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Temporomandibular Joint Pain
and Dysfunction
Kathleen Herb, DMD, MD, Sung Cho, DMD,
and Marlind Alan Stiles, DMD
Corresponding author
Marlind Alan Stiles, DMD
Department of Oral and Maxillofacial Surgery, Thomas Jefferson
University Hospital, 909 Walnut Street, Suite 300, Philadelphia,
PA 19107, USA.
E-mail: alan.stiles@jefferson.edu
Current Pain and Headache Reports 2006, 10:408 – 414
Current Science Inc. ISSN 1531-3433
Copyright © 2006 by Current Science Inc.
Pain caused by temporomandibular disorders originates
from either muscular or articular conditions, or both.
Distinguishing the precise source of the pain is a significant diagnostic challenge to clinicians, and effective
management hinges on establishing a correct diagnosis.
This paper examines terminology and regional anatomy
as it pertains to functional and dysfunctional states of
the temporomandibular joint and muscles of mastication. A review of the pathophysiology of the most
common disorders is provided. Trends in evaluation,
diagnosis, treatment, and research are presented.
Introduction
Signs and symptoms of temporomandibular disorders
(TMDs) may include pain, impaired jaw function,
malocclusion, deviation or deflection, limited range of
motion, joint noise, and locking. Headache, tinnitus,
visual changes, and other neurologic complaints may
also accompany TMDs. Because of many etiologic factors, the diagnosis and treatment of patients with TMDs
is complex. TMDs can be subdivided into muscular and
articular categories. Differentiation between the two is
sometimes difficult because muscle disorders may mimic
articular disorders, and they may coexist. Myogenic disorders include myalgia (myofascial pain, fibromyalgia),
myospasm, splinting, and fibrosis/contracture. Articular disorders include synovitis/capsulitis, joint effusion,
trauma/fracture, internal derangement, arthritis, and neoplasm. Accurate diagnosis allows for appropriate therapy
whether it is nonsurgical or surgical. Current trends favor
conservative (nonsurgical) therapy, and the surgical interventions have become less aggressive, moving away from
open arthroplasty and toward arthroscopic procedures.
Research continues to look toward biochemical markers
of disease. The interrelationship between the various disorders continues to be explored.
The temporomandibular joint (TMJ) is a compound
articulation formed from the articular surfaces of the
temporal bone and the mandibular condyle. Both surfaces are covered by dense articular fibrocartilage. Each
condyle articulates with a large surface area of temporal
bone consisting of the articular fossa, articular eminence,
and preglenoid plane. The TMJ functions uniquely in that
the condyle both rotates within the fossa and translates
anteriorly along the articular eminence. Because of the
condyle’s ability to translate, the mandible can have a
much higher maximal incisal opening than would be possible with rotation alone. The joint is thus referred to as
“gynglimodiarthrodial”: a combination of the terms ginglymoid (rotation) and arthroidial (translation) [1].
A cartilaginous disc resides between the articular
surfaces of the temporal bone and mandibular condyle.
Although other articular cartilages are composed of
hyaline cartilage, this disc is composed of fibrocartilage;
thus, the disc contains a much higher percentage of collagen, increasing its stiffness and durability. The disc does
not have any direct vascularization or innervation; however, the posterior attachment of the disc (also known as
retrodiscal tissue) is both highly vascularized and highly
innervated and, therefore, pertinent to the discussion of
joint pain. The superior lamina of the retrodiscal tissue
limits extreme translation, whereas the inferior lamina
limits extreme rotation. The lateral pterygoid muscle controls the opening of the mandible. The superior segment
of this muscle attaches to the anterior portion of the disc,
and the inferior segment attaches inferior to the condyle.
As both segments contract the condyle translates anteriorly along the articular eminence, and the disc remains
interposed between the condyle and the temporal bone at
all points of translation.
The joint is stabilized by three ligaments: collateral
(discal), capsular, and temporomandibular. These attach
to the disc at the medial and lateral poles of the mandibular condyle, as well as to the temporal fossa. These
ligaments limit extreme condylar movement. The capsular
Temporomandibular Joint Pain and Dysfunction Herb et al.
ligament surrounds the joint space and disc and acts to
contain the synovial fluid within the joint space.
The capsule is lined by a synovial membrane. Synovial
tissue covers all intra-articular surfaces except for the pressure-bearing fibrocartilage (ie, disc, condyle, eminence).
The synovial tissue is highly innervated and vascularized
and has regulatory, phagocytic, and secretory functions.
The synovial fluid has metabolic and nutritional functions
and is essential to joint surface lubrication [2].
The masseter, medial pterygoid, lateral pterygoid, and
temporalis muscles are the muscles of mastication. The
masseter, medial pterygoid, and temporalis are primarily
responsible for mandibular closure and bite force, whereas
the lateral pterygoid and infrahyoid muscles are responsible for mandibular opening. Mandibular movement is
also influenced by the digastric, geniohyoid, mylohyoid,
stylohyoid, sternohyoid, omohyoid, sternothyroid, and
thyrohyoid muscles, which as a group coordinate complex
mandibular movements including opening, protrusion,
retrusion, lateral excursion, and closure.
At rest, the condyle is seated passively in the temporal
fossa with the fibrocartilage disc interposed at the most
superior and anterior position of the condyle commonly
referred to as the 11-o’clock position. Mandibular opening commences with contraction of the lateral pterygoid
and infrahyoid muscles, which rotates the condyle.
Mandibular opening proceeds with lateral pterygoid
contraction pulling the condyle forward along the articular eminence (translation). The superior segment of the
lateral pterygoid muscle coordinates the translation of
the disc with the condyle. During jaw closing the ligaments and retrodiscal lamina pull the condyle and disc
back into resting position.
The TMJ receives its vascular supply from the
superficial temporal, maxillary, and masseteric arteries.
Innervation of the joint is provided mainly by the auriculotemporal nerve and, to a lesser extent, the masseteric
and posterior deep temporal nerves. The production
of synovial fluid is also under a certain amount of
neuronal control.
Temporomandibular Disorders
The term “TMJ pain” varies greatly in meaning among
clinicians, patients, and the general population. Historically, symptom-based classification of the disorder
has been problematic. As stated by Laskin [3,4], the
difficulty began with the introduction of a “TMJ syndrome.” Then clinicians erroneously grouped a “variety
of etiologically unrelated conditions into one diagnostic
category based on the fact that they produced similar
signs and symptoms,” and this led to “one diagnosis
equals one treatment.” Only later was it recognized that
many of these patients suffered from muscle-related
conditions. The terms myofascial pain (MFP) and myofascial pain and dysfunction (MPD) evolved [5], and
409
“TMJ disorders” became “TMDs.” For the purposes of
this article, we will differentiate the TMDs into articular (joint) and nonarticular (myogenic) disorders, with
a focus on disorders most commonly encountered in
clinical practice.
Myogenic Disorders
Within this category, MFP and MPD syndrome are
encountered frequently. Other muscular disorders
include myositis, fibrosis, tendonitis, whiplash injury,
and fibromyalgia. Patients suffering from MFP will have
tenderness to palpation of two or more muscle sites.
Myalgias involving the muscles of mastication predominate. MFP escalates to myofascial dysfunction when
there is concomitant limitation of jaw opening [6].
MFP and MPD are intertwined. Traditionally, it was
thought that structural abnormalities (ie, dental malocclusion, condylar malposition) led to muscular dysfunction
and pain [6,7]. Muscles were thought to be under an
increased burden in the presence of these skeletal and/or
dental misalignments. As such, a “vicious cycle” model
was proposed:
Structural → abnormality → muscle hyperactivity ↔
pain ↔ mandibular dysfunction where pain and muscle
hyperactivity potentiate each other and emotional stress
is thought to have an additive effect [6,7]. Over time,
there has been a lack of scientific evidence to support this
theory. Others have put forth a pain-adaptation model in
which motor behavior is altered or limited as a response to
pain, thus serving a protective purpose [8]. Many believe
that masticatory myalgias are instead “nonprogressive,
self-limited, or fluctuating over time,” with a significant
number of patients reportedly pain free at follow-up
examinations 1, 3, and 5 years later [8].
Consideration has also been given to the preponderance of female patients afflicted with TMDs. Many
researchers have examined the role of estrogen in the
etiology of masticatory myalgias [9]. The fact that the
condition is more severe in women than in men, and that
it occurs more frequently in women of reproductive age,
bears further investigation. The search for causative and
contributing factors is ongoing.
One must differentiate muscular from joint conditions in order to appropriately treat the patient. At the
same time, the clinician must understand the role of MPD
within the spectrum of TMDs. It has been reported that
approximately 50% of all TMDs are masticatory myalgias or painful masticatory muscle disorders [8].
MFP of the masticatory muscles is more frequently
induced by stress-related parafunctional habits (ie,
clenching and grinding) and rarely by mechanical causes
such as occlusal prematurities or high dental restorations.
MFP and MPD, although considered to be muscular disorders, are thought to possibly play a causative role in
degenerative disease of the TMJ.
410
Pain Aspects of Arthritis
TMJ pain from an articular disorder may conversely
lead to MFP. This is thought to occur due to reflex muscle contractions in the muscles of mastication [6,7]. This
is considered as a self-protective reflex and is referred to
as muscle “guarding” or “splinting.” Patients will present with tenderness and hyperalgesia at sites distant to
the joint that mimic MFP. They may also exhibit various
trigger points.
Treatment of masticatory MFP may include pharmacologic therapy (nonsteroidal anti-inflammatory
drugs, muscle relaxants, tricyclic antidepressants, anxiolytics), occlusal appliance/splint therapy, trigger point
therapy (spray and stretch, injections), and physical
therapy (mandibular exercises). Splint therapy is considered an adjunct to pharmacologic therapy and most
appropriate when nocturnal parafunctional activities
can be identified. Typically, a flat-plane maxillary occlusal splint designed for bilateral contact of all teeth is
fabricated. Such splints are thought to unload the joint
by disarticulating the dentition and increasing the vertical dimension of occlusion. By unloading the joint, there
will be a reduction in both synovitis and masticatory
muscle activity. Therefore, the result is a reduction in
symptoms. These appliances may also change condylar
position and the existing occlusal relationship, thereby
reducing abnormal muscle activity and spasm.
Articular Disorders
The etiology of articular disorders may be degenerative, traumatic, infectious, immunologic, metabolic,
neoplastic, congenital, or developmental.
Articular disc displacement (internal derangement)
Anterior disc displacement (ADD) is the most frequently
encountered articular disorder. Disc displacement (also
known as internal derangement) is defined as “a disturbance in the normal anatomic relationship between the
disc and condyle that interferes with smooth movement of
the joint and causes momentary catching, clicking, popping, or locking” [10]. Therapy is indicated if pain and
significant limitation in range of motion are present.
The incidence of ADD is unknown. Numerous radiographic, clinical, and cadaveric studies of asymptomatic
subjects have shown rates up to 30% [11]. The clinical
significance of this finding remains uncertain.
When the articular disc becomes displaced anteriorly, there is excessive stretching of the retrodiscal
tissue, which then bears repeated loading force from the
mandibular condyle. This tissue has been shown to have
some capacity to adapt to these forces and may transform into a “pseudodisc.” In many patients the disc is
recaptured and is known as “disc displacement with
reduction,” resulting in TMJ noise (clicking or popping)
and full translational movement of the condyle. With
mandibular closure, a reciprocal (closing) click repre-
sents the condyle returning to the retrodiscal tissue and
the disc returning to an anterior position. Many feel that
ADD with reduction does not require treatment unless
there is concomitant joint pain.
ADD without reduction, also known as closed lock,
will have a much different clinical presentation because
the condyle’s forward translation is limited by the
disc’s anterior position and is unable to reduce onto the
disc, allowing only for rotational and not translational
movement. Patients with acute or subacute closed lock
typically report a sudden onset of pain and inability to
open more than 20 to 30 mm. The patient may give a
history of joint noise that suddenly ceased with the onset
of signs and symptoms. Clinically, the mandible deviates on opening to the affected side due to the ability of
the unaffected joint to translate. Additionally, excursive
mandibular movements to the contralateral side are limited. This diagnosis of TMDs continues to present the
clinician with a significant challenge. Establishment of
an accurate diagnosis is necessary for effective management. The difficulty lies not in creating a distinction
between articular and muscular disorders, but in the
interrelation of the two entities. Although patients may
have isolated joint or muscular disorders, many have a
component of each. Simply stated, joint disorders may
lead to muscle dysfunction, and muscle disorders may
lead to joint dysfunction. This may not be possible to
elicit on examination because the patient will tend to
guard against pain.
In chronic disc displacement without reduction, the
patient can usually recount a history consistent with acute
closed lock that resolved over time. Recovery of function
is due to stretching the retrodiscal tissue over weeks to
months, restoring translational movement.
MRI allows for evaluation of soft tissue abnormalities of the TMJ. MRI is noninvasive and avoids radiation
exposure. The disc can be visualized making diagnosis
possible. T1 images show a hypodense biconcave disk
between the condyle and eminence. Effusion, bone marrow edema, and soft tissue pathology are well visualized
with T2 imaging. Multiplane views of the TMJ are available; with high-speed MRI, dynamic studies are also
available (Fig. 1).
The ability of the joint to adapt to biomechanical
stress and disc derangement has been a subject of debate.
In his classification system, Wilkes [12] promotes the
theory that internal derangement logically progresses to
degenerative joint disease (DJD). Historically, surgical
and nonsurgical approaches have been used to reposition
the displaced disc, with the goal of arresting this progression [13]. In an opposing view, Milam [9] states that
“the adaptive capacity of the TMJ is not infinite…some
individuals are… capable of mounting an adaptive
response to an articular disc displacement; other individuals may not adapt to these structural derangements,
and a progressive DJD may result.” Factors considered to
Temporomandibular Joint Pain and Dysfunction Herb et al.
411
Figure 1. MRI of the temporomandibular joint. Note the anterior
location of the disc in a closed position (arrow) (A), with recapture
on opening (arrow) (B), and without recapture (arrow) (C).
compromise the adaptive response include age, sex, stress,
and illness [9,14]. He concludes that disc derangement
may exist variably as cause or effect, but does not always
progress to disease.
Although patients without internal derangement
may develop osteoarthritis (OA) [15], a complex twoway relationship exists. Controversy continues as to
whether disc derangement is a cause or a result of DJD;
however, scientific evidence strongly supports the latter
conclusion [15–18,19•].
Capsulitis and synovitis
Inflammation of the capsular ligament may manifest
with swelling and continuous pain localized to the
joint. Movements that stretch the capsular ligament
cause pain with resultant limitation of such movement. Significant inflammation may increase joint fluid
volume. When this occurs, one may see an ipsilateral
posterior open bite (lack of contact between maxillary
and mandibular teeth) secondary to inferior displacement of the condyle [7]. Similarly, inflammation due to
trauma or abnormal function may affect the retrodiscal
tissue. Edema in this area may cause anterior displacement of the condyle and an acute malocclusion with
painful limitation of mandibular movements.
The highly innervated and vascularized synovial
membrane digests debris and pain mediators released
from cartilage degradation. When this ability is overwhelmed, inflammation (acute synovitis) results.
Inflammation of the synovial membrane is an early
sign of DJD [20]. Inflammatory and pain mediators
have been identified in TMJ synovial fluid [21,22].
Chemical breakdown of degenerative byproducts is
thought to stimulate the production of inflammatory
and pain mediators (prostaglandin E2 and leukotriene B4, among others) through the arachidonic acid
cascade. Prostaglandin E2 is a powerful vasodilator
and leukotriene B4 attracts inflammatory cells. Their
presence creates acute synovitis pain and stimulates
further damage from cytokines and proteases. For this
reason arthrocentesis and arthroscopy for joint lavage
and lysis of adhesions are believed to have a therapeutic
effect [23–25]. These procedures remove particulate
debris and pain mediators, aiding reduction of joint
inflammation and pain. Results are similar with and
without disc repositioning [23]. Lysis of adhesions may
improve range of motion. Steroid injections are also
used to reduce synovial inflammation and pain. Recent
investigations have looked at intra-articular morphine
for sustained pain relief in patients [26]. Research is
now focusing on the role of biochemical mediators in
the development and progression of TMJ pain and dysfunction [19•,22] and the identification of biochemical
“markers” of TMJ disease [14].
412
Pain Aspects of Arthritis
Figure 2. MRI of the right temporomandibular joint. Note the
anterior disc (arrow on left) dislocation and condylar head
(arrow on right) degenerative changes.
The arthritides
Arthritis of the TMJ has many etiologies: frequently
OA and rheumatoid arthritis (RA) and less often infectious, metabolic (gout), or immunologic (ankylosing
spondylitis, lupus). DJD, also known as OA, has a
multifactorial pathogenesis including biomechanical,
biochemical, inflammatory, and immunologic insults.
Excessive and repetitive mechanical stress has been implicated [19•]. Inflammatory mediators and waste products
may play a role in DJD [27–42]. Inflammatory states
cause changes in the viscosity of synovial fluid, which
changes its ability to nourish the articular cartilage, thus
changing cartilage metabolism.
OA is classified as primary (no known predisposing
factors) or secondary (associated with known abnormalities or injuries). Primary OA symptoms begin in the
fifth to sixth decade. Secondary OA produces symptoms
at an earlier age.
In contrast to the other arthritides, OA symptoms
will not necessarily be present in other joints. Patients
suffering from OA complain of increasing pain during
increased function and load bearing throughout the
day. Joints are tender and will exhibit decreased range
of motion. Crepitus may indicate loss of articular cartilage. Patients may have referred pain to head and neck
regions. Radiography may reveal joint space narrowing,
osteophyte formation, condylar head flattening, and
subchondral bone cysts.
In the osteoarthritic joint, there is progressive softening and loss of cartilage, which Quinn [20,31] calls
chondromalacia (softening of the articular cartilage)
of the TMJ. It is thought that repeated stress-related
microtrauma (ie, bruxism) eventually overloads the
joint’s articular cartilages leading to compression and
shearing of cartilage. Chondrocyte injury stimulates
release of proteolytic enzymes and other collagenases.
Eventually, there is loss of water and loss of cartilage
resilience [20,30–33].
Four stages of TMJ OA are based on the amount of
cartilage degeneration and the grade of synovitis. In stage
2, the early stage, patients may report pain and limited
range of motion. Joint noise may occur due to disc dis-
placement or perforation. This continues into the later
stages, and patients may develop crepitation secondary
to bone exposure. Pain and adhesion formation result in
limitation of joint movement. Dijkgraaf et al. [32] found
that “in many patients, the signs and symptoms of TMD
are attributable to osteoarthritis.” The authors place less
emphasis on the stage of internal derangement and more
emphasis on both the stage of cartilage degradation and
grade of synovitis.
Panoramic radiography is an excellent screening
tool for the presence of bony degenerative changes.
In addition to identifying disc displacement, MRI is
useful in the diagnosis of joint effusion, osteoarthritic
changes, bone marrow abnormalities of the mandibular condyle, retrodiscal tissue changes, and neoplasms
(Fig. 2) [43,44].
TMJ arthroscopy now allows clinicians to visualize
degenerative changes of both the articular cartilage and
disc at early stages [20]. Arthroscopy is considered to
be the “gold standard” in the diagnosis of OA because
degenerative changes are visualized earlier than with
radiographic techniques.
RA is a chronic systemic inflammatory disease
affecting the joints and other organs. A childhood form,
juvenile RA, also exists. The etiology is unknown, but an
autoimmune component has been identified (rheumatoid
factor). Of the patients who test positive for rheumatoid
factor, 50% to 75% will develop TMJ involvement [45].
The age of onset is younger (fourth to sixth decade) than
that seen with OA. In contrast to OA, patients with RA
typically have morning stiffness that lasts for more than
an hour, but report improvement of mobility with function throughout the day. They complain of deep, dull
preauricular pain that worsens with function. Patients
may also report fever, malaise, and fatigue. They will
eventually experience decrease in jaw mobility, joint
destruction, and fibrous ankylosis. Patients may progress
to loss of mandibular ramus height, retrognathia, and
open bite. Patients will have symptoms long before there
is radiographic evidence of disease. Early imaging with
MRI may be beneficial to evaluate disc morphology and
pathologic changes.
Temporomandibular Joint Pain and Dysfunction Herb et al.
Neoplasms
Pain and/or changes in occlusion may be presenting signs
and symptoms of a pathologic joint lesion. Neoplasms
of the condyle and joint space may be benign (osteoma,
chondroma, synovial chondromatosis, giant cell lesions)
or malignant (chondrosarcoma, osteosarcoma, synovial
sarcoma, multiple myeloma). The most common TMJ
neoplasms are the osteoma and osteochondroma. These
can be distinguished from condylar hyperplasia by the
presence of a normal condylar neck length. Pathologic
lesions may be first noted on screening panoramic
radiographs. Further evaluation of bony tumors is best
performed with CT.
Conclusions
The subject of TMJ pain and dysfunction is complex.
Signs and symptoms may be specific or nonspecific. The
strong relationship between articular and muscular disorders makes accurate diagnosis difficult. A thorough
knowledge of joint anatomy and function serves as a basis
for understanding the effect of dysfunction on the joint’s
component parts. Myogenic causes of pain are the majority and may coexist with articular disorders. Internal
derangement and DJD are the most frequently encountered
articular disorders. The etiology of each is multifactorial,
and the cause-effect relationship between the two remains
a controversial subject. Imaging techniques have greatly
advanced in the evaluation and diagnosis of TMDs. Treatment trends now involve a comprehensive conservative
plan along with surgical options. Treating these dysfunctions with only surgical techniques lessens the chance for
treatment success.
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