose of ionizing radiation possible,
based on the available equipment. For example, many newer panoramic machines can
provide excellent quality 4-view TMJ studies while limiting exposure to other regions of
the orofacial structures. In the same vein, limited field of view (FOV) cone-beam
computed tomography (CBCT) scans should be considered rather than large FOV scans.
Because CBCT examinations deliver a higher dose of ionizing radiation to the patient, the
potential benefit versus potential harm needs to be more carefully examined.
Imaging modalities that are used in TMJ studies include panoramic imaging, plain
film, arthrography, computed tomography, and MRI.
It should be stated that the prescriber is responsible for interpretation of the entire
imaging study and not just the ROI. MRI studies are typically done at imaging centers
and the attending radiologist will return the study with a report, whereas reporting in-
office imaging studies are the responsibility of the prescriber. Oral and maxillofacial
radiologists are able to assist in providing radiology reports for panoramic, CBCT,
MRI, and other imaging studies of the TMJs.3
The most common disabling condition affecting the TMJ is rheumatoid arthritis (RA).
Based on the American College of Rheumatology/European League Against Rheuma-
tism criteria for the diagnosis of RA.4 TMJ RA diagnosis in the absence of any other joint
involvement in the body can only be made if it is bilateral and the following criteria are met:
1. Abnormal C-reactive protein and erythrocyte sedimentation rates
2. Low-positive or high-positive rheumatoid factor and anticitrullinated protein
antibodies
3. Duration of symptoms is approximately 6 weeks or greater.
The radiographic diagnosis forms a key role in the assessment of TMJ RA (Figs. 1
and 2). TMJ is involved in approximately 50% of cases with rheumatoid diseases such
as RA, ankylosing spondylitis, and psoriatic arthritis.4–8
Fig. 1. CBCT axial, sagittal, and coronal projections of the right TMJ demonstrating signifi-
cant changes to the joints over time secondary to RA. Note the concomitant presence of sub-
chondral cysts in the coronal slice from September 2011. (Images courtesy of Dr. E. Eliav,
Rochester, NY.)
TMJ Imaging 3
Fig. 2. CBCT axial, sagittal, and coronal projections of the left TMJ demonstrating significant
changes to the joints over time secondary to RA. (Images courtesy of Dr. E. Eliav, Rochester,
NY.)
Imaging the TMJ allows clinicians to evaluate the integrity and relationships of the
TMJ osseous components and soft tissue. The choice of TMJ imaging depends on
several factors such as radiation dose, cost, availability, diagnostic information pro-
vided, and whether hard or soft tissue is imaged.8 When diagnosing TMD, hard tissues
are the first to be evaluated. Osseous contours, positional relationship of the condyle
and glenoid fossa and range of motion are assessed.5 Soft tissue imaging offers infor-
mation about disk position and morphology, as well as abnormalities surrounding the
muscle and soft tissue.9
PANORAMIC IMAGING
Panoramic images are curved surface tomograms. They provide broad coverage of
the orofacial structures at a relatively low dose of ionizing radiation and a minimum
of discomfort for the patient. Although there is variation based on the specifics of
the imaging systems used, it is reported that the effective dose for a single periapical
radiograph is approximately 0.001 and 0.007 mSv for a standard panoramic radio-
graph.10 The dose for a 4-view TMJ tomographic images may be lower (Figs. 3 and
4). Panoramic imaging of the joints allows for sagittal projections of the joints with
an adequate resolution for detecting anatomic changes as may be seen in
Fig. 3. TMJ tomographic view in closed mouth position. Typically, these tomographic projec-
tions are used to check the range of motion of the condyles as well as the anatomical var-
iations and pathologic condition within the joint. If there is a disc-related disorder, an MR
imaging of the joint will be needed to evaluate the disc position and morphology.
degenerative joint diseases such as osteoarthritis and RA or anatomic variants such as

bifid condyle, as well as fractures (Fig. 5). With proper splinting and patient posi-
tioning, condylar position in the glenoid fossa and along the articular eminence, dislo-
cations, hypermobility, and changes in joint space can be seen on a qualitative basis.
Panoramic radiographs, used along with reverse Towne’s views, can provide excellent
imaging of condylar fractures.
Fig. 4. TMJ tomographic view in open mouth position. Typically, these tomographic projec-
tions are used to check the range of motion of the condyles as well as the anatomical var-
iations and pathologic condition within the joint. If there is a disc-related disorder, an MR
imaging of the joint will be needed to evaluate the disc position and morphology.
TMJ Imaging 5
Fig. 5. Panoramic projection demonstrating fracture of the left condylar neck. Note the
entire glenoid fossa is not covered in this radiographic due to positioning issues related
to the patient after the trauma.
Inaccuracies in the measurable distance are a limitation of the panoramic technique.

Caution is recommended in making absolute measurements using panoramic
radiographs.11
PLANAR IMAGING (PLAIN IMAGING OR 2D IMAGING)
Due to compression and superimposition of the z-axis, most plain film views, such as
lateral and posteroanterior cephalometric and skull projections, are of limited use in
TMJ diagnosis. Exceptions are reverse Towne’s views, as well as transcranial, trans-
orbital, and transpharyngeal images. Although CBCT has superseded these imaging
modalities, CBCT or multidetector computed tomography (MDCT) imaging is not al-
ways easily accessible.
Reverse Towne’s projections are posteroanterior views taken with the patient’s chin
tilted downward and the mouth in an open position, providing a clear view of the
condylar neck and a portion of the condylar head. As mentioned earlier, along with
a panoramic image, the reverse Towne’s view can allow viewing of subcondylar
fractures.
Transcranial and transpharyngeal projections provide adjusted sagittal projections
of the TMJs. They may be taken in both the open and closed positions, with stenting
recommended for consistent open position views. These views are technically chal-
lenging, as care must be taken in positioning to avoid superimposition of the petrous
ridge of the temporal bone over the joint. Transorbital projections provide adjusted
coronal projections of the TMJ, allowing for visualization of medio-lateral changes
to the condylar head and glenoid fossa.
Although these extraoral plain film views have been all but replaced by CBCT, a
2019 study comparing the efficacy of transcranial views to CT imaging in the diagnosis
of osteoarthritis and RA found that both methods “are equally efficacious in evaluating
the osseous degenerative changes of TMJ in arthritis.”12
LINEAR AND PLURIDIRECTIONAL TOMOGRAPHY
Tomography (from Greek, meaning “picture of a slice”) uses motion to blur structures
that are located in front or in back of the ROI. This is especially helpful in projectional
imaging of the skull base, where many bony structures are in close proximity. Linear
tomography was developed initially but proved to be of questionable value due to
strong streaking artifacts created by structures outside of the image layer. These
artifacts were often superimposed over the ROI, rendering the imaging of little value.
During the 1990s, pluridirectional tomography systems, designed for orofacial imag-
ing, were developed. These provided higher quality images than linear tomography
but required a large amount of time for each study. They were ultimately retired
when CBCT image became more available.
Arthrography and Arthrocentesis

Arthrography is a technique where a radiopaque dye is injected into a joint and then
the joint is imaged. It has been used for TMJ imaging to determine if a disc is displaced
or perforated. Arthrography provides an indirect depiction of the disc because the dye
will be seen in the inferior joint space beneath the disc and in the superior joint space
above the disc. Great care must be taken to inject the proper amount of dye so as to
enter the joint spaces while not overwhelming the joint and obscuring the anatomic
structures. Arthrography can be used to depict the anterior–posterior relationship of
the disc, perforation, and joint function, when open and closed images are exposed.
It is considered to be inaccurate for medial and lateral displacement. Arthrography is
considered to be extremely technique sensitive.
Traditionally, the images were obtained following introduction of the dye into the
joint using plain film techniques, including transcranial and transpharyngeal projec-
tions. More recently, CBCT imaging has been used, providing three-dimensional
arthrography of the TMJ. The researchers were able to use the images to diagnose
disc displacement, both with and without reduction, disc perforation, and tears in
the articular capsule.13
Computed Tomography
Although MDCT may be used for TMJ imaging of both the hard and soft tissues, its use
in recent years has been superseded by CBCT for hard tissue imaging and MRI for
visualizing the soft tissues of the joint. CBCT has demonstrated its superiority over
MDCT for TMJ imaging through its high-quality images of the hard tissues of the
TMJ, versatile software that permits oblique views to accommodate the variable an-
gles of the joint, increasing accessibility in dental practices, small FOV scans that
may reduce artifact production, and significantly lower radiation dose. Thin cross-
sections of the joint may be obtained, and the resolution is usually adequate for diag-
nosis. Further, three-dimensional reconstructions are easily viewed and may be
rotated.
CBCT is able to reliably demonstrate the hard tissue changes commonly seen in pa-
tients with degenerative changes to the joint. These changes include remodeling of the
articulating surface of the condylar head, osteophyte formation, subchondral cysts,
osteosclerosis, and remodeling of the posterior slope of the articular eminence
(Figs. 6 and 7). Fig. 8 is a CBCT 3-D reconstruction of right TMJ showing significant
condylar erosion and morphological changes.
Further findings that are often seen on CBCT examinations include bifid condyles
(Fig. 9) and reduced joint space—a possible indirect indicator of disc displacement.
Condylar fractures are also nicely demonstrated in coronal and axial projections
(Figs. 10 and 11). Figs. 12 and 13 show sagittal and coronal projections of a separated
osteophyte in the superior joint space of the right TMJ. Ankylosis of the TMJs can also
be viewed using CBCT scans, especially if the ankylosis is bony (Figs. 14–16).
Most CBCT software programs allow for a “TMJ View.” This feature proves adjusted
sagittal slices at a variable angle for each joint. Axial and coronal views of the joints are
also provided (see Fig. 14; Fig. 17).
TMJ Imaging 7
Fig. 6. CBCT-based panoramic reconstruction showing significant TMJ changes within the
right condyle.
Magnetic Resonance Imaging

When imaging of the soft tissues of the TMJ is required, MRI provides the only viable
option for visualization of the articular disc.14 MRI is based on nonionizing radiation but
does have some absolute and relative contraindications. MRI yields fewer artifacts
from dense bone and metallic structures. It is accurate for both soft and hard tissues.
Timing of the radiofrequency pulses alters the appearance of the images. Although
there are several sequences available, T1-weighted (T1W) and T2W images are still
used most frequently for MR imaging of the TMJs.14 T1W imaging provides a bright
signal for fat, whereas T2W imaging yields images where both fat and water appear
bright. The contrast of the tissues in the image is, in general, based on the water con-
tent of the tissue. The higher the water content, the brighter the signal in the resultant
image. Therefore, dense bone (low water content) will usually appear black in an MRI,
Fig. 7. Adjusted bilateral sagittal projections demonstrating osteoarthritic changes of the

TMJs. Flattening of the anterior articulating surfaces of the condylar head and osteophyte
formation are seen in both joints, whereas more advanced degenerative changes, including
flattening of the posterior slope of the articular eminence, reduced joint space, and sub-
chondral cyst formation, are noted in the right TMJ.
Fig. 8. CBCT 3-D reconstruction of right TMJ showing significant condylar erosion and
morphological changes.
whereas fluids, such as fat, will appear brighter. In the images of the TMJ, the articular
disc will appear dark gray because it is composed of dense fibrous connective tissue
with a low water content. The retrodiscal tissue will appear brighter. T1W images pro-
vide excellent contrast resolution of soft tissues, displaying a wide range of interme-
diate gray densities that allow for visualization of the various tissues that comprise
the TMJs. T2W imaging is prescribed when fluid accumulation is suspected. This
might be in cases of joint effusion, osteonecrosis, or cystic lesions.
Absolute contraindications to MRI include cerebral aneurysm clips and cardiac
pacemakers. Relative contraindications are claustrophobia, metallic prosthetic heart
valves, ferromagnetic bodies, and implanted wires in critical locations. Surgical clips
outside of the brain and other nonferrous metal prostheses are not contraindications
to MRI. Additionally, dental implants that are made of titanium, zirconium, or other
nonferrous substances are not contraindications to MRI. If there is any doubt, consul-
tation with the patient’s physician to clarify the nature of the implanted device is appro-
priate. MRI is limited by relatively low resolution. When high-resolution MR imaging is
required, the prescriber should request that a minimum of a 1.5 Tesla scanner be
used. Tesla is a derived SI unit of magnetic field strength. Higher Tesla scanners will
provide improved resolution.
Fig. 9. CBCT coronal and axial projections of the TMJs. Left side exhibits bifid nature of the
condyle. The right condyle is unremarkable.
TMJ Imaging 9
Fig. 10. CBCT coronal projection at the level of the condyles demonstrating a right subcon-
dylar fracture.
Indications for MRI of the TMJs include suspected displacements, joint effusion
following trauma, osteomyelitis of the condylar head and/or articular eminence, and
neoplasia. Although functional MRI15 is not yet readily available, open and closed
MRI studies are often appropriate to distinguish between disc displacement with
and without reduction (Figs. 18 and 19).
Ultrasound Imaging
Ultrasound (US) imaging is an inexpensive and noninvasive diagnostic imaging modal-
ity that is widely available. US imaging has high sensitivity for disc evaluation, cartilage
displacement, joint effusion, and condylar erosion.16,17 However, MR diagnosis of
TMD is preferred over US diagnosis by clinicians due to its higher specificity.
Fig. 11. CBCT axial projection at the level of the maxilla demonstrating a right subcondylar
fracture.
Fig. 12. CBCT coronal projection of the right TMJ. In addition to the osteoarthritic changes
seen in the joint, a separated osteophyte is seen in the superior joint space.
Limitations in the use of US include image distortion and variability in the interpretation
of image data. US imaging can be used for the evaluation of TMD but it does not pro-
vide definitive diagnoses. Due to the nature of the US frequencies, only the osseous
surfaces but not the cortex or spongiosa can be visualized. There is limited accessi-
bility of deep structures by US evaluation due to the absorption of sound waves by
the lateral portions of condyles and the zygomatic process of the temporal bone.
Nuclear Imaging (Bone Scanning and Positron Emission Scanning)

Nuclear medicine scans can be used for the evaluation of osseous pathologic condi-
tions in the TMJ. Technetium-99 m bone scans are the most commonly used scinti-
graphic studies. Technetium bone scans have relatively high resolution and high
Fig. 13. CBCT sagittal projection of the right TMJ. In addition to the osteoarthritic changes
seen in the joint, a separated osteophyte is seen in the superior joint space.
TMJ Imaging 11
Fig. 14. TMJ CBCT. Ankylosis of the condylar heads to the posterior wall of the glenoid fossa
can be seen bilaterally. This condition is the result of RA.
Fig. 15. TMJ Sagittal CBCT showing ankylosis of the condylar heads to the posterior wall of
the glenoid fossa seen bilaterally. This condition is the result of RA.
Fig. 16. TMJ axial CBCT at the level of the condyles showing the bilateral ankylosis. This con-
dition is the result of RA.
sensitivity. Radiation exposure and lack of specificity are the drawbacks. Advantages
include low cost and high diagnostic accuracy for osseous pathologic conditions.
Bone scans are best suited for assessing the progress of TMD, especially the inflam-
matory conditions and/or remodeling of TMJ. This is especially true in the prediction of
painful temporomandibular joint osteoarthritis in juvenile patients.18
Inflammation of the TMJ has a high correlation to the late stages of RA. TMJ is the
freely moving joint between the condyle of the mandible and the squamous portion of
the temporal bone. The TMJ consists of six main parts: the ligaments, the lateral pter-
ygoid, the articular disc, the capsule, the articular surface to the temporal bone and the
mandibular condyles. Most of these structures can be seen by CT scans. Imaging the
Fig. 17. CBCT TMJ projections demonstrating bilateral osteoarthritic changes to the TMJs.
TMJ Imaging 13
Fig. 18. T1W MRI of the joint (open mouth) demonstrating normal disc position although
disc itself has some morphological changes.
TMJ using positron emission scanning (PET) is a new development. TMJ disorders are
generally diagnosed using full-skull radiograph, MRI, CBCT, or CT as describe earlier
in this article. MRI can demonstrate position of the articular disc (see Figs. 18 and 19)
and CT demonstrates the osseous detail of the joint. PET, however, can show not only
the bony structures but also soft tissue inflammation, as well as the impact on blood
flow (Fig. 20). The sensitivity of PET is expected to be a great advantage for diag-
nosing TMD. Both [18F]-fluoro-2-deoxy-D-glucose (FDG) and [18F]-sodium fluoride
(NaF) are used in the diagnosis of inflammatory disorders of TMJ. FDG is an analog
of glucose that contains the radionuclide, Fluorine F-18, which decays by positron
emission. Its efficacy comes from the optimal half-life and low degradability. Dr Abass
Alavi conducted the first human study with FGD-PET in 1976 leading to a
Fig. 19. T1W MRI of the joint (closed mouth) demonstrating anterior disc displacement.
Fig. 20. PET maximum intensity projections. The lit-up areas in color indicate TMJ increased
metabolic activity in a patient with rheumatoid arthritis. (Images courtesy Sophia Oak,
Temple University, Philadelphia, PA).
breakthrough in nuclear medicine.19 FDG-PET/CT and NaF-PET/CT have high TMJ

uptake in patients with RA. Overall, both FDG-PET/CT and NaF-PET/CT are reliable
imaging tools that can be helpful in a clinical setting for patients with TMD.
SUMMARY
Diagnostic imaging of the temporomandibular joint can provide confirmation of clini-

cally suspected temporomandibular disorders. Careful selection of the imaging exam-
ination with respect to the tissues being imaged and the radiation burden to the patient
will aid in obtaining the desired diagnostic yield. In general, ionizing radiation-based
imaging is most appropriate for hard tissue abnormalities, whereas MRI is indicated
for soft tissue pathologic conditions and anatomic variations.
CLINICS CARE POINTS
! Select imaging studies based on supected conditions.

! Consider the suspected anatomic changes and match the imaging study that is best suited to
visualize these changes.
! The practitioner is responsible for complete interpretation of the prescribed images.
! Consider the potential risk to the patient versus the potential benefit of the imaging study.
DISCLOSURE
S.R. Singer has nothing to disclose. M. Mupparapu has nothing to disclose.
REFERENCES
1. Oenning AC, Jacobs R, Pauwels R, et al, DIMITRA Research Group. Cone-beam

CT in paediatric dentistry: DIMITRA project position statement. Pediatr Radiol
2018;48(3):308–16. Available at: http://www.dimitra.be.
2. Oenning AC, Jacobs R, Salmon B, DIMITRA Research Group. ALADAIP, beyond
ALARA and towards personalized optimization for paediatric cone-beam CT. Int J
Paediatr Dent 2021;31(5):676–8. Available at: http://www.dimitra.be.
3. Kim IH, Singer SR, Mupparapu M. Review of cone beam computed tomography
guidelines in North America. Quintessence Int 2019;50(2):136–45.
P a t h o g e n e s i s an d
D i ffe re n t i a l D i a g n o s i s o f
D i s o rd e r s
Junad Khan, DDS, MSD, MPH, PhDa,*, Steven R. Singer, DDSb,
Andrew Young, DDS, MSDc,
Naruthorn Tanaiutchawoot, DMD, MSDb, Mythili Kallada, BDS, MSDa,
Mel Mupparapu, DMD, MDS, DipABOMRd
KEYWORDS
! Fibromyalgia ! Chronic overlapping pain conditions ! Comorbid
! Temporomandibular disorder
KEY POINTS
! Temporomandibular joint disorders (TMDs) are often chronic in nature, and underlying
mechanisms are poorly understood.
! TMDs can mimic as aodontogenic pain and result in unnecessary treatment and financial
burden.
! TMDs can be challenging to diagnose and manage. A proper understanding and training
can better help manage the patient.
INTRODUCTION
Temporomandibular disorders (TMDs) affect approximately 11.5 million individuals in

the United States, entailing a significant burden on economic and health care resources.
The annual incidence of clinically verified TMDs is estimated to be 4%. However, this
may reflect a “symptom iceberg.”1 The condition may have a significant association
with age and presents a similar incidence is men and women, with a nonsignificant
higher incidence in women. The condition also has a significantly higher incidence in Af-
rican Americans and whites in comparison to Asians. The variations may be explained
by an incidence-prevalence bias and study design.2 In 1992, the Research Diagnostic
a
Orofacial Pain and TMJD, Eastman Institute for Oral Health, 625 Elmwood Avenue, Rochester,
NY 14620, USA; b Department of Diagnostic Sciences Division of Oral & Maxillofacial Radiology,
Rutgers School of Dental Medicine, 110 Bergen Street | PO Box 1709, Newark, NJ 07101-1709,
USA; c Arthur A. Dugoni School of Dentistry, University of the Pacific, San Francisco, CA, USA;
d
Penn Dental Medicine, 240 S 40th Street, Philadelphia, PA 19104, USA

2 Khan et al
Criteria for Temporomandibular Disorders (RDC/TMD) was developed. RDC/TMD cate-

gorized TMDs into Axis I and Axis II. Axis I described the common physical TMD signs
and symptoms, whereas Axis II includes conditions that relate to the psychosocial and
behavior disorders. In 2008 to 2011, RDC/TMD was assessed and validated. Although
Axis II seemed to be reliable and valid, Axis I was redeveloped to be a validated diag-
nostic criterion for clinicians and researchers as now known as the Diagnostic Criteria
for Temporomandibular Disorders (DC/TMD).3,4
The etiopathogenesis of TMDs is complex and involves an interplay of multiple fac-
tors across various biological, psychological, social, and environmental domains in the
backdrop of genetic influences. The multiple factors may exert their influence over
time, resulting in manifestation, progression, remission, or exacerbations of the con-
dition.1,5 Early theories were mechanistic and focused on the role of mechanistic
occlusal factors as the primary factor in the genesis of these conditions. Current sci-
entific evidence has refuted and shown very low to no role of occlusion in the genesis
of TMDs and resulted in the shift of theories from biomechanistic models toward bio-
psychosocial models.6–8 The role of peripheral and central nociceptive inputs; envi-
ronmental, genetic factors; and interplay of biopsychosocial risk factors in the
initiation, sustenance, and progression of these conditions is currently hypothesized
to play a major role in evolution of TMDs.1
In spite of having validated diagnostic guidelines, insights into various pathophysi-
ological mechanisms and proper management of TMDs are still elusive and controver-
sial. This information is crucial for successful pain management and to prevent the
new incidence or recurrences in new or existing patients with TMD. The objective of
the present article is to provide a comprehensive evidence-based literature review
on the proposed pathophysiological mechanisms implicated in the genesis of TMDs
and the clinical implications of the same following the classification guidelines as
per the DC/TMD.
CAUSE AND RISK FACTORS
The Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study was
one of the most comprehensive studies to date assessing risk factors using prospec-
tive cohort, case-control, and nested case-control study designs. OPPERA studies
enabled significant inferences on risk factors and associations playing a vital role in
the initiation and sustenance of TMDs. The prospective cohort study explored the
temporal sequence of risk factors and onset of TMDs, whereas the case-control study
design provided information on significant associations between risk factors and
TMD. Comorbid health conditions, somatic symptoms, and nonpainful orofacial
symptoms emerged as the strongest predictors for incident TMDs.9–11
Comorbid health conditions included a list of approximately 20 different health con-
ditions administered as a screening questionnaire, and ill-defined, painful or nonpain-
ful conditions and cigarette smoking emerged as additional risk factors for TMDs.12
Hormonal contraceptive initiation also increased the risk of development of subse-
quent TMDs, headaches, and craniofacial pain, which reduced on cessation.13
Self-reports by patients were stronger predictors than examiner assessments. Self-
reports of temporomandibular joint (TMJ) noises and multiple parafunctional habits as
assessed by the Oral Behavioral Checklist were very strong indicators of chronic
TMDs and incident TMDs.14 Multiple parafunctional habits may result in a threshold
effect, elevating the risk of patients for TMDs possibly through mechanisms including
central dysregulation, reduction in proprioception and motor inhibition, enhanced mo-
tor activation, and constant psychophysiological reactivity.15 The extrinsic or intrinsic
Diagnosis of Temporomandibular Joint Disorders 3
injury also increased the odds of developing TMDs significantly, and single trauma had
a higher impact compared with multiple injuries to the jaw.16 The nested case-control
study reported that pressure pain thresholds were not reliable indicators of incident
TMD, rather coincided with onset and progression.17
Sleep quality was a significant factor for incident TMD. The rate of incident TMD
increased 40% for every standard deviation reduction in quality of sleep.12 Patients
with first-onset TMD had preceding OSA symptoms and 73% higher hazards of devel-
oping TMDs.18 Poor sleep quality has been hypothesized to increase the perception of
stress and additionally has a significant direct impact on pain perception through its
effect on immune, metabolic, and inflammatory pathways.19 Somatic and global psy-
chological symptoms were the most robust psychological risk predictors for incident
TMD. Previous life events, levels of perceived and measured stress, and negative ef-
fects also had important implications.20 Previous studies have also shown that health
anxiety in adults and life satisfaction, somatization, and depression in adolescents
may play a role in the development of chronic orofacial pain.21–23 Somatic symptoms
also exhibited strong associations with several chronic overlapping pain conditions
(COPC) and individual COPC,24 although the exact mechanism and role of somatic
symptoms in the evolution of TMD are under scrutiny. Somatic symptoms may also
alter biological pathways through their effects on the inflammatory and immune path-
ways, and certain risk factors such as parafunctional habits may induce somatic
symptoms or somatic symptoms may be manifestations of physiologic perturbations
and these may act in cohort with other risk factors and play a role in initiation and sus-
tenance or contribute to the chronicity of TMDs.15,25,26 Patients with new-onset TMD
may also exhibit greater pain and symptoms and exhibit deteriorating psychological
parameters, whereas patients with chronic TMD may exhibit better biopsychosocial
parameters signifying engagement of coping and adaptation skills, suggesting evolu-
tion of biopsychosocial parameters as the condition evolves, persists, or resolves.27
The transition from acute to chronic TMDs may also be facilitated by processes
such as catastrophizing.
Genes are upstream determinants of biological intermediate phenotypes that may
act with environmental factors and produce downstream phenotypic effects,
increasing an individual’s predisposition to TMDs.5 Studies have reported that
single-nucleotide polymorphisms (SNPs) affecting the serotonergic pathway and
gene-environment interaction on stress and pain were modified by the catechol O-
methyltransferase (COMT). SNPs in the glucocorticoid receptor gene and serotonin
receptor gene have been implicated through their action on the hypothalamic-
pituitary-adrenal axis and affective, nociceptive pathways, respectively. The OPPERA
study also implicated 4 other novel and previously unreported SNPs as risk factors for
TMDs; this included voltage-gated sodium channel Nav1.1 alpha subunit, angio-
tensin-I–converting enzyme, prostaglandin-endoperoxide synthase 1 gene, and amy-
loid beta (A4) precursor protein.28 However, it has been suggested that the complexity
of TMDs may involve multiple SNPs acting through distinct biological pathways. For
instance, it has been suggested that in localized TMD, the genetic interactions may
activate peripheral serotonergic pathways causing local hyperalgesia but with signif-
icant counteraction by the central serotonergic pathways limiting widespread effects
seen in TMDs with additional widespread body pain on palpation. Genetic factors may
also play a role in modulating inflammatory responses, nociceptive sensitivity, and
psychological and autonomic responses.
TMDs are no longer considered a localized condition. It may have a strong associ-
ation with certain chronic overlapping pain syndromes such as fibromyalgia (FM), and
the association may be influenced by the number of chronic overlapping pain
4 Khan et al
conditions. In patients developing incident TMD, headache frequency and prevalence

specifically migraine increased.29 The overlap between COPCs was more significant
for musculoskeletal conditions such as TMDs, low back pain, and FM. In addition to
the overlap of pain conditions in the body and orofacial pain, a significantly higher
anatomic overlap has been reported, especially in craniocervical pain reflecting differ-
ential amplification of pain inputs based on anatomic locations.30 Segmental central
sensitization (somatosensory inputs to the central nervous system (CNS) are segmen-
tally organized and thus sensitization may alter across the neuroaxis, resulting in pain
symptoms in specific sites) has also been suggested as a possible mechanism in
several pain conditions with anatomic overlap.31 Convergence of afferent nociceptive
inputs at the level of the cervical first dorsal horn has been suggested as a plausible
segmental sensitization mechanism in craniocervical pain conditions such as TMDs,
headache, neck pain, and whiplash injuries.32 In addition, cortical reorganization
due to continued nociceptive inputs and activation of afferent pain pathways may
play a role in pain processing and also contribute to this phenomenon.30,33,34
Significant lines of evidence seem to point to the role of peripheral and central sensi-
tization in the evolution of painful TMDs. Painful TMDs may be one of the pathways
contributing to increased synaptic efficacy of nociceptive neurons and thus drive upre-
gulation of pathways contributing to central sensitization.1 Inflammatory mediators
including serotonin, prostaglandin E2, bradykinin, and histamine seem to show involve-
ment in pain development in patients with muscle pain. Some studies showed the eleva-
tion of tumor necrosis factor alpha (TNF-a), interleukin-1 (IL-1), and IL-6 levels in
synovial fluid of patients with TMD pain.35,36 Upregulation of proinflammatory cytokines
such as TNF-a, interleukin- IL-6, 1b (IL-1b), and monocyte chemoattractant protein-1
may activate nociceptors and this coupled with downregulation of antiinflammatory cy-
tokines and omentin has been suggested to play a role in the development of pain.37–43
In addition, some nociceptive neuropeptides such as substance P, calcitonin gene–
related peptide (CGRP), neuropeptide Y, and vasoactive intestinal peptide have also
been shown to correlate with TMJ degeneration if imbalanced. Free radical such as
reactive oxygen species also plays an important role in TMJ disease.44
Pain amplification that may occur as a consequence of enhanced pain facilitatory
pathways in the peripheral/central nervous system or impaired modulatory pathways
has also been implicated.45 Pain amplification may be determined by genotypic or
phenotypic interaction with the environment and risk factors. Acute TMDs may thus
involve peripheral sensitization through injury or oral parafunctional behavior with sub-
sequent activation of nociceptors in the masticatory tissues or it may involve dysregu-
lation of systems beyond the local site with a more central mechanism. Peripheral
mechanisms may have a more significant role in the initiation of localized TMDs,
whereas the involvement of central mechanisms (central sensitization, neuroplasticity,
cortical reorganization) may contribute to the persistence and chronicity of TMDs
marked with widespread symptoms. Central sensitization and downregulation of
modulatory pathways has also been proposed to play an important role.15,46,47 Cluster
analysis in the case-control OPPERA group has identified 3 different clusters: adap-
tive, pain sensitive (characterized by greater experimental pain sensitivity), and global
clusters (characterized by heightened psychological distress and pain sensitivity) of
patients with TMD. Analysis of the TMD cases and controls revealed that an over-
whelming majority of TMD cases encompassed global symptoms and pain-sensitive
clusters (91.5%), whereas a significant proportion of controls (41.2%) could be clas-
sified into the adaptive cluster. The global symptom cluster had a greater predilection
for developing first-onset TMD, and the global symptom and pain-sensitive cluster
exhibited grater, functional limitation, increased pain, and multiple comorbidities.48
A proper diagnosis of TMDs is considered the first important step to allow re-
searchers to develop well-designed rigorous studies with reliable and validated infer-
ences, which can then be applied by clinicians to enable evidence-based
management of TMDs. At present, the standard diagnostic guideline recommended
for clinicians and researchers is the DC/TMD. This section will only describe Axis I
of the classification of TMDs. As per DC/TMD protocol, TMDs can be categorized
into 2 dual axes. Accordingly, as per Axis I protocol, TMDs can be categorized into
4 major categories including temporomandibular joint disorders, masticatory muscle
disorders, headaches, and associated structures. In this article, the authors provide
an overview of the pathophysiologic mechanisms as per Axis 1 DC/TMD49 (Figs. 1
and 2).
JOINT PAIN
Arthralgia
The diagnosis of pain in the TMJ is termed “arthralgia.” It could be confirmed by the repro-
duction of chief complaint with TMJ palpation and/or with jaw movement. The palpation
force recommended by DC/TMD during TMJ examination should be around 1 kg/cm2. It
is described as joint pain affected by functional or parafunctional jaw movements.
Arthritis
Arthritis is a localized joint pain condition presenting with characteristics of inflamma-
tion or infection. In addition to pain, if the clinical presentation shows signs of inflam-
mation including redness, swelling, or increased skin temperature, the diagnosis
“arthritis” shall be made instead. It is often secondary to mechanical, metabolic, infec-
tious, and/or inflammatory factors.50
JOINT DISORDERS
Degenerative Joint Disease, Disc Displacements, and Subluxation
The diagnostic criteria for the degenerative joint disease do not include pain; the diag-
nosis refers to the TMJ’s erosion of the articular surface. If pain is present, this is
Fig. 1. The flow chart shows the classification of temporomandibular joint disorders.
6 Khan et al
Fig. 2. The flow chart shows the classification of masticatory muscle disorders.
referred to as “temporomandibular joint pain attributed to degenerative joint disease”

in the ICOP1; in the DC/TMD, for this presentation, 2 diagnoses would be given:
“degenerative joint disease” and “arthralgia.3”
The same diagnostic criteria approach holds for pain with TMJ disc displacement
and subluxation: if they are painful, the diagnoses “TMJ pain” or “arthralgia” are
attached. TMJ subluxation and disc displacement with reduction (DDWR) have very
similar presentations. Subluxation has a loud, late pop with a wide opening and
may have a closing pop as well. DDWR can have a loud pop, or a fainter click, and
these noises may occur anywhere from early to late in the condylar translation.3
One distinguishing factor is the intensity of the joint sound. Only DDWR can have a
faint click; a louder pop can be either. Another distinguishing feature is the timing of
the pop. An early pop is not a feature of subluxation, so would have to be diagnosed
as DDWR; a late pop can be either. Lastly, the direction of jaw deviation can help
differentiate. In subluxation, the mandible deviates toward the side contralateral to
the pop, at the time of the pop; in DDWR, the mandible deviates toward the side ipsi-
lateral to the pop.
If the disc is displaced anterior to the condylar head in a closed mouth position and
is recaptured to the normal position while opening, then this condition should be diag-
nosed as anterior DDWR. In instances when the disc is displaced anteriorly to the
condylar head in mouth closing position and maintained anteriorly even with mouth
opening, this condition should be diagnosed as “anterior disc displacement without
reduction.” Several hypotheses have been proposed, and one of the hypotheses on
etiopathogenesis in articular disc disorders suggests that it may involve alterations
in the intraarticular lubrication, leading to increased articular friction. However, this
may become symptomatic generally only in a predisposed joint with other risk factors
(trauma, alterations in joint or disc morphology, dynamics, hypermobility, and so
forth). Trauma may induce an inflammatory response primarily in the retro discal tissue
and damage the ligaments and posterior attachment of the joint, enhancing suscep-
tibility to articular disc disorders. Instances of articular overloading exceeding the
adaptive remodeling capacity of the joint may also induce changes in the articular
disc that has limited remodeling capacity in comparison to the bony structures of
the joint and lead to articular disc disorders.51
Temporomandibular Joint Hypomobility

TMJ hypomobility is a condition that does not allow the jaw to be able to move to the
normal limit, may be a sequela of intraarticular fibrotic adhesions or due to fibrous or
bony ankylosis. In most instances, they may be sequelae of trauma (macrotrauma/
fractures) and occasionally due to systemic diseases (such as psoriatic or rheumatoid

arthritis, fibrodysplasia ossificans progressiva,52–54 infections [middle ear and
mastoid]).55,56
Temporomandibular Joint Hypermobility

It is a condition characterized by the ability of the jaw to move beyond the normal limit
(hypermobility). Pathophysiologic alterations in the supporting structures (ligaments,
bony, and muscle components) of TMJ have been proposed to be the primary factors
in the etiopathogenesis of hypermobility disorders; this may be secondary to trauma,
systemic conditions, and other factors.57 Animal models of traumatic TMJ hypermo-
bility have demonstrated changes in the synovium of the upper joint compartment,
deposition of fibrin in inflamed synovial tissues, adhesions, capillary hyperemia, the
proliferation of surface cells, and synovitis.58 A systematic review on the role of gener-
alized joint hypermobility (GJH) in TMD is still unclear and suggests that the condition
warrants further research.59 GJH may be seen in conditions such as Ehlers Danlos
syndrome. GJH may be associated with several conditions affecting the locomotor
system such as myalgia, arthralgia, soft tissue lesions, dislocations, traumatic synovi-
tis, and so forth. It has been proposed that the increased range of movement may
overload the joint and increase susceptibility to mechanical damage, or the alterations
in the quality of collagen in these disorders may terminate in degenerative changes or
clinical manifestations of the condition. GJH may frequently be associated with TMDs
such as osteoarthritis.
JOINT DISEASES
Imaging of the TMJ is an important aspect of diagnosis especially if the bony compo-
nents of the joint are affected. Plain digital radiography (planar radiography), cone-
beam computed tomography (CBCT), multidetector computed tomography, and
MR imaging can be used to image joints, and functional imaging such as PET and
PET-CT imaging can be used to identify malignant disorders. Three-dimensional re-
constructions help in displaying the TMJ in all 3 dimensions (Fig. 3).
Osteoarthrosis and Osteoarthritis

These are degenerative joint conditions. According to DC/TMD, both conditions show
similar signs of TMJ degeneration, but osteoarthrosis presents without arthralgia,
whereas osteoarthritis presents with arthralgia. Often the terms are used interchange-
ably. Osteoarthritis is a multifactorial condition with a complex pathogenesis involving
sustained inflammation. Mechanical and metabolic factors may initiate early damage
of articular cartilage, triggering immune and biochemical responses in the hard and
soft tissues of the joint. Immune cells may release inflammatory mediators including
cytokines and chemokines and activate the complement system, causing the release
of factors that can damage articular cartilage including prostaglandin E and matrix
metalloproteinase. The local inflammatory response can damage and degrade the
articular cartilage and cause remodeling changes in the subchondral bone60 (Figs.
4 and 5).
Systemic Arthritides
Systemic arthritides are pain and structural changes secondary to joint inflammation
resulting from systemic conditions such as juvenile idiopathic arthritis, rheumatoid
arthritis spondyloarthropathies (psoriatic arthritis, ankylosing spondylitis, Reiter
8 Khan et al
Fig. 3. Three-dimensional reconstruction (Recon) of the right TMJ using CBCT.
syndrome, infectious arthritis), and crystal-induced (chondrocalcinosis, gout) and

autoimmune conditions (lupus erythematosus, Sjögren syndrome, scleroderma).61
TMJ arthritis caused by systemic disease is generally painful, and diagnosis is made
by a combination of clinical presentation, consideration for existing systemic disease,
imaging, and serologic studies.61,62
In cases where the joints are completely degenerated or destroyed, a total joint
replacement is recommended, which will bring back function and reduce pain in the
patient (Fig. 6).
Idiopathic Condylar Resorption

The etiopathogenesis is still unclear, and it has been suggested to be idiopathic (Figs.
7–10). Previously, estrogen, reduced 17b-estradiol levels, mechanical loading, and
dysfunctional remodeling of the condyle have been suggested as possible factors.
Condylar resorption may also be secondary to surgeries such as orthognathic surgery
and often these cases are also classified into the category of ICR. A systematic review
reported that at present there is a lack of evidence to suggest estrogen deficiency as a
contributor. However, the quality of evidence is low and the investigators suggest
further rigorous studies to investigate the matter.63
Osteochondritis Dissecans
Osteochondritis dissecans is the presence of loose osteochondral fragments in the
joint due to detachment of cartilage and a fragment of bone from a bony extremity.
The pathophysiological mechanisms are yet to be elucidated in the TMJ.61
Osteonecrosis
This condition is characterized by necrotic bone and pain. When it occurs in the TMJ
condyle, it is difficult to distinguish from arthritis. When it occurs in nonarticular areas
of the maxillofacial region, where arthritis does not occur, and where it can be clinically
observed when it penetrates the soft tissue, it is more easily diagnosed. The history
generally must be positive for trauma or surgery and antiresorptive medication or
radiation.61
Fig. 4. T1W sagittal MR image showing significant erosion and osteophyte formation in the
superior and anterior aspects of the condylar head due to degenerative joint disease.
BENIGN BONE TUMORS
Although often asymptomatic, these conditions may present with swelling when pain-
ful. Osteoid osteoma may be confused with myofascial orofacial pain (MOP). It pro-
gressively worsens, is often worst at night, and is relieved by nonsteroidal
antiinflammatory drugs (NSAIDs). However, pain intensity is unrelated to activity,
which may cue the diagnostician to a non-TMD diagnosis.62 Osteoblastoma has
continuous pain that is not relieved by NSAIDs. Clinically aggressive bone lesions
Fig. 5. CBCT in TMJ reconstruction mode shows the extensive degeneration of the left
condyle in comparison to the normal right condyle.
10 Khan et al
Fig. 6. A panoramic radiograph showing total joint replacement of the TMJ bilaterally in a
patient with significant TMJ arthritis, leading to the destruction of left and right condyles.
such as ameloblastomas (Fig. 11) can essentially affect the body or the ramus of the
mandible and can mimic orofacial pain due to bone expansion and compression of the
neurovascular bundles.
Synovial Chondromatosis
In synovial enchondromatosis, metaplasia of the TMJ synovial tissue results in carti-
laginous nodules that may detach, becoming loose bodies. In osteochondromatosis,
the nodules are calcified. Pain, TMJ swelling, progressive limitation in mouth opening,
posterior open bite, and/or crepitus may develop. Although clinically it can be
confused with simple TMJ pain, or with lateral pterygoid spasm, differentiation is
achieved by imaging.61
The pathogenesis involves chronic inflammation and metaplasia of the synovial
membrane progressing to a stage of synovial progressive metaplasia with detached
particles (active chondrocytes partially encased in the synovial membrane), and finally,
only detached particles are present.64 Synovial macrophages, tenascin, transforming
Fig. 7. CBCT 3D reconstruction showing the condylar resorption on the left. The patient had
bilateral condylar resorption.
Fig. 8. Right oblique sagittal CBCT slice showing the condylar resorption on the right side.
growth factor beta, and fibroblastic growth factor receptor have also been implicated
in the etiopathogenesis of SC due to their role in chondrogenesis.65–67
MALIGNANT BONE TUMORS
Osteosarcoma can occur in jaw bones, although such occurrences are rare; the pain
often begins after an injury and may fluctuate over weeks to months. Langerhans cell
histiocytosis may have a soft tissue mass and pain. Multiple myeloma presents with
osteolytic lesions and bone pain.62
Primary malignant lesions or metastatic lesions can be detected via nuclear
medicine–based scans, more precisely via PET-CT, and Fig. 12 shows the active up-
take of radiolabeled glucose absorption at the potentially malignant site near the right
ramus.
Fig. 9. Left oblique sagittal CBCT slice showing the condylar resorption on the left side.
12 Khan et al
Fig. 10. A variant of idiopathic condylar resorption—this resorptive process included part of
the right ramus, condylar neck, and the head of the condyle. The patient only had mild
discomfort during the opening and closing of the mouth.
SINUSITIS
Inflammation in the sinus, whether acute or chronic (Fig. 13), is typically painful.
Although the maxillary sinuses are not immediately adjacent to the masticatory mus-
cles, sinusitis-related pain can be confused with masseter, medial pterygoid, or lateral
pterygoid MOP if the pain is diffuse enough or if it refers to the proximity of those mus-
cles. Sinusitis pain differs from MOP in that it is not altered with jaw function or palpa-
tion, does not limit the range of motion, often worsens with bending forward, and
usually has a history of current or recent allergies or upper respiratory tract
infection.68,69
Fractures: if the patients report a history of traumatic incidence, fractures of jaw-
related structures should be considered. The diagnosis should be proposed with
radiographic evidence of fracture. On occasion, the fractured portion of the elongated
styloid process can also lead to diffuse pain in the neck and may radiate to the ipsilat-
eral TMJ. The reliable and valid radiographs suggested in DC/TMD to confirm the frac-
ture are CT scan or CBCT imaging.
Congenital: anatomic abnormality of the TMJ condyle may be encountered. In the
case of a total absence of the condyle, either ipsilateral or bilaterally, the diagnosis
should be “aplasia.” “Hypoplasia” describes the condyle to be smaller, whereas
normal “hyperplasia” refers to an enlargement of the condyle. These conditions can
Fig. 11. A panoramic radiograph shows significant destruction of the right body of the
mandible and right ramus due to ameloblastoma. A small well-defined radiolucency within
the left ramus is the medial sigmoid depression, which is developmental.
Fig. 12. An FDG PET-CT image of a metastatic tumor near the right ramus closer to the
condyle showing a high amount of uptake of the radionuclide tracer. FDG,
fluorodeoxyglucose.
affect unilateral or bilateral TMJs. Congenital TMDs may be isolated occurrences (in-
trauterine defects during the prenatal period of TMJ development) or part of various
syndromes affecting first and second branchial arches such as Treacher Collins syn-
drome, Goldenhar syndrome, Hallermann-Streiff syndrome, Hemifacial microsomia,
Hurler syndrome, Morquio syndrome, Proteus syndrome, and Auriculocondylar syn-
drome.67 Condylar hyperplasia is secondary to a nonneoplastic proliferative increase
in normal cells, resulting in overdevelopment of condyle or entire mandible/facial
bones.61
MASTICATORY MUSCLE DISORDERS
According to DC/TMD, myofascial pain is a subcategory under the diagnosis of

myalgia. Myalgia can be diagnosed based on the patient’s chief complaint of pain
in the masticatory muscle location, and the pain can be reproduced by muscle palpa-
tion. Recommended force for muscle palpation suggested in DC/TMD is 1 kg/cm2. If
the pain seems to be localized under the palpation area, the diagnosis of “local
myalgia” should be given. If the pain spreads beyond the palpation area but is
restricted to the muscle boundary, it is recognized as “myofascial pain without
referral.” In the case that the pain travels beyond the boundary of palpated muscle
and refers to a remote area, which is perceived and reported by the patients, the diag-
nosis should be “myofascial pain with referral.”
Myofascial Pain
Pain with jaw function (whether the force of chewing or the act of stretching the jaw),
pain with palpation, and limitation in jaw range of motion due to pain distinguish masti-
catory MOP from headaches and neuropathic pain, which at times overlap with MOP
by location and pain quality.62 Neuropathic pain can also be triggered by jaw function
or palpation but tend to be disproportional to the stimulus. Trigeminal neuralgia, for
example, is often characterized by explosive pain with normally innocuous touch or
gentle jaw movements.62 MOP pain, on the other hand, increases in proportion to
14 Khan et al
Fig. 13. Coronal CBCT at the level of the maxillary sinuses showing severe bilateral maxillary
sinusitis.
the degree or duration of force applied during chewing, the distance of jaw movement,
or the amount of pressure applied during palpation. Some muscles, such as the medial
and lateral pterygoid muscles, are difficult or impossible to palpate; these muscles
therefore can only be tested with load or range-of-motion testing.61
Myalgia
Although specific pathophysiologic mechanisms for masticatory myalgia in the orofa-
cial region are yet to be completely elucidated, they may share certain common mech-
anisms involved in myofascial pain. It is currently hypothesized that myofascial pain is
initiated and sustained by the presence of myofascial trigger points that are hyperirrita-
ble spots in taut bands of muscle and occur when the adaptive capacity of muscles is
exceeded by functional demands. Excess acetylcholine, CGRP-related mechanism,
and acidic environment may lead to dysfunctional neuromuscular endplates and result
in sustained sarcomere contraction; this may lead to restriction in blood flow, local hyp-
oxia, the cumulation of waste products, and a deficit of adenosine triphosphate; this
causes an energy crisis and the formation of trigger points. Various other mechanisms
and theories have been proposed including the role of peripheral and central sensitiza-
tion, Cinderella theory (hierarchical recruitment patterns of muscle fibers result in small-
est fibers being subjected to longest duration of contraction and increased
susceptibility to initiating energy crisis in phasic muscles), and shift theory (tonic mus-
cles with the shift pattern of recruitment are susceptible with prolonged periods of
contraction and insufficient relaxation), the possible role of descending modulation.70
Myositis
Muscle pain associated with signs of inflammation is referred to as myositis. It is
generally secondary to trauma, infection, or in chronic cases, it may be secondary
autoimmune conditions. The allogenic inflammatory mediators released at the site
of inflammation/tissue damage can lower the detection threshold and result in periph-
eral sensitization and pain as mentioned in the introductory section. This infectious
and/or inflammatory muscle condition is usually caused by direct trauma or acute
infection to the muscle or a chronic autoimmune disease. It must be accompanied by

edema, erythema, or increased temperature of the muscle. Serologic testing may be
done, which may reveal elevated inflammatory markers such as creatine kinase.61
Tendonitis
It is described as pain restricted to the masticatory tendon, most commonly temporal
tendon with replication of pain with functional or parafunctional movements of the
jaw.61 The pain of this inflammatory condition seems as MOP, differing only by the pre-
cise location of the pain. Differentiation relies on a strong familiarity with the anatomy
of masticatory muscles and associated structures. Due to varied anatomy amongst in-
dividuals, location of the muscle-tendon junction, tendonitis and MOP cannot always
be distinguished with absolute certainty. The temporalis tendon is the most common
site of tendonitis in the masticatory system.61
Spasms
Spasm is defined by the DC/TMD as a “sudden, involuntary, reversible tonic contraction
of a muscle.” It must be accompanied by pain and limitation of the jaw opening
(<40 mm) and/or laterotrusion (<7 mm), which differentiates it from MOP; if a patient
has muscle pain without a limitation in jaw range, the diagnosis is simply MOP.61
TMJ pain attributed to a disc displacement without reduction can also cause limitation
in jaw range, but spasm differs in that the sense of pain and range limitation is felt within
a muscle and the offending event occurred in the muscle. If those parameters are too
unclear for a definitive diagnosis of spasm over a disc displacement, the description
of “TMJ pain” discussed in this article may be used to further differentiate.62
Temporomandibular Joint Pain
TMJ pain (also known as “arthralgia” in the DC/TMD), similar to MOP, is characterized
by pain with jaw function, pain with palpation, and limitation in jaw range of motion due
to pain. When the pain is located in a site remote from the TMJ, differentiation is rela-
tively simple. However, MOP can occur in the proximity of the TMJ, as portions of
every masticatory muscle pass near the TMJ. In such cases, other parameters of dif-
ferentiation are needed. If palpation of the TMJ causes pain, TMJ pain is
confirmed61,62; if palpation of the TMJ does not cause pain, that does not definitively
rule out TMJ pain, as most of the TMJ cannot be reached for palpation. TMJ arthralgia
is more likely to be aggravated by jaw laterotrusion, so that test can suggest TMJ
arthralgia rather than MOP. If a pop or click is present and hurts, or if the patient re-
ports the pain to be in the same location as the joint sounds, TMJ pain is very likely.
Contracture
Extended immobilization periods following surgery, trauma, radiation therapy, or
infection may result in fibrosis of muscle fibers or supporting structures such as ten-
dons and ligaments, resulting in painless limitation unless the involved muscle is
extended beyond the functional length.61 This shortening of a muscle due to fibrosis
of the muscle, ligaments, or tendons may seem similar to MOP, nonreducing disc
displacement, and TMJ pain, except that contracture does not usually hurt unless
the muscle is stretched beyond the point of resistance.61
Hypertrophy
Most commonly, it is a painless condition associated with enlargement in the mastica-
tory muscle possibly related to overuse, familial, genetic, or chronic bracing of
muscles.61
16 Khan et al
MASTICATORY MUSCLE PAIN ATTRIBUTED TO SYSTEMIC/CENTRAL PAIN

DISORDERS
Fibromyalgia
The diffuse chronic widespread pain, hyperalgesia, and allodynia in FM have been
previously hypothesized to be due to central mechanisms. However, recently it is hy-
pothesized that the condition may be a spectrum secondary to multiple potential
mechanisms with varying degrees of peripheral and central components across the
spectrum of presentations. The mechanisms may include biological amplification of
sensory pain inputs, affective components of pain processing, alterations in neuro-
transmitters and their receptors, enhanced connections with the insula in the resting
state, reduced connectivity among antinociceptive areas, augmented pain process-
ing, altered immunologic, inflammatory mechanisms, and defective pain modulation
in descending inhibitory systems.71 Patients with TMD may share many features
with FM. Both are characterized by musculoskeletal pain. Although FM diagnosis
generally requires more locations than just the jaw, the American College of Rheuma-
tology Preliminary Diagnostic Criteria for FM allows for as few as 3 locations (the right
jaw, left jaw, and neck, for example), so long as other symptoms are more severe or
abundant. Those other symptoms include fatigue, waking unrefreshed, muscle weak-
ness, depression, nervousness, and so forth; such symptoms are nonspecific and
may occur in patients with TMD. Patients with TMD also may have pains elsewhere
in the body, further increasing the chance of confusing TMD for FM or vice versa.
The use of a validated FM diagnostic is the most certain way to achieve an accurate
diagnosis.72
HEADACHES
Headache has been reported in many TMDs cases, but the relationship between these
2 conditions is still controversial.3 A study in the US population reported that 61.3% of
patients with orofacial pain reported headaches with migraine (with or without aura)
specifically affecting 38% of this population,73 and specifically 72.7% of patients
with TMD reported headaches.74 A 5-year prospective study reported that in patients
with migraine and tension-type headaches (TTHs), prevalence and frequency of head-
aches were strong indicators for the development of TMD. Multiple mechanisms
including genetics, trigeminocervical sensitization, and biopsychosocial and environ-
mental factors have been hypothesized to play a role.29
Tension-Type Headache
TTH is a primary headache characterized by bilateral mild or moderate pressing or
tightening pain, which is not worsened by routine physical activity. Because TTH often
overlaps with the temporalis region, feels as a physical pressure, lacks nausea and
vomiting, and often lacks photophobia and phonophobia,6 it at times is confused
with temporalis MOP. Differentiation is made by the fact that temporalis MOP is aggra-
vated by palpation and jaw function.3,62
Migraine Headache
Migraine headache is a primary headache characterized by moderate-to-severe uni-
lateral pulsating pain aggravated by routine physical activity, as well as nausea, vom-
iting, photophobia, and/or phonophobia.75 Because migraine headaches may overlap
with the temporalis region and are worsened with physical activity, migraine patients
are more likely to have TMD, and TMD and migraine headaches can trigger or aggra-
vate each other,76,77 migraines are sometimes confused with temporalis MOP.
However, the associated signs of nausea, vomiting, photophobia, and phonophobia,

as well as the response to migraine-specific medications, help the clinician recognize
migraine headaches. The absence of pain with jaw function and palpation of the tem-
poralis also suggest migraine headaches over temporalis MOP.
CORONOID HYPERPLASIA
An abnormal enlargement of the coronoid process should be considered as a TMD

condition that lies in the subcategory of associated structures.61
PERSISTENT IDIOPATHIC FACIAL PAIN
Persistent idiopathic facial pain is characterized by poorly localized dull, aching, or

nagging pain that does not follow the distribution of a peripheral nerve. The pain
can feel deep and can be aggravated by stress. When the location overlaps mastica-
tory muscles and/or the TMJ, this fairly nonspecific pain condition can seem to be a
TMD. The main points of differentiation are the aggravation of TMD by palpation
and/or jaw function.62
CLINICAL IMPLICATIONS
Although the complexity of the etiopathogenic domains may seem overwhelming,

there are significant clinical implications in terms of diagnosis and management. First
and foremost, the incorporation of validated questionnaires, screening tools, or
checklists assessing risk factors may help in the identification of the patient population
at risk for developing these conditions and enable the clustering of patients. Risk fac-
tors are a significant contributor to the development of TMDs. Identification and
addressing these risk factors may result in a substantial reduction in the incident,
and recurrent TMDs curtailing and addressing the deleterious oral parafunctional
risk factors and enhancing positive modifying factors are crucial to success; this
may also be an effective way to prevent the development of incident TMD and reduce
dependence on health care resources. In addition to promoting features for peripheral
management; emphasis may also be placed on improving general health outcomes
and addressing health and pain comorbidities. Traditionally home care instructions
have included local measures to provide pain relief. Emphasis on general health
care measures may help in addressing additional comorbidities and COPCs, thus
improving general health. The distinction between acute, chronic, single versus recur-
rent, persistent pain and regional/localized versus widespread TMD and the etiopa-
thological mechanism is critical to developing a management or treatment
strategies. Identification of distinct pathophysiological pathways, biopsychosocial
risk factors, and pain profiling in patients may help in developing clusters of individual
patients, predict prognosis, and use precision medicine to enhance success rates of
management. Current research suggests that simple therapy may suffice in patients
without significant psychological symptoms, whereas multimodal, interdisciplinary
management may be required for complex patients with major psychological risk fac-
tors. Identifying the complexity may form a platform for the clinician to initiate discus-
sion and patient education for interdisciplinary management. Hence it is also
important to follow the progression of individual parameters across various time points
in an individual to assess the development of systemic confounders affecting treat-
ment prognosis and management. Finally, the identification of pathophysiological
mechanisms may enable targeted pharmacologic interventions. For instance, if pe-
ripheral factors predominate, topical and pharmacologic medications targeting
18 Khan et al
peripheral sensitization mediators may be more effective, whereas in chronic condi-

tions centrally acting medications may be required.
CLINICS CARE POINTS
! The understanding of peripheral and centrally mediated pain can better help manage
patientsReferral pain from non-odontogenic regions can reflect as odontogenic pain.
DISCLOSURE
REFERENCES
1. Slade GD, Ohrbach R, Greenspan JD, et al. Painful temporomandibular disorder:

decade of discovery from OPERA studies. J Dent Res 2016;95(10):1084–92.
2. Slade GD, Bair E, Greenspan JD, et al. Signs and symptoms of first-onset TMD
and sociodemographic predictors of its development: the OPPERA prospective
cohort study. J Pain 2013;14(12 Suppl):T20–32 e1-3.
3. Schiffman E, Ohrbach R, Trueloveet E, et al. Diagnostic Criteria for Temporoman-
dibular Disorders (DC/TMD) for Clinical and Research Applications: recommen-
dations of the International RDC/TMD Consortium Network* and Orofacial Pain
Special Interest Groupdagger. J Oral Facial Pain Headache 2014;28(1):6–27.
4. Rongo R, Ekberg E, Nilsson I, et al. Diagnostic criteria for temporomandibular
disorders (DC/TMD) for children and adolescents: An international Delphi
study-Part 1-Development of Axis I. J Oral Rehabil 2021;48(7):836–45.
5. Slade GD, Fillingim R, Sanders A, et al. Summary of findings from the OPPERA
prospective cohort study of incidence of first-onset temporomandibular disorder:
implications and future directions. J Pain 2013;14(12 Suppl):T116–24.
6. Manfredini D, Lombardo L, Siciliani G. Temporomandibular disorders and dental
occlusion. A systematic review of association studies: end of an era? J Oral Re-
habil 2017;44(11):908–23.
7. Gesch D, Bernhardt O, Kirbschus A. Association of malocclusion and functional
occlusion with temporomandibular disorders (TMD) in adults: a systematic review
of population-based studies. Quintessence Int 2004;35(3):211–21.
8. Kalladka M, Young A, Thomas D, et al. The relation of temporomandibular disor-
ders and dental occlusion: a narrative review. Quintessence Int 2022;53(5):
450–9.
9. Bair E, Ohrbach R, Fillingim R, et al. Multivariable modeling of phenotypic risk
factors for first-onset TMD: the OPPERA prospective cohort study. J Pain 2013;
14(12 Suppl):T102–15.
10. Moin Anwer HM, Albagieh H, Kalladka M, et al. The role of the dentist in the diag-
nosis and management of pediatric obstructive sleep apnea. Saudi Dent J 2021;
33(7):424–33.
11. Ozasa K, Nishihara C, Watanabe K, et al. Somatosensory profile of a patient with
mixed connective tissue disease and Sjogren syndrome. J Am Dent Assoc 2020;
151(2):145–51.
12. Sanders AE, Slade G, Bair E, et al. General health status and incidence of first-
onset temporomandibular disorder: the OPPERA prospective cohort study. J
Pain 2013;14(12 Suppl):T51–62.
Biomechanics and
D e r a n g e m e n t s o f th e
Sowmya Ananthan, BDS, DMD, MSDa,*, Richard A. Pertes, a
DDS ,
Steven D. Bender, DDSb
KEYWORDS
! Temporo-mandibular joint ! Internal derangements ! Disc displacements
! Limited mouth opening
KEY POINTS
! In disc displacement with reduction, there is an opening click (disk reduction) and a clos-
ing click (discdisplacement).
! In disc displacement with reduction with intermittent locking, there is a high probability of
progression to a discdisplacement without reduction.
! In disc displacement without reduction, there is no click. The jaw is locked, with limited
mandibular opening, protrusion, and lateral excursion to the contra-lateral side.
INTRODUCTION
The human temporomandibular joint (TMJ), described as a ginglymoarthrodial joint, is

a highly complex synovial joint in which the two condyles function at the same time.
The complex is capable of both ginglymoid and arthrodial movements. It is the only
joint structure in the body with two distinct compartments separated by a fibrocartilag-
enous disc. The two compartments of the joint are filled with synovial fluid which pro-
vides lubrication and nutrition to the joint structures. The gliding movements, also
referred to as translatory movements, occur in the upper joint compartment between
the articular disc and glenoid fossa, whereas the hinge or rotary joint movements
occur in the lower compartment between the disc and the condyle. The bony aspects
of the complex are held together with ligaments. These ligaments surround the TMJ to
form the joint capsule. The lateral aspect of the capsule is formed by the temporoman-
dibular ligament. The joint capsule serves to limit the movements of the mandible. A
more detailed description of the anatomy can be found in other chapters of this
a
Department of Diagnostic Sciences, Center for Temporomandibular Disorders & Orofacial
Pain, Rutgers School of Dental Medicine, 110 Bergen Street, Newark, NJ 07101, USA;
b
Department of Oral and Maxillofacial Surgery, College of Dentistry, Texas A & M Health, 3302
Gaston Avenue, Dallas, TX 75246, USA

0011-8532/22/ª 2022 Published by Elsevier Inc.
2 Ananthan et al
edition. The movements of the mandible are mostly determined by the shape of the
boney architecture, the muscles of mastication, the ligaments, and the unique pattern
of occlusion for each individual.
The muscles of mastication consist of four paired muscle groups that include the
masseter, temporalis, medial pterygoid, and lateral pterygoid muscles. The digastric
muscles are not generally considered to be muscles of mastication but do serve an
important role in the movement of the mandible. These muscle groups will work in
concert with one another in positioning and movement of the mandible to accomplish
important functions such as chewing, speaking, and swallowing. The lateral pterygoid
muscle is thought to influence the articular disc position and movement due to the
small portion of the superior aspect of this muscle that attaches to the disk. However,
there is debate as to the amount of attachment and the significance this may have on
the movement of the disc1,2 (Table 1).
BIOMECHANICS OF THE TEMPOROMANDIBULAR JOINT
Movements of the mandible will cause both static and dynamic alterations in the TMJ
by generating forces such as compressive, tensile, and shear loading on the articular
surfaces.
The articular disc serves as a very fibrous and viscoelastic structure that allows
force distribution and smooth movement of the joint in its normal arrangement during
these processes. Most studies suggest that the normal disc position is where the pos-
terior band is located at the 120 o clock position within the glenoid fossa in the closed
mouth posture.3 The force of the condyle will be directed toward the intermediate zone
of the articular discwhich will lie against the anterior slope of the glenoid fossa. Anterior
to the disc is the anterior attachment which joins the disk to the TMJ capsule. The pos-
terior discattachment is sometimes referred to as the bilaminar zone. This highly vas-
cularized tissue consists of two parts; the superior fibroelastic layer that attaches the
disc to the posterior aspect of the glenoid fossa and the inferior fibrous layer that
Table 1
Muscles involved in mandibular movements
Action
Muscles Involved in Jaw Opening
Digastrics Rotation
Superior and inferior lateral pterygoids Translation
Muscles involved in jaw closing
Masseter
Medial pterygoid
Superior lateral pterygoid Minimal involvement
Muscles involved in protrusion
Superior and inferior lateral pterygoids
Superficial masseter Limited involvement
Medial pterygoid Limited involvement
Muscles involved in lateral excursions
Superior and inferior lateral pterygoids Contra-lateral to the direction of movement
Medial pterygoid
Masseter and temporalis Ipsilateral: keep condyle braced within the
articular fossa
Derangements of the Temporomandibular Joint 3
attaches the disc to the posterior portion of the condylar neck. The upper and lower
layers are separated by the intermediate layer, which contains loose connective tissue
and attaches to the posterior wall of the joint capsule. The posterior attachment will
elongate as the condyle translates anteriorly in the fossa and then shortens with jaw
closing as the condyle repositions in the fossa. The disk is very tightly attached to
the medial and lateral aspects of the condylar head by the discal ligaments. The
disk is not attached to the medial and lateral aspects of the joint capsule. This arrange-
ment appears to allow for a small amount of anterior and posterior rotation of the artic-
ular disc along the head of the condyle as the condyle moves within the fossa.
In the early mouth opening phase, condylar movement will occur in an inferior and
anterior direction beneath the intermediate zone of the articular disc by approximately
6 to 9 mm, causing an elongation of the retro discal tissues.4 Even with early opening,
both rotation and translation will be observed in the TMJ. As mentioned, the rotation
will occur between the condyle and the articular disc whereas the translation is simul-
taneously occurring between the disc and the fossa. The muscles involved in jaw
opening include the digastric muscles (rotation) and the bilateral lateral pterygoid mus-
cles (translation) involving both the superior and inferior aspects.4,5 With later mouth
opening the condylar movement will occur in an inferior and anterior direction loading
a portion of the anterior band of the articular disk as it rotates posteriorly in relation to
the condyle.4 With jaw closing, condylar translation occurs in the posterior direction
along with rotation as the mouth closes completely. The articular disc will rotate ante-
riorly with jaw closing. The masseter muscles as well as the medial pterygoid, tempo-
ralis, along with minimal activity of the superior aspect of the lateral pterygoid muscle
are all involved in the closing action.5 For a protrusive movement, bilateral and simul-
taneous contractions of the lateral pterygoid muscles involving both the superior and
inferior aspects will occur. There is also some involvement of the superficial masseter
muscle as well as potentially the medial pterygoid muscle.5 This is mostly a transla-
tional movement with the articular disk interposed between the condyle and glenoid
fossa. In a unilateral eccentric movement, the superior and inferior portions of the
lateral pterygoid contralateral to the direction of movement of the mandible will con-
tract. Also involved will be the masseter and temporalis muscles on the ipsilateral
side keeping the ipsilateral condyle braced within the articular fossa. The medial pter-
ygoid on the contralateral side of the direction of the movement may also be involved.5
The condyle on the contralateral side of the direction of the mandibular movement will
show translation within the articular fossa. In an ideal condyle to disc arrangement, the
articular disc will remain interposed between the two structures with the load being
placed primarily on the intermediate zone of the articular disc.
DERANGEMENTS OF THE TEMPOROMANDIBULAR JOINT
In a healthy joint, the posterior band of the articular disc ends at the apex of the
condyle when the teeth are in occlusion. However, when the biomechanics of the joint
is altered, the disc may be displaced creating an abnormal relationship between the
disc, condyle, and the eminence that is often referred to as an internal derangement.
Usually, the disc is displaced in an anterior or anteromedial direction, but medial,
lateral, and even posterior displacements have been reported.
The disc is maintained in its proper relationship by tight discal ligaments and a self-
seating capacity provided by thick posterior and anterior borders of the disk, which act
as wedges holding it in position. Because the only physiologic movement occuring be-
tween the condyle and disk is rotation, any sliding movement between the disk and
condyle is considered abnormal.
4 Ananthan et al
Several possible causes for disc displacements have been proposed, but trauma is
the most common etiologic factor contributing to a change in biomechanics in the
joint. It can take the form of macro-trauma from a sudden blow to the jaw, especially
when the mouth is open. Most cases of internal derangement, however, are caused by
micro-trauma involving mild, frequent, and repetitive forces on the joint over a pro-
longed period. A common example of microtrauma is bruxism.6
As a result of prolonged clenching, hard biting, or trauma with the teeth together,
excessive pressure on the joint may cause the expression of the synovial fluid that lu-
bricates the junction between the superior surface of the disc and the articular
eminence. This may introduce a harmful frictional component into normal translatory
movement and cause an adhesion to develop between these surfaces. When this oc-
curs, the disk may become temporarily fixated to the eminence sometimes referred to
as a “sticky disk”.7,8 With opening, the disc will lift off the condyle accompanied by a
single-clicking noise, and lubrication to the joint surfaces will return leading to a
resumption of normal joint function. But in the process of breaking the adhesion be-
tween the disc and eminence, the discal ligaments may become stretched. These lig-
aments do not have the property of elasticity and function to limit movement and when
they become elongated, the stage is set for a disc displacement.9
If the disc is displaced, the inferior retrodiscal lamina, which limits anterior rotations
of the disc on the condyle may also become elongated allowing the disc to become
positioned more anteriorly on the condyle. Now, any pressure on the TMJ will cause
thinning of the posterior border of the disc resulting in a loss of its self-seating capacity
further encouraging displacement of the disc.
In the diagnostic criteria for temporomandibular disorders (DC/TMD) classification,10
the most common intra-articular disorders involving a disc displacement include:
! Disc displacement with reduction
! Disc displacement with reduction with intermittent locking
! Disc displacement without reduction with limited opening
! Disc displacement without reduction without limited opening
Although disc displacements are presented as a series of progressively worsening
clinical stages starting with disc displacement with reduction, studies indicate that few
patients follow this progression.11 Most patients remain in the initial stage of disc
displacement with reduction for years and are able to adapt to their dysfunction
with little or no discomfort.12 Why this occurs is not clear, but it has been suggested
that patients with a lack of posterior dental support, systemic ligament laxity, and par-
afunctional activity may be more susceptible.
DISC DISPLACEMENT WITH REDUCTION
The DC/TMD describes this stage as “An intracapsular biomechanical disorder char-
acterized by displacement of the disc in an anterior position relative to the condylar
head in the closed mouth position and the disc reduces on mouth opening with a re-
turn to a more normal position relative to the condyle on opening”.
Clinical Signs and Symptoms

The most characteristic feature is a clicking, popping, or snapping sound detected
with palpation during opening and closing. The opening click can occur at any point
in the translatory cycle as the condyle traverses under the posterior border of the
disc into a normal relationship with the disk. This is referred to as reduction or recap-
ture of the disc. At or near the intercuspal position, a soft click may also be detected as
the disc again becomes displaced. The dual opening and closing clicks are often
referred to as reciprocal clicking with disc displacement on closing and disc reduction
on opening (Fig. 1).
Disc displacement with reduction is also characterized by deviation of the mandib-
ular midline toward the affected joint on early opening because of the displaced disk
preventing condylar translation. With further opening, a clicking noise can be detected
as the condyle passes under the posterior border of the disc indicating that the disc
has been reduced. At that point in translation, the mandibular midline returns to
normal. Mandibular vertical opening is usually relatively normal and any limitation on
opening is due to secondary elevator masticatory muscle involvement, not mechanical
obstruction by the disc.
For many years, the stage of disc displacement with reduction was thought to be a
precursor to the stage of disc displacement without reduction. But studies show that
most of the patients with disc displacement with reduction do not progress to disc
displacement without reduction.13 Further, disc displacement with reduction is not
usually accompanied by pain.
But why is pain absent in most patients when the disc is displaced and the condyle
able to press against the highly vascularized and well-innervated retrodiscal tissues in
the posterior attachment, especially when the teeth are in contact? Most patients are
able to adapt to this dysfunction because the posterior attachment has undergone
fibrotic changes and is no longer innervated or vascularized.14 These adaptive
changes are often referred to as "pseudodisk formation" and allow the posterior
attachment to function as an extension of the disc.15,16 Therefore, when the condyle
presses against the posterior attachment, there is no pain. In some cases, however,
when pseudodisc adaptation does not occur, pain may be present as a result of
inflammation in the posterior attachment or strained discal ligaments.
Diagnosis
The diagnosis of disc displacement with reduction is based on a history of any TMJ
noise with jaw movement in the past 30 days or a patient report of jaw noise during
the clinical exam. In addition, a clicking, popping, and/or snapping noise must be
detected with palpation during at least one of three repetitions of opening and closing
movements (DC/TMD). Joint sounds commonly occur in the general population. In
the DC/TMD, the sensitivity (ie, ability of a test to correctly identify patients with the dis-
ease) for diagnosing disc displacement with reduction without imaging is 0.34 and the
sensitivity (ie, ability of a test to correctly identify people without the disease) is 0.92. This
indicates that most clinicians encounter difficulty diagnosing a disc displacement and
questions the accuracy of using only palpation of the joint for this purpose.
Fig. 1. Disc displacement with reduction showing late reduction of the disc in the transla-
tory cycle. As the condyle passes under the posterior border of the disk, an opening click
is usually heard. (A) the displaced disc in closed mouth position, (B) condyle passing under
the posterior border of the disc. (C) disc reduction has been accomplished. (From Pertes,RA,
Gross SG. Clinical Management of Temporomandibular Disorders and Orofacial Pain. Chi-
cago, Quintessence, 1995.)
6 Ananthan et al
In a study involving 273 consecutive patients with TMD, clicking was detected in
143 joints using digital palpation during mouth opening and closing, but the accuracy
of identifying disc displacement / with (DD/W) reduction was relatively low as verified
with MRI in these patients. However, with the use of a Clicking Elimination Test the ac-
curacy of detecting DD/W reduction significantly improved.17 In this test, the patient to
open his/her mouth until a clicking noise occurs indicating the disk has been reduced.
Then the patient is instructed to close in a protruded edge-to-edge position. At that
point, the disc is still reduced and when the patient opens there will be no joint noise.
But if clicking is not eliminated, the patient should be asked to repeat opening and
closing the mouth in a more protruded position until clicking is no longer present.
If the diagnosis is still unclear, MRI of the TMJs may be needed. To correctly diag-
nose DD W/red using MRI, the DC/TMD states that the posterior band of the disc
should be located anterior to the 11:30 position and the intermediate zone of the
disk anterior to the condylar head in maximum intercuspation. On full opening, the in-
termediate zone of the disc should be between the condylar head and the articular
eminence (Fig. 2).
Management
When there is no pain and minimal interference with function, no treatment is indi-
cated. However, it is important to educate the patient about the biomechanics
involved in disc displacement and the benign nature of this disorder to allay any fears
the patient might have. However, there remains a small possibility of progression to
disc displacement without reduction and the patient should be periodically monitored
for any changes.
Because the disc is displaced, it seemed obvious that the goal of treatment should
be to restore a normal disc-condyle relationship. This led to the concept of using
mandibular repositioning appliances to advance the mandible forward into a new
therapeutic position to “recapture” or reduce the disc and eliminate clicking.18 On a
Fig. 2. MRI showing disc displacement with reduction. Note displacement of the disc (arrow)
anterior to the condyle in closed position and reduction of the disk to a more "normal" loca-
tion between the condyle and eminence in open position.
short-term basis, mandibular repositioning appeared to be successful, but long-term

efforts to permanently recapture the disc were not as successful, with studies showing
that in most cases, that the disc remained displaced when the appliance was discon-
tinued.18,19 This result was not surprising, since a disc displacement causes irrevers-
ible elongation of the tight discal ligaments that hold the disc in place. When this is
accompanied by flattening of the posterior border of the disc and a loss in shape of
the disc,20 it results in a loss of its self-seating capacity on the condyle.
Despite these limitations, anterior repositioning appliances did help to reduce
pain.21 With the mandible in a forward position, the condyle did not impinge upon
the posterior attachment, thereby decreasing inflammation and pain. Not only did
this relieve pressure on the posterior attachment, it also encouraged pseudodisc for-
mation. After repositioning therapy, some clinicians advocate a second phase ("Phase
II") of dental therapy to preserve the newly acquired occlusal relationship. This
approach often involves extensive dental reconstruction or orthodontics and should
be reserved for those few patients whose pain can only be managed by maintaining
a forward mandibular position.22 It appears that the main role of repositioning therapy
may be to control pain while allowing the injured tissues to undergo adaptation.6
The most reasonable approach to the management of DDW/red is to concentrate on
reducing pain without attempting to recapture the disk starting with a joint stabilization
appliance to be worn at night. This is the most commonly used appliance for TMD and
is often used for masticatory myalgia and TMJ arthralgia. However, it may also be
effective for some cases of DD/W reduction as well, especially when the disk is
reduced early in the translatory cycle.
This appliance is made in the patient’s habitual arc of closure and is designed to
provide a stable occlusal posture by creating contacts between the occlusal surface
of the appliance and all opposing teeth. It does not involve any change in mandibular
position. But if this approach is not effective, an anterior repositioning appliance
should be fabricated mainly for use when sleeping. As pain decreases, the appliance
can be gradually “walked back" and converted to a stabilization appliance. If symp-
toms return, repositioning therapy may need to be restarted despite the problems
associated with repositioning, such as a posterior open bite.23
When pain is present, supportive therapy is needed. Nonsteroidal analgesic medi-
cations may be needed to reduce inflammation and if the masticatory muscles are
secondarily involved, muscle relaxants can also be prescribed. The patient should
be advised to follow a home regimen and decrease loading on the joint by eating softer
foods, taking smaller bites, and reducing clenching of the teeth whenever possible.
CLINICS CARE POINTS
! A click on opening (disk reduction) and closing (disk displacement) is present.

! Pain is usually absent
! A relatively normal vertical opening is present
! If pain is present, management should focus on encouraging adaptive changes in the
posterior attachment, not recapturing the disk
DISK DISPLACEMENT WITH INTERMITTENT LOCKING
Some patients with DD W/reduction may experience short episodes of limited mouth
opening or locking. In these patients, the disc is in an anterior position relative to the
8 Ananthan et al
condylar head when the mouth is closed, and the disc intermittently reduces with
mouth opening. This stage represents a progressive deterioration of TMJ structures
from the stage of DD W/reduction.
The episodes of locking occur because of additional elongation of the discal liga-
ments and more flattening of the posterior border of the disk. In addition, there is
stretching and a loss of elasticity in the superior retro discal lamina of the posterior
attachment, which is the only structure capable of retracting the disk on opening.6
Clinical Presentation
Joint noise is present on palpation during both opening and closing movement of the
mandible. When the disc does not reduce on mouth opening, however, the jaw is
locked and limited mandibular movement is present. When the jaw is locked, there
will be no joint noise.
When the joint is locked and limited opening is present, the patient may have to ma-
neuver his/her jaw to unlock the jaw and reduce the disc by moving the mandible to the
contralateral side.
Diagnosis
A diagnosis of DDW/reduction with intermittent locking should be suspected when a
patient reports a history of episodes of limited opening, especially upon awakening. It
should be noted that these episodes may be extremely short, even momentarily. Dur-
ing the clinical examination, a clicking, popping or snapping noise is detected with
palpation during opening and closing movements, which is indicative of DDW/red.
The clicking elimination test can be used to confirm the diagnosis. Sometimes during
the examination, the jaw may lock, and the clinician may have to perform a maneuver
to reduce the disk. In the DC/TMD criteria for diagnosis, the sensitivity for diagnosing
the disorder is 0.38 and the specificity is 0.98. However, in the authors’ opinion, most
cases can be diagnosed based on the history and clinical examination, and imaging is
rarely needed.
Management
The prognosis is poor, with a greater likelihood of progression to disc displacement
without reduction. However, some clinicians recommend the use of a maxillary appli-
ance at night with a ramp to take pressure off the posterior attachment and encourage
pseudodisc formation (Fig. 3).
Fig. 3. Maxillary appliance with ramp.
CLINICS CARE POINTS
! Disk displacement with reduction present except when locked

! Diagnosis is mainly by the patient report of locking or if it occurs during the examination
! High probability of progression to disk displacement without opening
DISK DISPLACEMENT WITHOUT REDUCTION WITH LIMITED OPENING
In the DC/TMD, this stage is described a disorder in which the disc is in an anterior
position relative to the condylar head in the closed mouth position and does not
reduce on mouth opening. Medial and lateral displacement of the disc can also occur.
When the disc does not reduce on opening during translation, the condyle is unable to
pass under the displaced disc and there is a loss of contact between the condyle, disc,
and articular eminence. Because the disc is trapped in front of the condyle, there is a
limited translatory movement that is often referred to as a “closed lock.” Except where
acute microtrauma is involved, this stage usually represents a progressive deteriora-
tion in joint structures starting with the stage of disc displacement with reduction
(Fig. 4).
These patients often report a history of clicking that was interrupted by periods of
locking. They usually remember when the clicking stopped and limited opening and
pain started. Why this progression occurs in only a small number of patients and
not in most cases of disc displacement with reduction is not clear. It has been sug-
gested that contributing factors, such as the loss of posterior dental support, systemic
ligament laxity, or the presence of parafunctional habits (clenching), may play a role.
Clinical Characteristics
This stage is relatively acute and clinical examination will reveal a severely restricted
opening (25–30 mm) with a marked midline deflection of the mandible to the side of
the affected joint (ipsilateral). Protrusive excursion is also limited and accompanied
by a deflection to the ipsilateral side (Fig. 5). Lateral movement to the opposite (contra-
lateral) side is also restricted, but mandibular movement to the ipsilateral side is
normal since this only requires rotational movement of the condyle and not condylar
translation.
Fig. 4. Disc displacement without reduction. In the acute stage, failure to reduce the disc
prevents normal condylar movement in the affected joint. With time, a more normal range
of motion returns. (A) the displaced disc in closed mouth position. (B) the condyle is unable
to pass under the displaced disc. (C) the disc is unable to reduce. (From Pertes, RA, Gross SG.
Clinical Management of Temporomandibular Disorders and Orofacial Pain. Chicago, Quin-
tessence, 1995.)
10 Ananthan et al
Fig. 5. Deviation of the incisal path is characteristic of disk displacement with reduction. The
midline shifts to the ipsilateral side on opening and returns to a centered position after disc
reduction. Deflection is characteristic of acute disc displacement without reduction where
the midline continuously displaces to the ipsilateral side. (From Pertes, RA, Gross SG. Clinical
Management of Temporomandibular Disorders and Orofacial Pain. Chicago, Quintessence,
1995.)
The restricted jaw movement interferes with the patient’s ability to eat. Generally,
this stage is accompanied by pain due to inflammation in the articular capsule, discal
ligaments, and posterior attachment. Activity of the masseter and temporalis muscles
on the affected side is usually increased adding to limited opening and pain.
Diagnosis
During the examination, the jaw is locked, and opening is severely limited to less than
40 mm. Because there are other causes of limited opening (hypomobility), it is impor-
tant to differentiate DD W/reduction and limited opening from a masticatory elevator
muscle problem. Clinically, if the elevator muscles are in spasm, only vertical opening
will be limited, and lateral excursions and protrusive excursion will be normal. This
contrasts with disc displacement without reduction with limited opening where vertical
opening, contralateral excursion, and protrusive excursion are all restricted and only
movement toward the affected joint (ipsilateral) is normal.
When opening is limited, another diagnostic test that may help in determining the
nature of the restriction is the end feel. This test involves the clinician placing the
thumb and middle finger between the upper and lower incisors and gently applying
pressure to increase mouth opening (Fig. 6). If opening is increased, the end feel is
considered to be soft and the restriction is due to masticatory muscle involvement.
However, if opening is not increased, the end feel is termed hard, and the restricted
opening is most likely due to a displaced disk that prevents condylar translation.
Management
The main goal of treatment is to decrease any pain that is present by encouraging
pseudodisc formation. The chances for recapturing the disc and maintaining it on
the condyle are poor because of changes in the morphology of the disc along with irre-
versible changes in the posterior attachment and discal ligaments. The use of an
Fig. 6. Testing for end feel.
anterior repositioning appliance should be avoided because it may force the disk for-
ward causing more pain.
Encouraging pseudodisc formation in patients with disc displacement with limited
opening and leaving the disc in place is often referred to as "off the disk" treatment.
It is important to note, however, that if the disc is permanently displaced, the patient
is predisposed to degenerative changes in the TMJ. Without a disc between the
condyle and eminence, the articular tissues covering the bony components of the joint
can be distorted when subjected to heavy compressive forces. In clinical and radio-
logical studies, a strong association was found between disc displacement without
reduction and osteoarthritis.24,25
However, if the disc displacement was caused by a single traumatic event to a
healthy joint, or occurred suddenly, an attempt should be made to reduce the disc
through manual mobilization as soon as possible (see Fig. 6). The success of this pro-
cedure is dependent upon a functioning superior retro discal lamina, which is the only
structure capable of retracting the disk.
Self-mobilization by the patient should be attempted first. The patient should be
instructed to open slightly and then move the mandible as far as possible to the
contralateral side. At that point, the patient should open to his/her maximum opening.
If a click is heard or if the patient can open further with minimum difficulty, the disc is
probably reduced. However, if after a few attempts, the disc is still displaced, manual
mobilization by the clinician is indicated. With the thumb over the last molar on the side
of the affected joint and the fingers placed on the inferior border of the mandible, the
12 Ananthan et al
Fig. 7. Manual mobilization of the TMJ to reduce a displaced disk. Applying a downward
force on the ipsilateral molars separates the condyle from the eminence to allow the supe-
rior retro discal lamina in the posterior attachment to retract the disk. Because this proced-
ure can be painful, some patients may need a local anesthetic block of the joint.
clinician should exert downward pressure to move the condyle inferiorly increasing the
space between the condyle and eminence to allow retraction of the disc (Fig. 7). The
patient should protrude the mandible while the clinician moves the mandible to the
contralateral side. If mobilization is successful, the patient should be able to achieve
a normal vertical opening. At that point, cotton rolls or gauze pads should be placed
between the posterior teeth on the affected side for about 10 minutes to maintain the
disc reduction. As soon as possible, an appliance should be placed to move the
mandible forward and allow the disc to recover its original shape. This appliance
should be worn full time for about 3 to 4 days and then at night. The prognosis is fairly
good, indicating that the superior retro discal lamina is still functioning and able to
reduce the disc.
CLINICS CARE POINTS
! Jaw is locked causing limited mandibular opening, protrusive and lateral excursion to
contralateral side
! Clicking, popping, and snapping not present in affected joint
! Usually, painful
DISK DISPLACEMENT WITHOUT REDUCTION WITHOUT LIMITED OPENING
In this stage, the disc is still displaced in an anterior position relative to the condylar
head and does not reduce on opening. Although the disc is permanently displaced,
as the posterior attachment elongates most patients can achieve a more normal range
of motion and function normally.
Clinical Presentation
The maximum passive (operator assisted) opening is about 40 mm, which is slightly
restricted. There may also be a slight deflection to the ipsilateral side and some restric-
tion to the contralateral side.
This condition is not usually painful indicating that adaptive changes in the form of a
pseudo disc occurred. A crunching or grating noise (crepitus) may be present because
of degenerative changes in the joint. However, a clicking noise is absent.
Diagnosis
The patient will usually present with a prior history of jaw locking and limited mouth
opening that caused difficulty with eating. Because these patients have a range of
mandibular movement that is close to normal, diagnosis can be difficult, and MRI
may be needed to confirm the diagnosis (Fig. 8). However, it is appropriate to raise
the question about whether imaging is worth the expense, especially when the patient
has little, if any, discomfort, and relatively normal function.
Management
Placement of a joint stabilization appliance, along with elimination of contributing fac-
tors, may also help pseudodisc formation. For those patients who do not gradually
achieve a normal range of opening with time, a course of physical therapy using
various types of distraction procedures is recommended. This may include the use
of an increasing number of tongue blades to increase the opening range, or mechan-
ical devices such as the Therabite26 or EZ-Flex. The presence of persistent pain in the
joint, however, may indicate that adaptation is not occurring and an invasive proced-
ure such as arthrocentesis (joint lavage) or arthroscopy should be considered.
Differential Diagnosis of Disc Displacements

Disc displacement with reduction can usually be diagnosed with considerable accu-
racy by clinical examination only, without the need for imaging.17 Most cases of
disc displacement without reduction with limited opening can also be diagnosed
based on clinical findings along with a prior history of clicking or recent trauma. How-
ever, the accuracy of detecting disk displacement without reduction without limited
opening using only history and clinical examination is not high, especially when vertical
opening is close to normal and deflection to the ipsilateral side is minimal. In these
cases, MRI of the TMJ may be needed to confirm the diagnosis.27 Although a variety
of electronic instruments have been developed to help evaluate disc displacements
Fig. 8. Disc position in anterior disc displacement without reduction, without limited open-
ing, in the closed and open mouth positions. Both arrows show the anteriorly displaced disc
in closed and open mouth positions in disc displacement without reduction.
14 Ananthan et al
and are used by many clinicians, the validity of these diagnostic devices is
questionable.
Most cases of limited mouth opening (hypomobility) are related to a masticatory
muscle disorder, although a displaced disc can also limit mouth opening. From the
viewpoint of a differential diagnosis, contraction of elevator muscles only restricts ver-
tical opening, but does not significantly affect lateral or protrusive excursions. In
contrast, an acute disc displacement (closed lock) will severely limit contralateral
and protrusive movement.
Another cause of hypomobility is coronoid process hyperplasia, a rare disorder
caused by progressive elongation of the coronoid process. As a result, the coronoid
process is unable to pass between the zygomatic process and the lateral surface of
the maxilla. Clinically, all mandibular movements will be restricted, especially
protrusion.
DISCLOSURE
REFERENCES
1. Meyenberg K, Kubik S, Palla S. Relationships of the muscles of mastication to the

articular disc of the temporomandibular joint. Schweiz Monatsschr Zahnmed
(1984) 1986;96(6):815–34.
2. Wilkinson TM. The relationship between the disk and the lateral pterygoid muscle
in the human temporomandibular joint. J Prosthet Dent 1988;60(6):715–24.
3. Murakami S, Takahashi A, Nishiyama H, et al. Magnetic resonance evaluation of
the temporomandibular joint disc position and configuration. Dentomaxillofac Ra-
diol 1993;22(4):205–7.
4. Bhargava D, Gurjar P. Anatomy and Basic Biomechanics of the Temporomandib-
ular Joint. In: Bhargava D, editor. Temporomandibular Joint Disorders. Singapore:
Springer; 2021. p. 9–21.
5. Hargitai IA, Hawkins JM, Ehrlich AD. The Temporomandibular Joint. In:
Gremillion HA, Klasse GD, editors. Temporomandibular Disorders. Berlin/Heidel-
berg, Germany: Springer; 2018. p. 91–107.
6. Okeson JP. Joint intracapsular disorders: diagnostic and nonsurgical manage-
ment considerations. Dent Clin North Am 2007;51(1):85–103, vi.
7. Nitzan DW. The process of lubrication impairment and its involvement in tempo-
romandibular joint disc displacement: a theoretical concept. J Oral Maxillofac
Surg 2001;59(1):36–45.
8. Nitzan DW, Etsion I. Adhesive force: the underlying cause of the disc anchorage
to the fossa and/or eminence in the temporomandibular joint–a new concept.
J Oral Maxillofac Surg 2002;31(1):94–9.
9. Nitzan DW, Marmary Y. The "anchored disc phenomenon": a proposed etiology
for sudden-onset, severe, and persistent closed lock of the temporomandibular
joint. J Oral Maxillofac Surg 1997;55(8):797–802, discussion 802-3.
10. Schiffman E, Ohrbach R, Truelove E, et al. Diagnostic Criteria for Temporoman-
dibular Disorders (DC/TMD) for Clinical and Research Applications: recommen-
dations of the International RDC/TMD Consortium Network* and Orofacial Pain
Special Interest Groupdagger. J Oral Facial Pain Headache 2014;28(1):6–27.
11. Poluha RL, Canales GT, Costa YM, et al. Temporomandibular joint disc displace-
ment with reduction: a review of mechanisms and clinical presentation. J Appl
Oral Sci 2019;27:e20180433.

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Classification and Diagnosis

Dent Clin N Am - (2022) -–-

Currently, classification is broadly defined as a “systematic arrangement in groups or

CLASSIFICATION SYSTEMS FOR TEMPOROMANDIBULAR DISORDERS

Among the significant improvements of the ICD 11 is the addition in Chapter 21 of a

ACTTION-APS Pain Taxonomy

American Academy of Orofacial Pain

American Academy of Craniofacial Pain

Temporomandibular Joint Disorders 5.Congenital/developmental disorders

The International Classification of Orofacial Pain

Okeson Classification of Temporomandibular Disorders (8th Edition)

2. Myofascial orofacial pain 3. Temporomandibular Joint (TMJ) pain

DIAGNOSTIC SYSTEMS FOR TEMPOROMANDIBULAR DISORDERS

Diagnostic Criteria for Temporomandibular Disorders

Most Common Pain-Related Temporomandibular Disorders

Expanded Diagnostic Criteria for Temporomandibular Disorder taxonomy

International Classification for Orofacial Pain

CLINICS CARE POINTS

The authors have nothing to disclose.

Veronica Iturriaga, DDS, MSc, PhDa,*, Thomas Bornhardt, DDS, MSc

The masticatory or stomatognathic system has to be understood as a physiologic,

Dent Clin N Am - (2022) -–-

In the evolution of the osseous components of the current temporomandibular joint

Fig. 1. Localization of the temporomandibular joint (human cadaveric specimen, sagittal

Fig. 2. Temporomandibular joint anatomy components (human cadaveric specimen, sagittal

which is formed by fibrous connective tissue with islands of fibrocartilage devoid of

GENERAL CHARACTERISTICS OF THE TEMPOROMANDIBULAR JOINT

OSSEOUS AND CARTILAGINOUS COMPONENTS OF THE TEMPOROMANDIBULAR

Mandibular Fossa and Articular Tubercule

Fig. 3. Temporomandibular joint of rabbit (Oryctolagus cuniculus). (A). Sagittal section of a

which, as a consequence of joint inflammation, edema or effusion may occur. Currently,

LIGAMENTS AND SYNOVIAL MEMBRANE OF THE TEMPOROMANDIBULAR JOINT

MAIN MUSCLE COMPONENTS RELATED TO THE TEMPOROMANDIBULAR JOINT

CLINICS CARE POINTS

1. Mejia C, Salazar L. Desarrollo ontogénico de la articulación temporomandibular

Comorbidity is largely defined in medical literature as a specific additional condition that

Dent Clin N Am - (2022) -–-

A. Any headache fulfilling criteria

TMD pain include nonsteroidal anti-inflammatory drugs (NSAIDs), muscle relaxants,

LOWER BACK PAIN

There is an abundance of literature showing significant association between LBP and

ANXIETY AND DEPRESSION

IRRITABLE BOWEL SYNDROME

CHRONIC FATIGUE SYNDROME

MANAGEMENT OF TEMPOROMANDIBULAR JOINT DISORDERS WITH

Comorbidities should be addressed in an attempt to manage TMD and TMD-

Dent Clin N Am - (2022) -–-

degenerative joint diseases such as osteoarthritis and RA or anatomic variants such as

Inaccuracies in the measurable distance are a limitation of the panoramic technique.

PLANAR IMAGING (PLAIN IMAGING OR 2D IMAGING)

LINEAR AND PLURIDIRECTIONAL TOMOGRAPHY

Arthrography and Arthrocentesis

Magnetic Resonance Imaging

Fig. 7. Adjusted bilateral sagittal projections demonstrating osteoarthritic changes of the

Nuclear Imaging (Bone Scanning and Positron Emission Scanning)

breakthrough in nuclear medicine.19 FDG-PET/CT and NaF-PET/CT have high TMJ

Diagnostic imaging of the temporomandibular joint can provide confirmation of clini-

CLINICS CARE POINTS

! Select imaging studies based on supected conditions.