TEMPOROMANDIBULAR JOINT PAIN AND DYSFUNCTION

Temporomandibular Joint Pain
and Dysfunction

Kathleen Herb, DMD, MD, Sung Cho, DMD,
and Marlind Alan Stiles, DMD

Corresponding author open arthroplasty and toward arthroscopic procedures.
Marlind Alan Stiles, DMD Research continues to look toward biochemical markers
Department of Oral and Maxillofacial Surgery, Thomas Jefferson of disease. The interrelationship between the various dis-
University Hospital, 909 Walnut Street, Suite 300, Philadelphia, orders continues to be explored.
PA 19107, USA.
E-mail: [email protected] The temporomandibular joint (TMJ) is a compound
articulation formed from the articular surfaces of the
Current Pain and Headache Reports 2006, 10:408–414 temporal bone and the mandibular condyle. Both sur-
Current Science Inc. ISSN 1531-3433 faces are covered by dense articular fibrocartilage. Each
Copyright © 2006 by Current Science Inc. condyle articulates with a large surface area of temporal
bone consisting of the articular fossa, articular eminence,
Pain caused by temporomandibular disorders originates and preglenoid plane. The TMJ functions uniquely in that
from either muscular or articular conditions, or both. the condyle both rotates within the fossa and translates
Distinguishing the precise source of the pain is a sig- anteriorly along the articular eminence. Because of the
nificant diagnostic challenge to clinicians, and effective condyle’s ability to translate, the mandible can have a
management hinges on establishing a correct diagnosis. much higher maximal incisal opening than would be pos-
This paper examines terminology and regional anatomy sible with rotation alone. The joint is thus referred to as
as it pertains to functional and dysfunctional states of “gynglimodiarthrodial”: a combination of the terms gin-
the temporomandibular joint and muscles of mastica- glymoid (rotation) and arthroidial (translation) [1].
tion. A review of the pathophysiology of the most
common disorders is provided. Trends in evaluation, A cartilaginous disc resides between the articular
diagnosis, treatment, and research are presented. surfaces of the temporal bone and mandibular condyle.
Although other articular cartilages are composed of
Introduction hyaline cartilage, this disc is composed of fibrocartilage;
thus, the disc contains a much higher percentage of col-
Signs and symptoms of temporomandibular disorders lagen, increasing its stiffness and durability. The disc does
(TMDs) may include pain, impaired jaw function, not have any direct vascularization or innervation; how-
malocclusion, deviation or deflection, limited range of ever, the posterior attachment of the disc (also known as
motion, joint noise, and locking. Headache, tinnitus, retrodiscal tissue) is both highly vascularized and highly
visual changes, and other neurologic complaints may innervated and, therefore, pertinent to the discussion of
also accompany TMDs. Because of many etiologic fac- joint pain. The superior lamina of the retrodiscal tissue
tors, the diagnosis and treatment of patients with TMDs limits extreme translation, whereas the inferior lamina
is complex. TMDs can be subdivided into muscular and limits extreme rotation. The lateral pterygoid muscle con-
articular categories. Differentiation between the two is trols the opening of the mandible. The superior segment
sometimes difficult because muscle disorders may mimic of this muscle attaches to the anterior portion of the disc,
articular disorders, and they may coexist. Myogenic dis- and the inferior segment attaches inferior to the condyle.
orders include myalgia (myofascial pain, fibromyalgia), As both segments contract the condyle translates anteri-
myospasm, splinting, and fibrosis/contracture. Articu- orly along the articular eminence, and the disc remains
lar disorders include synovitis/capsulitis, joint effusion, interposed between the condyle and the temporal bone at
trauma/fracture, internal derangement, arthritis, and neo- all points of translation.
plasm. Accurate diagnosis allows for appropriate therapy
whether it is nonsurgical or surgical. Current trends favor The joint is stabilized by three ligaments: collateral
conservative (nonsurgical) therapy, and the surgical inter- (discal), capsular, and temporomandibular. These attach
ventions have become less aggressive, moving away from to the disc at the medial and lateral poles of the man-
dibular condyle, as well as to the temporal fossa. These
ligaments limit extreme condylar movement. The capsular

Temporomandibular Joint Pain and Dysfunction Herb et al. 409

ligament surrounds the joint space and disc and acts to “TMJ disorders” became “TMDs.” For the purposes of
contain the synovial fluid within the joint space. this article, we will differentiate the TMDs into articu-
lar (joint) and nonarticular (myogenic) disorders, with
The capsule is lined by a synovial membrane. Synovial a focus on disorders most commonly encountered in
tissue covers all intra-articular surfaces except for the pres- clinical practice.
sure-bearing fibrocartilage (ie, disc, condyle, eminence).
The synovial tissue is highly innervated and vascularized Myogenic Disorders
and has regulatory, phagocytic, and secretory functions.
The synovial fluid has metabolic and nutritional functions Within this category, MFP and MPD syndrome are
and is essential to joint surface lubrication [2]. encountered frequently. Other muscular disorders
include myositis, fibrosis, tendonitis, whiplash injury,
The masseter, medial pterygoid, lateral pterygoid, and and fibromyalgia. Patients suffering from MFP will have
temporalis muscles are the muscles of mastication. The tenderness to palpation of two or more muscle sites.
masseter, medial pterygoid, and temporalis are primarily Myalgias involving the muscles of mastication predomi-
responsible for mandibular closure and bite force, whereas nate. MFP escalates to myofascial dysfunction when
the lateral pterygoid and infrahyoid muscles are respon- there is concomitant limitation of jaw opening [6].
sible for mandibular opening. Mandibular movement is
also influenced by the digastric, geniohyoid, mylohyoid, MFP and MPD are intertwined. Traditionally, it was
stylohyoid, sternohyoid, omohyoid, sternothyroid, and thought that structural abnormalities (ie, dental malocclu-
thyrohyoid muscles, which as a group coordinate complex sion, condylar malposition) led to muscular dysfunction
mandibular movements including opening, protrusion, and pain [6,7]. Muscles were thought to be under an
retrusion, lateral excursion, and closure. increased burden in the presence of these skeletal and/or
dental misalignments. As such, a “vicious cycle” model
At rest, the condyle is seated passively in the temporal was proposed:
fossa with the fibrocartilage disc interposed at the most
superior and anterior position of the condyle commonly Structural → abnormality → muscle hyperactivity ↔
referred to as the 11-o’clock position. Mandibular open- pain ↔ mandibular dysfunction where pain and muscle
ing commences with contraction of the lateral pterygoid hyperactivity potentiate each other and emotional stress
and infrahyoid muscles, which rotates the condyle. is thought to have an additive effect [6,7]. Over time,
Mandibular opening proceeds with lateral pterygoid there has been a lack of scientific evidence to support this
contraction pulling the condyle forward along the artic- theory. Others have put forth a pain-adaptation model in
ular eminence (translation). The superior segment of the which motor behavior is altered or limited as a response to
lateral pterygoid muscle coordinates the translation of pain, thus serving a protective purpose [8]. Many believe
the disc with the condyle. During jaw closing the liga- that masticatory myalgias are instead “nonprogressive,
ments and retrodiscal lamina pull the condyle and disc self-limited, or fluctuating over time,” with a significant
back into resting position. number of patients reportedly pain free at follow-up
examinations 1, 3, and 5 years later [8].
The TMJ receives its vascular supply from the
superficial temporal, maxillary, and masseteric arteries. Consideration has also been given to the prepon-
Innervation of the joint is provided mainly by the auric- derance of female patients afflicted with TMDs. Many
ulotemporal nerve and, to a lesser extent, the masseteric researchers have examined the role of estrogen in the
and posterior deep temporal nerves. The production etiology of masticatory myalgias [9]. The fact that the
of synovial fluid is also under a certain amount of condition is more severe in women than in men, and that
neuronal control. it occurs more frequently in women of reproductive age,
bears further investigation. The search for causative and
Temporomandibular Disorders contributing factors is ongoing.

The term “TMJ pain” varies greatly in meaning among One must differentiate muscular from joint condi-
clinicians, patients, and the general population. His- tions in order to appropriately treat the patient. At the
torically, symptom-based classification of the disorder same time, the clinician must understand the role of MPD
has been problematic. As stated by Laskin [3,4], the within the spectrum of TMDs. It has been reported that
difficulty began with the introduction of a “TMJ syn- approximately 50% of all TMDs are masticatory myal-
drome.” Then clinicians erroneously grouped a “variety gias or painful masticatory muscle disorders [8].
of etiologically unrelated conditions into one diagnostic
category based on the fact that they produced similar MFP of the masticatory muscles is more frequently
signs and symptoms,” and this led to “one diagnosis induced by stress-related parafunctional habits (ie,
equals one treatment.” Only later was it recognized that clenching and grinding) and rarely by mechanical causes
many of these patients suffered from muscle-related such as occlusal prematurities or high dental restorations.
conditions. The terms myofascial pain (MFP) and myo- MFP and MPD, although considered to be muscular dis-
fascial pain and dysfunction (MPD) evolved [5], and orders, 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 sents the condyle returning to the retrodiscal tissue and
lead to MFP. This is thought to occur due to reflex mus- the disc returning to an anterior position. Many feel that
cle contractions in the muscles of mastication [6,7]. This ADD with reduction does not require treatment unless
is considered as a self-protective reflex and is referred to there is concomitant joint pain.
as muscle “guarding” or “splinting.” Patients will pres-
ent with tenderness and hyperalgesia at sites distant to ADD without reduction, also known as closed lock,
the joint that mimic MFP. They may also exhibit various will have a much different clinical presentation because
trigger points. the condyle’s forward translation is limited by the
disc’s anterior position and is unable to reduce onto the
Treatment of masticatory MFP may include phar- disc, allowing only for rotational and not translational
macologic therapy (nonsteroidal anti-inflammatory movement. Patients with acute or subacute closed lock
drugs, muscle relaxants, tricyclic antidepressants, anx- typically report a sudden onset of pain and inability to
iolytics), occlusal appliance/splint therapy, trigger point open more than 20 to 30 mm. The patient may give a
therapy (spray and stretch, injections), and physical history of joint noise that suddenly ceased with the onset
therapy (mandibular exercises). Splint therapy is con- of signs and symptoms. Clinically, the mandible devi-
sidered an adjunct to pharmacologic therapy and most ates on opening to the affected side due to the ability of
appropriate when nocturnal parafunctional activities the unaffected joint to translate. Additionally, excursive
can be identified. Typically, a flat-plane maxillary occlu- mandibular movements to the contralateral side are lim-
sal splint designed for bilateral contact of all teeth is ited. This diagnosis of TMDs continues to present the
fabricated. Such splints are thought to unload the joint clinician with a significant challenge. Establishment of
by disarticulating the dentition and increasing the verti- an accurate diagnosis is necessary for effective manage-
cal dimension of occlusion. By unloading the joint, there ment. The difficulty lies not in creating a distinction
will be a reduction in both synovitis and masticatory between articular and muscular disorders, but in the
muscle activity. Therefore, the result is a reduction in interrelation of the two entities. Although patients may
symptoms. These appliances may also change condylar have isolated joint or muscular disorders, many have a
position and the existing occlusal relationship, thereby component of each. Simply stated, joint disorders may
reducing abnormal muscle activity and spasm. lead to muscle dysfunction, and muscle disorders may
lead to joint dysfunction. This may not be possible to
Articular Disorders elicit on examination because the patient will tend to
guard against pain.
The etiology of articular disorders may be degenera-
tive, traumatic, infectious, immunologic, metabolic, In chronic disc displacement without reduction, the
neoplastic, congenital, or developmental. patient can usually recount a history consistent with acute
closed lock that resolved over time. Recovery of function
Articular disc displacement (internal derangement) is due to stretching the retrodiscal tissue over weeks to
Anterior disc displacement (ADD) is the most frequently months, restoring translational movement.
encountered articular disorder. Disc displacement (also
known as internal derangement) is defined as “a distur- MRI allows for evaluation of soft tissue abnormali-
bance in the normal anatomic relationship between the ties of the TMJ. MRI is noninvasive and avoids radiation
disc and condyle that interferes with smooth movement of exposure. The disc can be visualized making diagnosis
the joint and causes momentary catching, clicking, pop- possible. T1 images show a hypodense biconcave disk
ping, or locking” [10]. Therapy is indicated if pain and between the condyle and eminence. Effusion, bone mar-
significant limitation in range of motion are present. row edema, and soft tissue pathology are well visualized
with T2 imaging. Multiplane views of the TMJ are avail-
The incidence of ADD is unknown. Numerous radio- able; with high-speed MRI, dynamic studies are also
graphic, clinical, and cadaveric studies of asymptomatic available (Fig. 1).
subjects have shown rates up to 30% [11]. The clinical
significance of this finding remains uncertain. The ability of the joint to adapt to biomechanical
stress and disc derangement has been a subject of debate.
When the articular disc becomes displaced ante- In his classification system, Wilkes [12] promotes the
riorly, there is excessive stretching of the retrodiscal theory that internal derangement logically progresses to
tissue, which then bears repeated loading force from the degenerative joint disease (DJD). Historically, surgical
mandibular condyle. This tissue has been shown to have and nonsurgical approaches have been used to reposition
some capacity to adapt to these forces and may trans- the displaced disc, with the goal of arresting this pro-
form into a “pseudodisc.” In many patients the disc is gression [13]. In an opposing view, Milam [9] states that
recaptured and is known as “disc displacement with “the adaptive capacity of the TMJ is not infinite…some
reduction,” resulting in TMJ noise (clicking or popping) individuals are… capable of mounting an adaptive
and full translational movement of the condyle. With response to an articular disc displacement; other indi-
mandibular closure, a reciprocal (closing) click repre- viduals 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, from cartilage degradation. When this ability is over-
and illness [9,14]. He concludes that disc derangement whelmed, inflammation (acute synovitis) results.
may exist variably as cause or effect, but does not always Inflammation of the synovial membrane is an early
progress to disease. sign of DJD [20]. Inflammatory and pain mediators
have been identified in TMJ synovial fluid [21,22].
Although patients without internal derangement Chemical breakdown of degenerative byproducts is
may develop osteoarthritis (OA) [15], a complex two- thought to stimulate the production of inflammatory
way relationship exists. Controversy continues as to and pain mediators (prostaglandin E2 and leukotri-
whether disc derangement is a cause or a result of DJD; ene B4, among others) through the arachidonic acid
however, scientific evidence strongly supports the latter cascade. Prostaglandin E2 is a powerful vasodilator
conclusion [15–18,19•]. and leukotriene B4 attracts inflammatory cells. Their
presence creates acute synovitis pain and stimulates
Capsulitis and synovitis further damage from cytokines and proteases. For this
Inflammation of the capsular ligament may manifest reason arthrocentesis and arthroscopy for joint lavage
with swelling and continuous pain localized to the and lysis of adhesions are believed to have a therapeutic
joint. Movements that stretch the capsular ligament effect [23–25]. These procedures remove particulate
cause pain with resultant limitation of such move- debris and pain mediators, aiding reduction of joint
ment. Significant inflammation may increase joint fluid inflammation and pain. Results are similar with and
volume. When this occurs, one may see an ipsilateral without disc repositioning [23]. Lysis of adhesions may
posterior open bite (lack of contact between maxillary improve range of motion. Steroid injections are also
and mandibular teeth) secondary to inferior displace- used to reduce synovial inflammation and pain. Recent
ment of the condyle [7]. Similarly, inflammation due to investigations have looked at intra-articular morphine
trauma or abnormal function may affect the retrodiscal for sustained pain relief in patients [26]. Research is
tissue. Edema in this area may cause anterior displace- now focusing on the role of biochemical mediators in
ment of the condyle and an acute malocclusion with the development and progression of TMJ pain and dys-
painful limitation of mandibular movements. function [19•,22] and the identification of biochemical
“markers” of TMJ disease [14].
The highly innervated and vascularized synovial
membrane digests debris and pain mediators released

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 placement or perforation. This continues into the later
Arthritis of the TMJ has many etiologies: frequently stages, and patients may develop crepitation secondary
OA and rheumatoid arthritis (RA) and less often infec- to bone exposure. Pain and adhesion formation result in
tious, metabolic (gout), or immunologic (ankylosing limitation of joint movement. Dijkgraaf et al. [32] found
spondylitis, lupus). DJD, also known as OA, has a that “in many patients, the signs and symptoms of TMD
multifactorial pathogenesis including biomechanical, are attributable to osteoarthritis.” The authors place less
biochemical, inflammatory, and immunologic insults. emphasis on the stage of internal derangement and more
Excessive and repetitive mechanical stress has been impli- emphasis on both the stage of cartilage degradation and
cated [19•]. Inflammatory mediators and waste products grade of synovitis.
may play a role in DJD [27–42]. Inflammatory states
cause changes in the viscosity of synovial fluid, which Panoramic radiography is an excellent screening
changes its ability to nourish the articular cartilage, thus tool for the presence of bony degenerative changes.
changing cartilage metabolism. In addition to identifying disc displacement, MRI is
useful in the diagnosis of joint effusion, osteoarthritic
OA is classified as primary (no known predisposing changes, bone marrow abnormalities of the mandibu-
factors) or secondary (associated with known abnor- lar condyle, retrodiscal tissue changes, and neoplasms
malities or injuries). Primary OA symptoms begin in the (Fig. 2) [43,44].
fifth to sixth decade. Secondary OA produces symptoms
at an earlier age. TMJ arthroscopy now allows clinicians to visualize
degenerative changes of both the articular cartilage and
In contrast to the other arthritides, OA symptoms disc at early stages [20]. Arthroscopy is considered to
will not necessarily be present in other joints. Patients be the “gold standard” in the diagnosis of OA because
suffering from OA complain of increasing pain during degenerative changes are visualized earlier than with
increased function and load bearing throughout the radiographic techniques.
day. Joints are tender and will exhibit decreased range
of motion. Crepitus may indicate loss of articular carti- RA is a chronic systemic inflammatory disease
lage. Patients may have referred pain to head and neck affecting the joints and other organs. A childhood form,
regions. Radiography may reveal joint space narrowing, juvenile RA, also exists. The etiology is unknown, but an
osteophyte formation, condylar head flattening, and autoimmune component has been identified (rheumatoid
subchondral bone cysts. factor). Of the patients who test positive for rheumatoid
factor, 50% to 75% will develop TMJ involvement [45].
In the osteoarthritic joint, there is progressive soft- The age of onset is younger (fourth to sixth decade) than
ening and loss of cartilage, which Quinn [20,31] calls that seen with OA. In contrast to OA, patients with RA
chondromalacia (softening of the articular cartilage) typically have morning stiffness that lasts for more than
of the TMJ. It is thought that repeated stress-related an hour, but report improvement of mobility with func-
microtrauma (ie, bruxism) eventually overloads the tion throughout the day. They complain of deep, dull
joint’s articular cartilages leading to compression and preauricular pain that worsens with function. Patients
shearing of cartilage. Chondrocyte injury stimulates may also report fever, malaise, and fatigue. They will
release of proteolytic enzymes and other collagenases. eventually experience decrease in jaw mobility, joint
Eventually, there is loss of water and loss of cartilage destruction, and fibrous ankylosis. Patients may progress
resilience [20,30–33]. to loss of mandibular ramus height, retrognathia, and
open bite. Patients will have symptoms long before there
Four stages of TMJ OA are based on the amount of is radiographic evidence of disease. Early imaging with
cartilage degeneration and the grade of synovitis. In stage MRI may be beneficial to evaluate disc morphology and
2, the early stage, patients may report pain and limited pathologic changes.
range of motion. Joint noise may occur due to disc dis-

Temporomandibular Joint Pain and Dysfunction Herb et al. 413

Neoplasms 7. Okeson JP, ed: Fundamentals of Occlusion and Temporo-
Pain and/or changes in occlusion may be presenting signs mandibular Disorders. St. Louis: C.V. Mosby; 1985.
and symptoms of a pathologic joint lesion. Neoplasms
of the condyle and joint space may be benign (osteoma, 8. Stohler CS: Masticatory myalgias. In Oral and Maxillofacial
chondroma, synovial chondromatosis, giant cell lesions) Surgery. Temporomandibular Disorders. Edited by Fonseca
or malignant (chondrosarcoma, osteosarcoma, synovial RJ, et al.: Philadelphia: WB Saunders; 2000:38–45.
sarcoma, multiple myeloma). The most common TMJ
neoplasms are the osteoma and osteochondroma. These 9. Milam SB: Pathophysiology of articular disk displace-
can be distinguished from condylar hyperplasia by the ments of the temporomandibular joint. In Oral and
presence of a normal condylar neck length. Pathologic Maxillofacial Surgery. Temporomandibular Disorders.
lesions may be first noted on screening panoramic Edited by Fonseca RJ, et al.: Philadelphia: WB Saunders;
radiographs. Further evaluation of bony tumors is best 20 0 0 : 46 –72 .
performed with CT.
10. Laskin DM: Internal derangements. Oral Maxillofac Surg
Conclusions Clin North Am 1994, 5:217–222.

The subject of TMJ pain and dysfunction is complex. 11. Westesson PL, Eriksson L, Kurita K: Reliability of a
Signs and symptoms may be specific or nonspecific. The negative clinical temporomandibular joint examination:
strong relationship between articular and muscular dis- prevalence of disk displacement in asymptomatic temporo-
orders makes accurate diagnosis difficult. A thorough mandibular joints. Oral Surg Oral Med Oral Pathol 1989,
knowledge of joint anatomy and function serves as a basis 68:551–554.
for understanding the effect of dysfunction on the joint’s
component parts. Myogenic causes of pain are the major- 12. Wilkes CH: Internal derangement of the temporomandibular
ity and may coexist with articular disorders. Internal joint. Pathological variations. Arch Otolaryngol Head Neck
derangement and DJD are the most frequently encountered Surg 1989, 115:469–467.
articular disorders. The etiology of each is multifactorial,
and the cause-effect relationship between the two remains 13. Greene CS, Laskin DM: Long-term status of TMJ clicking
a controversial subject. Imaging techniques have greatly in patients with myofascial pain and dysfunction. J Am
advanced in the evaluation and diagnosis of TMDs. Treat- Dent Assoc 1988, 117:461–465.
ment trends now involve a comprehensive conservative
plan along with surgical options. Treating these dysfunc- 14. Milam SB, Schmitz JP: Molecular biology of temporo-
tions with only surgical techniques lessens the chance for mandibular joint disorders: proposed mechanisms of
treatment success. disease. J Oral Maxillofac Surg 1995, 53:1448–1454.

References and Recommended Reading 15. de Bont LGM, Boering G, Liem RSB, et al.: Osteoarthrosis
and internal derangement of the temporomandibular joint.
Papers of particular interest, published recently, A light microscopic study. J Oral Maxillofac Surg 1986,
have been highlighted as: 44: 634 – 643.
• Of importance
•• Of major importance 16. Stegenga B, de Bont LGM, Boering G: Osteoarthrosis
as the cause of craniomandibular pain and dysfunc-
1. Fletcher MC, Piecuch JF, Lieblich SE: Anatomy and patho- tion: a unifying concept. J Oral Maxillofac Surg 1989,
physiology of the temporomandibular joint. In Peterson’s 47: 249 –2 56 .
Principles of Oral and Maxillofacial Surgery, edn 2.
Edited by Miloro M. Hamilton (Ontario): BC Decker; 17. Nickerson JW, Boering G: Natural course of osteoarthrosis
20 0 4 :933 –947. as it relates to internal derangement of the temporoman-
dibular joint. Oral Maxillofac Surg Clin North Am 1989,
2. Howerton DW, Zysset M: Anatomy of the temporoman- 1:27– 43.
dibular joint and related structures with surgical anatomic
considerations. Oral Maxillofac Surg Clin North Am 1989, 18. Stegenga B, de Bont LGM, Boering G, Van Willigen JD:
1:229–247. Tissue responses to degenerative changes in the temporo-
mandibular joint: a review. J Oral Maxillofac Surg 1991,
3. Laskin DM: Putting order into temporomandibular 49:1079–1088.
disorders. J Oral Maxillofac Surg 1998, 56:121.
19.• Israel HA, Langevin CJ, Singer MD, Behrman DA: The
4. Laskin DM: Diagnosis and etiology of myofascial pain relationship between temporomandibular joint synovitis
and dysfunction. Oral Maxillofac Surg Clin North Am and adhesions: pathogenic mechanisms and clinical impli-
1995, 7:73–78. cations for surgical management. J Oral Maxillofac Surg
2006, 64:1066–1074.
5. Dworkin SF, LeResche L: Research diagnostic criteria for
temporomandibular disorders: review, criteria, examina- This article explores the role of mechanical stress on the TMJ in
tions and specifications, critique. J Craniomandib Disord the development of synovitis, osteoarthritis, and adhesions. The
1992, 6:301–355. author supports the idea that disc displacement is a result of the
above-mentioned conditions.
6. Ogle OE, Hertz MB: Myofascial pain. Oral Maxillofac 20. Quinn JH: Pathogenesis of temporomandibular joint
Surg Clin North Am 2000, 12:217–231.
chondromalacia and arthralgia. Oral Maxillofac Surg Clin
North Am 1989, 1:47–57.
21. Kopp S: The influence of neuropeptides, serotonin, and
interleukin 1beta on temporomandibular joint pain and
inflammation. J Oral Maxillofac Surg 1998, 56:189–191.
22. Milam SB: Chronic temporomandibular joint arthralgia.
Oral Maxillofac Surg Clin North Am 2000, 12:5–26.
23. Moses JJ, Sartorius D, Glass R, et al.: The effect of
arthroscopic surgical lysis and lavage of the superior joint
space on TMJ disc position and mobility. J Oral Maxillofac
Surg 1989, 47:674–678.
24. Nitzan DW, Dolwick MF, Heft MW: Arthroscopic lavage
and lysis of the temporomandibular joint: a change in
perspective. J Oral Maxillofac Surg 1990, 48:798–801.
25. McCain JP, Sanders B, Koslin MG, et al.: Temporoman-
dibular joint arthroscopy: a 6-year multicenter retrospective
study of 4831 joints. J Oral Maxillofac Surg 1992,
50:926–930.
26. Brennan PA, Ilankovan V: Arthrocentesis for temporoman-
dibular joint pain dysfunction syndrome. J Oral Maxillofac
Surg 2006, 64:949–951.

414 Pain Aspects of Arthritis

27. Milam SB, Zardeneta G, Schmitz JP: Oxidative stress and 37. Takahashi T, Kondoh T, Fukada M, et al.: Proinflammatory
degenerative temporomandibular joint disease: a proposed cytokines detectable in synovial fluids from patients with
hypothesis. J Oral Maxillofac Surg 1998, 56:214–223. temporomandibular disorders. Oral Surg Oral Med Oral
Pathol Oral Radiol Endod 1998, 85:135–141.
28. Shibata T, Murakami KI, Kubota E, Maeda H: Glycosami-
noglycan components in temporomandibular joint synovial 38. Murakami KI, Shibata T, Kubota E, Maeda H: Intra-
fluid as markers of joint pathology. J Oral Maxillofac Surg articular levels of prostaglandin E2, hyaluronic acid, and
1998, 56:209–213. chondroitin-4 and -6 sulfates in the temporomandibular
joint synovial fluid of patients with internal derangement.
29. Moses JJ: Temporomandibular joint arthrocentesis and J Oral Maxillofac Surg 1998, 56:199–203.
arthroscopy: rationale and technique. In Peterson’s Principles
of Oral and Maxillofacial Surgery, edn 2. Edited by Miloro 39. Nishimura M, Segami N, Kaneyama K, et al.: Relation-
M. Hamilton (Ontario): BC Decker; 2004:963–988. ships between pain-related mediators and both synovitis
and joint pain in patients with internal derangements
30. Dijkgraaf, LC, Zardeneta G, Cordewener FW, et al.: and osteoarthritis of the temporomandibular joint. Oral
Crosslinking of fibrinogen and fibronectin by free radicals: a
possible initial step in adhesion formation in osteoarthritis of Surg Oral Med Oral Pathol Oral Radiol Endod 2002,
94:328–332.
the temporomandibular joint. J Oral Maxillofac Surg 2003,
61:101–111. 40. Ratcliffe A, Israel HA, Saed-Nejad F, Diamond B: Proteo-
glycans in the synovial fluid of the temporomandibular joint
31. Quinn JH: Pain mediators and chondromalacia in internally as an indicator of changes in cartilage metabolism during
deranged tempormandibular joints. In Modern Practice in
Orthognathic and Reconstructive Surgery. Edited by Bell primary and secondary osteoarthritis. J Oral Maxillofac
Surg 1998, 56:204–208.
WH. Philadelphia: WB Saunders; 1992:471–481.
41. Quinn JH, Bazan NG: Identification of prostaglandin
32. Dijkgraaf LC, de Bont LGM, Boering G, Liem RSB: The E2 and leukotriene B4 in the synovial fluid of painful,
structure, biochemistry, and metabolism of osteoarthritic
cartilage. A review of the literature. J Oral Maxillofac Surg dysfunctional temporomandibular joints. J Oral Maxillofac
Surg 1990, 48:968–971.
1995, 53:1182–1192.
42. Kaneyama K, Segami N, Nishimura M, et al.: The ideal
33. Dijkgraaf LC, Milam SB: Osteoarthritis: histopathology lavage volume for removing bradykinin, interleukin-6, and
and biochemistry of the TMJ. In Oral Maxillofacial Surgery
Knowledge Update, vol 3. Edited by Piecuch JF. Rosemont, protein from the temporomandibular joint by arthrocentesis.
J Oral Maxillofac Surg 2004, 62:657–661.
IL: American Association of Oral and Maxillofacial
Surgeons; 2001:5–28. 43. Sano T, Yamamoto M, Okano T: Temporomandibular
joint: MR imaging. Neuroimaging Clin N Am 2003,
34. Israel HA: Synovial fluid analysis. Oral Maxillofac Surg 13:583–585.
Clin North Am 1989, 1:85–92.
44. Larheim TA: Role of magnetic resonance imaging in the
35. Yih WY: Pathology of arthroscopic tissue of the temporo- clinical diagnosis of the temporomandibular joint. Cells
mandibular joint. Oral Maxillofac Surg Clin North Am
1989, 1:93–109. Tissues Organs 2005, 180:6–21.

36. Kubota E, Kubota T, Matsumoto J, et al.: Synovial fluid 45. Silverstein K: Arthritis of the temporomandibular joint.
In Oral and Maxillofacial Surgery. Temporomandibular
cytokines and proteinases as markers of temporoman- Disorders. Edited by Fonseca RJ, et al.: Philadelphia: WB
dibular joint disease. J Oral Maxillofac Surg 1998,
56:192–198. Saunders; 2000:73–92.