Internal Derangements of the Temporomandibular Joint · Cross-References ..... 32 References ........

Internal Derangementsof the Temporomandibular Joint

James J.R. Huddleston Slater and Reny de Leeuw

AbstractAn internal derangement of the temporoman-dibular joint (TMJ) is anatomically describedas a deviation in position or in form of thetissues within the capsule of the joint that inter-feres with smooth joint movement. Althoughoften regarded as such, an internal derange-ment is not a diagnostic entity, but it is merelya description of symptoms and signs of a num-ber of clinical problems that involve the joint.Among these clinical problems are disc con-dyle complex disorders, hypomobility disor-ders, adherences, hypermobility disorders,fractures, inflammatory disorders, crystaldeposition diseases, hyperplasia, andhypoplasia.

Clinical features include a snapping or tear-ing sensation during mouth opening, a sensa-tion of significant instability in the TMJ, or asignificant injuring force in the TMJ area.Some patients may have more serious com-plaints, such as the sudden inability to openthe mouth, or the occasional locking of thejoint on maximal mouth opening and somemay experience significant pain or discomfort.

Some patients with these conditions may notrequire treatment, while others may causemajor disturbances for which pervasive inter-ventions are necessary. Conservative treatmentis advocated for the management of discderangements, arthralgia, osteoarthritis, andadherences, although minimally invasive pro-cedures such as lysis and lavage(arthrocentesis) can be considered for refrac-tory cases.

KeywordsTemporomandibular joint • TMJ mobility dis-orders • TMJ inflammatory disorders • TMJfractures • TMJ internal derangement • Crystaldeposition disorders

ContentsIntroduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Etiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Disc Derangements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5Hypomobility and Adherences . . . . . . . . . . . . . . . . . . . . . . . . 9Hypermobility Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11Inflammatory Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12Crystal Deposition Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . 12Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13Hypoplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14

Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Disc Derangements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16Hypomobility and Adherences . . . . . . . . . . . . . . . . . . . . . . . . 18Hypermobility Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

J.J.R. Huddleston SlaterPrivate Practice, Groningen, The Netherlandse-mail: [email protected]

R. de Leeuw (*)Division of Orofacial Pain, College of Dentistry,University of Kentucky, Lexington, KY, USAe-mail: [email protected]

# Springer International Publishing AG 2017C.S. Farah et al. (eds.), Contemporary Oral Medicine,https://doi.org/10.1007/978-3-319-28100-1_31-1

1

mailto:[email protected]

mailto:[email protected]

https://doi.org/10.1007/978-3-319-28100-1_31-1

Arthralgia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19Rheumatoid Arthritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Spondyloarthritides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20Crystal Deposition Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . 21Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21Hypoplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Clinical–Pathological Features . . . . . . . . . . . . . . . . . . . . . 22Disc Derangements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22Hypomobility and Adherences . . . . . . . . . . . . . . . . . . . . . . . . 22Hypermobility Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Arthralgia and Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . 24Crystal Deposit Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Hypoplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25

Patient Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Disc Derangements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25Adherences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29Adhesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29Hypermobility Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Fractures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 30Arthralgia and Osteoarthritis . . . . . . . . . . . . . . . . . . . . . . . . . . 31Crystal Deposit Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31Hypoplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

Conclusions and Future Directions . . . . . . . . . . . . . . . . . 32

Cross-References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 33

Introduction

The temporomandibular articulation comprisestwo distinct temporomandibular joints (TMJ)connecting the base of the skull with the mandi-ble. The TMJ is a complex joint both morpholog-ically and functionally. The joint itself is made upof two incongruent parts: the mandibular condyleand the glenoid fossa of the temporomandibularbone; referred to further here as condyle and fossa.The articular disc is formed of dense fibrous tissueand is positioned between the condyle and fossa.The disc divides the joint cavity in two compart-ments: an upper and a lower compartment (Fig. 1).

The central part of the disc is considerablythinner than the posterior and anterior parts. Thedisc compensates for the incongruence betweenthe condyle and the eminence, as it fits like a capover the condyle, thereby distributing compres-sion forces over a broader articular surface

(Fig. 2). The architecture of the TMJ enables itto make rotational and sliding movements. Mostof the rotational movements occur in the lowercompartment between the condyle and the disc,whereas most of the sliding movements occur inthe upper compartment, between the disc and thefossa. The joint itself is encapsulated: a fibrouscapsule is attached to the temporal bone along thelimits of the fossa and the condyle. It consists of aloose arrangement of connective tissue that isreinforced laterally by the temporomandibular lig-aments (Fig. 3).

TMJ disorders are generally characterized bypain and impairment of joint function and jointsounds. Problems with TMJ functioning were rec-ognized in the thirtieth century B.C. when the

Fig. 1 The articular disc divides the joint cavity in twocompartments; an upper and a lower compartment. E emi-nence, C condyle, D disc, L lower joint compartment, Uupper joint compartment

Fig. 2 Histology of the TMJ. Blue dye represents carti-lage, burgundy dye is bone. E eminence,C condyle,D disc,L lower joint compartment, U upper joint compartment.Staining: Heidenhain’s AZAN trichrome stain

2 J.J.R. Huddleston Slater and R. de Leeuw

ancient Egyptians described a technique for thereduction of a mandibular dislocation. Later, inthe fifth century B.C., Hippocrates also describedsuch a technique (Schwartz 1966). During thefollowing centuries, interest in TMJ problemsremained, though mainly from an anatomicalpoint of view. Clicking and locking of the TMJwere attributed to an anteriorly displaced articulardisc by Annandale in 1887 (Annandale 1887). Itwas only a few decades ago that advances inimaging techniques, such as tomography,arthrography, computed tomography (CT), andlater, magnetic resonance imaging (MRI), resultedin an improved visualization of the inner struc-tures of the TMJ in living humans which resultedin better understanding of its functional disorders.Farrar (Farrar 1971) and McCarty (McCarty1980) emphasized the role of disc interferenceswithin this group of functional problems and usedthe term “internal derangements”. “Internalderangement” is an orthopedic term, defined as“a localized mechanical fault interfering withsmooth joint movement” (Adams and Hamblen1990; Stegenga 1996).

An internal derangement is anatomicallydescribed as a deviation in either the position orthe form of the tissues within the capsule of thejoint. Clinical features that are likely to indicate aninternal derangement of the TMJ are a snapping ortearing sensation during movements of the mouth,a sensation of significant instability in the TMJ, ora significant injuring force in the TMJ area. These

complaints may be accompanied by the inabilityto get the teeth into a full, comfortable, occlusion.Most patients, however, will only report clickingsounds that arise from the TMJ during mouthopening and/or closing. Some patients may havemore serious complaints, such as the suddeninability to open the mouth, or the occasionallocking of the joint on maximal mouth openingand may experience significant pain ordiscomfort.

Although often regarded as such, an internalderangement is not a diagnostic entity. Rather, it isa description of symptoms and signs. In fact,internal derangements of the TMJ are symptomsof a number of clinical problems that involve theTMJ. Among these clinical problems are disccondyle complex disorders, hypomobility disor-ders, hypermobility disorders, fractures, inflam-matory disorders, crystal deposition diseases,hyperplasia, and hypoplasia.

Condyle disc complex disorders (Table 1) arecharacterized by a displacement of the disc in theclosed jaw position that improves its structuralrelationship with the condyle during mouth open-ing, usually accompanied by a click (Fig. 4) (Far-rar and McCarty 1982).

In joints with an internal derangement andhypomobility, often the capsule undergoes fibro-sis resulting in the synovial surfaces being linedwith fibrin. In extreme cases, often occurring aftersevere intraarticular trauma, this may lead toadherences/adhesions (Katsnelson et al. 2012;Al-Baghdadi et al. 2014). In hypermobile joints,there is an excessive range of motion of the con-dyle without overstretching of the structures(Garcia-Campayo et al. 2011). A fracture of thecondylar structures may involve a fracture of themandibular caput (head of mandible) and/or afracture of the mandibular collum (neck of themandible) (Afrooz et al. 2015). Inflammatory dis-orders involve inflammation or inflammatorysymptoms of the intra-articular structures thatcan be sterile (e.g., arthritis, traumatic arteritis,rheumatoid arthritis) or bacterial (e.g., infectiousarthritis, abscess, or more systemic disease (syph-ilis, tuberculosis, actinomyocosis) (Kalladka et al.2014). Crystal deposition diseases are mostlyfound in knee joints, but a few reports describe

Fig. 3 The encapsulated TMJ: a fibrous capsule isattached to the temporal bone along the limits of the fossaand the condyle. It consists of a loose arrangement ofconnective tissue that is reinforced laterally by the tempo-romandibular ligaments. C capsule, CP coronoid process,M mastoid, ZA zygomatic arch

Internal Derangements of the Temporomandibular Joint 3

Table 1 Internal derangements

Disc derangements

Clicking in early mouth opening

Clicking in later mouth opening

Intermittent locking

Permanent or so-called closed lock

Hypomobility and adherences

Temporarily

Permanent

Adhesions

Ankylosis

Impedance of the coronoid process

Hypermobility disorders

Subluxations

Luxations

Fractures of the condylar process

Fractures of the mandibular caput (the head of the mandible)

Fractures of the mandibular collum (the neck of the mandible)

Inflammatory disorders

Sterile (e.g., arthritis, traumatic arthritis, rheumatoid arthritis)

Bacterial (e.g., infectious arthritis, abscess)

Systemic disease (e.g., syphilis, tuberculosis, actinomyocosis)

Crystal deposition diseases

Gout (hyperuricemia, arthritides, sodium urate crystal deposition in and around joints, renal disease, and urolithiasis)

Osteochondromatosis

Condylar hyperplasia

Condylar hypoplasia

Fig. 4 In a condyle disc complex disorder, the disc usuallyis located anterior to the head of the condyle in the closedposition (a) and improves its relationship with the condyle

during mouth opening (b). C condyle, D articular disc,E eminence


crystal formation in the TMJ (Phelan et al. 2011).These disorders will be described in detail below.

Epidemiology

A number of, and surely not all, internal derange-ments of the TMJ have one particular feature: asnapping, clicking, popping, or tearing sound onjoint movement (da Silva et al. 2016). Tradition-ally, epidemiological studies have mainly focusedon the clinical symptoms of internal derange-ments, such as either the simple clicking sounds,or reciprocal clicking that occurs on opening andclosing of the mouth. Little focus has been givenon the underlying causes of the internal derange-ment that result in the clicking sounds, such asdisc condyle complex disorders, hypermobilitydisorders, or deviation in form. As a result, manyepidemiological studies describe the incidenceand prevalence of clicking sounds and largelyignore the diagnostic entities of the clinical symp-toms and signs (Keeling et al. 1994; Gazit et al.1984; Locker and Slade 1988).

Studies that have assessed disc condyle com-plex disorders and hypermobility disorders haveusually used clinical evaluation of joint sounds(Gazit et al. 1984). However, other techniqueshave also been used to assess the prevalence ofinternal derangements. Among these techniquesare questionnaires (Locker and Slade 1988), mag-netic resonance imaging (MRI) (Nebbe andMajor

2000), and autopsy studies (Kondoh et al. 1998).In general, clicking sounds are frequently seen,with the reported prevalence ranging from 17.5%to 74.7% (Haiter-Neto et al. 2002; Nebbe andMajor 2000). The most commonly reported inter-nal derangements are disc condyle complex dis-orders (Vogl et al. 2016). Disc displacement hasbeen described as partial or complete, and thedirection of the displacement may be anterior,anteromedial, medial, anterolateral, lateral, andposterior, though the latter position is rare(Huddleston Slater et al. 2005; Okochi et al.2008). The reported prevalence, and evaluationmethod utilized, is outlined in Table 2.

Not surprisingly, there is little research on theincidence of other types of internal derangementswithout clicking sounds, such as hypomobilitydisorders, adhesions, fractures, inflammatory dis-orders, and crystal deposition diseases, simplybecause the lack of clinical symptoms did notwarrant any investigation on the incidence.

Etiology

Disc Derangements

Over the years, a variety of possible etiologicalfactors have been proposed to explain the occur-rence of disc derangements. Previously, it wasthought that the superior head of the lateral pter-ygoid muscle pulled the disc anteriorly during

Table 2 Reported prevalence of internal derangements

Study Diagnosis PopulationEvaluationmethod Prevalence N

Gazit et al.1984

Joint sounds Children 10–18 years of age Clinicalexamination

35.8% 369

Locker andSlade 1988

Joint sounds 18 yrs. and over Questionnaire 48.8% 1002

Keeling et al.1994

Joint sounds Children 6–12 years of age Clinicalexamination

10.0% 3428

Kondoh et al.1998

Discdisplacements

Cadavers Autopsy 57% 30

Nebbe andMajor 2000

Discdisplacements

Nonconsecutive adolescent sample MRI 61.8% (male),74.7% (female)

194

Haiter-Netoet al. 2002

Discdisplacements

Symptom-free healthy subjects(mean age of 26.9 years)

MRI 17.5% 40


mouth opening. In that perspective, disc displace-ment was regarded as the result of a spasm of thatmuscle. Research could not corroborate theseideas, because in autopsy specimens only a lim-ited number of cases were found where the fiberswere shown to insert directly in the disc (Savalle1988; Bittar et al. 1994). The main function of themuscle seems to be merely reflected by its contin-uous holding action, which is enabled by itslow-stimulation threshold and fatigue resistantfibers (Eriksson and Thornell 1983).

It has, however, been observed that the inci-dence of clicks develops with an increasing age,especially during childhood and adolescence(Egermark-Eriksson et al. 1981; Dibbets and vander Weele 1992; Thilander et al. 2002). Unfortu-nately, the interpretation of these studies is ham-pered by firstly a lack of classification, as only theclinical symptom of “clicking” has been studied,secondly relatively large age increments wereused, and finally orthodontic samples have beenstudied (Egermark-Eriksson et al. 1981; Dibbetsand van derWeele 1992). Orthodontic samples arenot representative for the study of condylar devel-opment, because in this patient population discdisplacement is seen more in class II patients(Gökalp 2016). Conversely, in joints from adoles-cents, rather prominent progressive remodelingchanges have been shown to occur (Krisjaneet al. 2012). It was suggested that the developmentof disc derangements is related to various anatom-ical relations between components of the TMJ(Pullinger et al. 2002). Thus, a disc derangementin this younger age group could be related toprogressive remodeling associated with growth.This is in agreement with observations that thecondyle undergoes considerable change in shapeduring the period of transition from birth to adult-hood (Petrovic 1972). In these individuals withthe symptom of a clicking joint, the anterior discposition could indeed be within the range of nor-mal anatomic variation. In line with this sugges-tion and the finding that the closing click oftenoccurs just before the condyle re-enters the fossa(Farrar and McCarty 1982; Huddleston Slateret al. 2002), an anterior disc displacement maybe the result of a space insufficiency within thejoint, so that the condyle and disc cannot be

jointly accommodated in the fossa. As a result,the disc becomes anteriorly displaced. In supportof this notion is the fact that individuals withskeletal class II profiles and hyperdivergentgrowth patterns have been shown to have anincreased frequency of TMJ disc displacementand degenerative disorders (Manfredini et al.2016).

Clicking due to anterior disc displacement inearly or later mouth opening is often termed asanterior disc displacement with reduction (Figs. 5and 6). A permanent or so-called closed lock ofthe TMJ movement is often termed as a non-reducing disc displacement (Figs. 5 and 7). Ret-rospective studies support the general idea that adisc displacement is likely to progress to osteoar-thritis (Rasmussen 1981; Wilkes 1989). It hasbeen postulated that individuals with disc dis-placements show a temporal progression thatcommences with clicking in early mouth opening(i.e., disc displacement with early reduction), toclicking in later mouth opening (i.e., disc dis-placement with late reduction) to intermittentlocking (i.e. disc displacement with occasionalreduction), and finally ending in a permanent orso-called closed lock of the TMJ movement (i.e.,disc displacement without reduction) (Rasmussen1981; Wilkes 1989). Since a permanent orso-called closed lock is an acute sign suggestiveof an early osteoarthritis, these observationssupported the idea that a disc displacement even-tually progresses to osteoarthritis.

Apart from the fact that it has been shown thatthe position of the click on mouth opening ispoorly correlated with the actual position of thecondyle (Huddleston Slater et al. 2002), longitu-dinal epidemiological studies do not support theconcept of temporal progression outlined above(de Leeuw et al. 1994, 1995a). In one study,293 subjects with clicking were followed for aperiod of 10 years and found only one subjectwho reported intermittent locking during thistime (Magnusson et al. 1993). Additionally, thislack of progression of internal derangement froma clicking (or better: a reducing disc to anon-reducing disc condition) was confirmed inseveral studies (Greene and Laskin 1988;Könönen et al. 1996). Given a disc displacement


with reduction may persist for decades, impliesthat a progressive course does not seem to be ageneral rule. By contrast, it has often beendescribed that a disc displacement may persistfor decades (de Leeuw et al. 1994) and can evensubside for some time, to reappear again later(Könönen et al. 1996).

Trauma to the TMJ or mandible has also beenthought to be a cause for disc displacements. Mostoften an acceleration-deceleration or an indirecttrauma is appointed as cause for pathology(McKay and Christensen 1998; Brown 1997).An acceleration-deceleration injury is an injuryresulting from a collision between a body part

and another object or body part while both are inmotion (Mosby’s Medical Dictionary 2013). Anindirect injury is an injury that is not the result of adirect blow (Oxford Dictionary of Sports Science& Medicine 2006). Trauma is further subdividedin macrotrauma and microtrauma (Speck et al.1979). Macrotrauma is the direct result of amajor traumatic event to the TMJ or mandible,resulting in overextension of the joint. It can alsoresult from (open) joint surgery. Other examplesof macrotrauma can be extreme and prolongedmouth opening during a dental procedure (e.g.,extraction, root canal treatment) or during intuba-tion prior to general anesthesia. Microtrauma are

Fig. 5 Anterior displacement of the articular disc, relativeto the head of the condyle. (a) Disc relationship with thecondyle in the closed mouth position. (b) Anterior discdisplacement with reduction: On mouth opening, thedisplaced disc acts as a localized mechanical fault thatinterferes with smooth joint movement. This is the causeof the clinically observed clicking sound with joint move-ments as the disc “clicks” onto the head of the condyle. (c)

Disc displacement without reduction: On mouth opening,the displaced disc once again acts as a localized mechanicalfault that interferes with smooth joint movement. However,the disc fails to “click” onto the head of the condyle withmouth opening. Mouth opening is limited resulting in aclosed lock condition (Original drawing by Dr. Hala AlJanaby, Perth, WA, Australia)


small repetitive injuries to the joint that repeatedlycause a soft tissue response, such as plastic defor-mation of the ligaments. Diurnal clenching isthought to be an example of microtrauma (Specket al. 1979). In adolescence, diurnal clenchingmay be a risk factor for intermittent locking inindividuals with disc displacements (Kalaykovaet al. 2011). Diurnal clenching is thought to resultin viscoelastic deformation of the disc that, duringnormal circumstances, are temporary and have nofurther consequences. However, if the burden onthe system is severely upregulated, the delicate

balance between synthesis and breakdown (i.e.,between anabolic and catabolic activity) withinthe articular tissues may become disturbed suchthat morphologic changes within the joint permitadaptation of the shape of the joint components,which in turn lead to locking of the joint(Fujimura et al. 2005).

The natural course of anterior disc displace-ment without reduction has been studied in 44 sub-jects who agreed to observation without treatment(Sato et al. 1997). The incidence of successfulresolution of the condition without treatment was

Fig. 6 Anterior disc displacement (a) with reduction (b)on opening. D disc, C condyle, GF glenoid fossa, AEarticular eminence. Dotted white lines indicate extent of

the disc. (Images courtesy of Clinical Associate ProfessorAndy Whyte, Perth Radiological Clinic, Perth, WA,Australia)

Fig. 7 Anterior disc displacement (a) without reduction(b) on opening. D disc, C condyle, GF glenoid fossa, AEarticular eminence. Dotted white lines indicate extent of

the disc. (Images courtesy of Clinical Associate ProfessorAndy Whyte, Perth Radiological Clinic, Perth, WA,Australia)


68% at 18 months (Sato et al. 1997). This findingsuggests that the signs and symptoms of anteriordisc displacement without reduction tend to bealleviated during the natural course of thecondition.

To summarize, clinical evidence does notsupport progressive worsening of the disc dis-placement in most patients. It is not exactly clearwhich patients have the greatest risk of pro-gressing to more advanced stages. Conse-quently, clinicians who justify aggressivetreatment of asymptomatic TMJ clicking basedon their belief in a high progression rate to anonreducing state should instead exercisepatience and clinical vigilance in their manage-ment of this condition. At present, considerableevidence has been obtained that disc displace-ment cannot be regarded as the sole predominantprimary etiologic factor for TMJ disorders(de Leeuw et al. 1994, 1995a; Magnussonet al. 1993; Westesson et al. 1989).

Hypomobility and Adherences

Adherences, due to a prolonged pressure of thejoint structures (e.g., clenching the teeth), are usu-ally temporary and can be eliminated by mobili-zation of the joint via external force to the jointstructures to free its movements. However, if theadherence cannot be freed (e.g., permanentdisplaced disc), the immobilization may

eventually become permanent (adhesion) (Leiet al. 2017). Damage to the synovial membranemay result in an inflammatory reaction that trig-gers the development of fibrotic connective tissue(Katsnelson et al. 2012). Further, fibrosis of theconnective tissue that lines the synovial surfacesmay result in adhesions (Al-Baghdadi et al. 2014).Finally, it is also known that open TMJ surgery isa risk factor for the development of hypomobilityand adhesions (DeMerle et al. 2017; Rastogi et al.2015). The relative risk, however, largely variesbetween studies and depends upon indication forthe surgery and the surgeon (Cevidanes et al.2010). Ankylosis is a fibrotic or bony connectionbetween the articular surfaces that may lead to apersistent intra-articular hypomobility (DeMerleet al. 2017; Rastogi et al. 2015). Ankylosis usuallyoccurs after intra-articular bleeding, for exampleafter a severe trauma (Fig. 8). Ankylosis after acondylar fracture in juveniles may lead to growthdisturbances of the lower face (retrognathia).Another form of hypomobility can be caused byimpedance of the coronoid process (Fig. 9)(Mulder et al. 2012). During opening, thecoronoid process passes antero-inferiorly betweenthe zygomatic process and the posterior lateralsurface of the maxilla. If the coronoid process iselongated, or if fibrosis has developed in this area,its movement may be inhibited and chronic hypo-mobility of the mandible can result (Kim et al.2014; Tavassol et al. 2012; Zhong et al. 2009).

Fig. 8 Ankylosis of the left TMJ. Between the zygomaticarch and the condyle on the right side (nonankylotic side) adistinct dark line is visible. On the left side, the dark line is

not visible, because the condyle is connected to the zygo-matic arch or better said the fossa. ConeBeam CT image,coronal section. C condyle, ZA zygomatic arch


Hypermobility Disorders

A common cause of (sub)luxation is iatrogenicand may occur during a lengthy surgical proce-dure or during the intubation process for the treat-ment of trauma or systemic diseases. Patients withcertain anatomical features, such as those with ashallow or steep articular eminence or abnormalcondylar shape, may also be more prone to luxa-tions or subluxations (Liddell and Perez 2015).

Luxations, or subluxations, can also occurspontaneously during yawning or singing in theabsence of any pathologic condition. In a hyper-mobile joint, the ligaments are loose. The loose-ness of ligaments should be regarded as avariation of normal anatomy. As the condylemoves beyond the crest of the articular eminence,it appears to jump forward into a more-wide openposition. The patient usually reports that the jaw“goes out” anytime he or she opens wide. Symp-tomatic TMJ hypermobility seems to be relatedwith gender, as women tend to be more

hypermobile than men (Seow et al. 1999; Larssonet al. 1993). TMJ hypermobility seems to beunrelated to either disc displacement or to inter-mittent closed locking (Kalaykova et al. 2011).

Hypermobile joints are common and occur inabout 10–25% of the population (Garcia-Campayoet al. 2011). It is usually not associated with anysymptoms, but a minority develop other conditionscaused by their unstable joints. The most commonheritable connective tissue disorder is the Ehlers-Danlos syndrome (EDS). EDS is a clinically andgenetically heterogeneous group of disorders,including an increasing number of variants whichshare the variable combination of dermal fragility,internal organ and vessel ruptures, and joint hyper-mobility (Table 3).

Fractures

Since the introduction of various security mea-sures in the last decades, the number facial

Fig. 9 Coronal reconstruction (a) of the coronoid pro-cesses (arrows) from a multidetector CT scan with a 3-Dreconstruction of the left TMJ and coronoid process(arrow) (b), illustrating bilateral coronoid hyperplasia.Hypomobility will result secondary to impingement

between the laterally flared and elongated coronoid pro-cesses as they abut and impinge upon the zygomatic arches(za) limiting further mouth opening. (Images courtesy ofClinical Associate Professor AndyWhyte, Perth Radiolog-ical Clinic, Perth, WA, Australia)


fractures (helmets, air bags, cage constructions incar design) that arise from traffic accidents havesteeply declined. By contrast, the number of frac-tures caused by violent crimes in relation to alco-hol and illicit drugs has not declined, and in fact,for illicit drugs in particular have increased(Afrooz et al. 2015). In addition, sports accidentsare also causes of facial injuries (Afrooz et al.2015; Yamamoto et al. 2015; Zhou et al. 2015;de Lucena et al. 2016; Farneze et al. 2016). Of allmandibular fractures, between 25% and 50% alsoinvolve fractures of the condylar process (Powers2017; Kruger and Tennant 2016; Afrooz et al.2015). Fractures of the condylar process can besubdivided in fractures of the mandibular caput(the head of the mandible) and fractures of themandibular collum (the neck of the mandible).Fractures of the collum are most frequently seen

and these fractures (Fig. 10) are caused by traumato the corpus (body) of the mandible (Afrooz et al.2015). Forces are distributed to the condylar pro-cess and damage occurs at the weakest point,which is apparently the collum. This is generallybeneficial because, if this does not occur, themandibular caput could be displaced through thethin base of the skull. The potential for repair ofthese fractures without intervention is significant.The long-term implications of condylar and sub-condylar fractures are generally good and seemnot to have any increased likelihood for the devel-opment of arthritis or clicking (Hovinga et al.1999; Zachariades et al. 2006; Laskin 2009;Lekven et al. 2011), unless undiagnosed and leftuntreated (Nagori et al. 2014).

Inflammatory Disorders

Most of the current understanding of articularcartilage maintenance and degradation is derivedfrom large load-bearing synovial joints, in partic-ular the knee joint. Both the knee joint and theTMJ are complex synovial joints with comparablemechanical features. Furthermore, the cartilagedegenerative processes are believed to developsimilarly. An important difference between thesejoints is the type of cartilage that forms the artic-ular lining. In the knee joint, articular surfaces are

Fig. 10 Condylar (left; black arrows), mandibular frac-ture (right; blue arrows) and coronoid process fracture(white arrow). C condyle, CP coronoid process (Image

courtesy of Dr. Larry Cunningham, University of Ken-tucky, Lexington, KY, USA)

Table 3 Classification of Ehlers-Danlos syndrome(Castori 2012)

Major forms

Hypermobility/JHS

• Vascular

• Kyphoscoliotic

• Arthrochalasia

• Dermatosparaxis

Rare/emerging forms

• Cardiac-valvular

• Periodontitis


covered with hyaline cartilage, whereas in theTMJ, this lining consists of fibrocartilage. Boththe knee joints and TMJs share similar risk factorsfor osteoarthritis including age, gender, over-loading, joint injuries, and genetics. The risk ofosteoarthritis increases with age, probablybecause the quality of the tissues is reduced withaging. Epidemiologic studies indicate a femalepredisposition for osteoarthritis of the TMJ, andinterestingly, women between the ages of44–55 years are most likely to seek treatment,suggesting a role for estrogen in the disease pro-cess of the TMJ (Manfredini et al. 2010). Themandibular condylar cartilage differs from otherarticular cartilages as it undergoes endochrondralossification. In long bones, estrogen is responsiblefor endochondral growth plate fusion in bothmales and females, and the role of estrogen recep-tors (ERs) has been characterized (Chen et al.2014). For example, estrogen via ER alpha isresponsible for growth plate fusion in both maleand female mice. In contrast, ER beta is involvedin growth inhibition in only young female mice(Nelson et al. 2013). The exact mechanism is yetto be elucidated. Also, repetitive microtraumaticoverloading may damage the delicate structuresbeyond their healing capacity. Injuries, such asopen joint surgery, may increase the risk of oste-oarthritis (Fig. 11). There is little doubt that agenetic background is a significant determinantof an individual’s susceptibility to disease. Oste-oarthritis is covered in detail in another chapter ofthis book.

Crystal Deposition Diseases

Gout is the traditional term for a heterogenousgroup of diseases that among other structuresmay affect the TMJs. The diseases include hyper-uricemia, arthritides, sodium urate crystal deposi-tion in and around joints, renal disease, andurolithiasis. The crystallization of uric acid,often related to relatively high levels in theblood, is the underlying cause of gout. This canoccur for a number of reasons, including diet,genetic predisposition, or underexcretion ofurate, the salts of uric acid. Underexcretion ofuric acid by the kidney is the primary cause ofhyperuricemia in about 90% of cases. Calciumpyrophosphate deposition disease is characterizedby the presence of crystal deposits in the affectedjoint. It is also called pseudogout (Fig. 12).

Crystal deposition diseases are mostly found inknee joints, but a few reports describe crystalformation in the TMJ (Dijkgraaf et al. 1998).Osteochondromatosis (also known as synovialchondromatosis) is a rare disease that formsbony cartilaginous nodules by a cartilaginousmetaplasia in the synovium or joint-lining tissue.The nodules move freely within the synovial fluid,which they require for nutrition and growth. Pro-gressive enlargement and ossification occur withtime. In severe cases, they may occupy the entirejoint space or penetrate to adjacent tissues. Also,they can reestablish a blood supply and becomereplaced by bone. In most cases, the disease isunilocular and involves either the knee, the hip, or

Fig. 11 Osteoarthritis ofthe TMJ. Sagittal (a) andcoronal (b) view of rightcondyle with flattening,erosion, pseudocysts, andosteophyte (arrow).C condyle, EAC externalauditory canal


the elbow. Rarely does it involve the TMJ(Fig. 13) (Phelan et al. 2011). The etiology isunknown.

Hyperplasia

Condylar hyperplasia is an increased develop-ment of one mandibular condyle. It is not knownwhen condylar hyperplasia begins and how long itlasts. Statistically it affects more women in ado-lescence, although it does not discriminate by ageor gender (Fig. 14).

Hypoplasia

Condylar hypoplasia (Fig. 15a) is an underdevel-opment of the mandibular condyle, due to damageof the condylar growth or due to ankylosis of thejoint at youth. Among possible causes are atrauma, irradiation, surgical intervention (e.g.,gross tumor resection), juvenile idiopathic arthri-tis, or an infection of the joint. The level of defor-mation depends upon the age at which thecondylar growth was interrupted. If the hypopla-sia is inherited, the underdevelopment is observedat early ages (Fig. 15b).

Fig. 12 Seventy-year-old female with chondrocalcinosisdue to pseudogout (calcium pyrophosphate deposition)with advanced arthropathy: Axial (a), oblique sagittal (b),and coronal bone (c), and soft-tissue window (d) recon-structions from a multidetector CT scan; there is extensivechondrocalcinosis (white dotted arrows and oval in b).This calcification is situated both in the joint capsule aswell as being intra-articular in location. A more discreteossified body is present, posterior to the condyle (white

arrow in b). All images show marked joint spacenarrowing, articular surface flattening, irregularity andperipheral osteophytosis consistent with osteoarthritis.The axial image (a) shows scalloped erosion of the articu-lar surfaces corresponding to the foci of chondrocalcinosis(white dotted arrows) typical of pseudogout (Images cour-tesy of Clinical Associate Professor Andy Whyte, PerthRadiological Clinic, Perth, WA, Australia)


Pathophysiology

Disc Derangements

During function of the TMJ forces generated bythe masticatory muscles are transferred to theinner structures of the temporal bone and as aresult these structures become loaded. The articu-lar disc compensates for the incongruity of thebony surfaces during its joint movements and adirect response of the loading of the tissues is the

viscoelastic deformation of the disc. In normalcircumstances, the deformations are temporaryand have no further consequences. If necessary,the biological system reacts with remodeling ofthe joint to adapt to the increased loading. Sincethe ability of the disc to remodel is very limited(if present at all) remodeling is the result of resorp-tion of the subchrondal bone by osteoclasts. If theoutline of the tissues alters in such a way that thedisc cannot slide smoothly during articulation, thedisc may displace into an altered position to allowfor movement of the condyle. Displacement of the

Fig. 13 Synovial chondromatosis of the upper TMJspace. (a) CT –multiple faintly calcified bodies are presentin the distended upper joint space (white dotted margin).(b) MRI – a fat saturation T2 sagittal sequence demon-strates marked distension of the upper joint space (whitemargin) by high signal synovial proliferation containinglower signal foci (white dotted arrows) representingchondroid or osseous bodies. (c) MRI – a post gadoliniumT1 sagittal sequence demonstrates enhancement

(hyperintense signal) of the synovial proliferation in thedistended upper joint space (black dotted margin). The discis shown as nonenhancing structure, apposed to the con-dylar head; it is of similar signal to the multiple small intra-articular bodies (black arrows). (d) Histopathology – mul-tiple small ossified bodies (Images courtesy of ClinicalAssociate Professor Andy Whyte, Perth, RadiologicalClinic, Perth WA, Australia)


Fig. 14 Condylar hyperplasia of the right condyle. Boththe neck and the condyle on the right side are enlarged(black arrows). The unilateral growth resulted in an open

bite on the ipsilateral side (white arrow). C condyle (Imagecourtesy of Dr. Joseph van Sickels, University of Ken-tucky, Lexington, KY, USA)

Fig. 15 Condylar hypoplasia and agenesis: (a) Right con-dylar hypoplasia and marked mandibular asymmetry. (b)Agenesis of the right condyle apart from a small separate

ossified fragment. There is marked mandibular asymmetry(Images courtesy of Clinical Professor Andy Whyte, PerthRadiological Clinic, Perth, WA, Australia)


disc can only happen by stretching of the firmretrodiscal ligaments that connect the disc withthe condyle. This means that the disc does notdisplace spontaneously, but will only do so afteradvanced intra-articular remodeling. Thisremodeling is not always visible on panoramicor on CT imaging, but has been shown in acadaver study (De Bont et al. 1986). Displaceddiscs may elicit responses, particularly in the discand retrodiscal tissues (De Bont et al. 1986).These responses are a normal reaction of thebody to adapt to changing circumstances.Remodeling of the TMJ associated with normaladaptation to altered functional demands seems tobe particularly prominent during late growth and

early maturity, which is when the joint compo-nents undergo considerable changes in overallshape (Solberg et al. 1985).

Discs can displace in an anterior, lateral,medial, and even posterior direction (HuddlestonSlater et al. 2005). Anteromedial and anterolateraldisplacements are most frequently observed(Tasaki et al. 1996; Montagnani et al. 2005;Whyte et al. 2006; Ikeda and Ikeda 2016).

Reduction of the disc is the repositioning of thedisc from a displaced position into its originalposition on the condyle during mouth opening(Fig. 16). On opening of the mouth, the condylepushes the disc forward until there is enoughpressure that the condyle can “jump” past the

Fig. 16 Disc displacement with reduction. (1) The artic-ular disc is anteriorly displaced relative to the head of thecondyle when the mouth is fully closed. (2, 3) As themouth begins to open, the condyle further displaces thearticular disc anteriorly. (4) A click is noted as the discreduces and assumes its original position on the condylarhead. (5) The mouth is wide open and the articular disc

remains in its original position relative to the condylarhead. (6, 7, 8) The mouth begins to close, where occasion-ally another click might be noted as the disc slips anteriorlyoff the head of the condyle when the mouth is fully closedagain (1) (Original drawing by Dr Hala Al Janaby, Perth,WA, Australia)


posterior band of the disc and assumes its positionunder the intermediate zone of the disc. The elas-ticity of the tissues, together with the degree ofdeformation of the disc and the degree of theoverstretching, determine whether “reduction” ofthe displacement can occur. Not all disc displace-ments have the capacity of a reduction; some discshave a semipermanent displacement and othersare chronic displacements without any form ofreduction (Fig. 17). When a disc is chronicallydisplaced (i.e., without reduction), the anteriorband undergoes atrophy or folds over the interme-diate zone, while the posterior band becomes flat-tened and elongated in the superior joint space andenlarged inferiorly (de Leeuw et al. 1995b).Responses to disc displacement observed in the

retrodiscal tissues include increased presence ofdense connective tissue, decreased vascularity,and decreased innervation, suggesting that duringaltered disc position, the retrodiscal tissue mayeventually adapt and function as a pseudodisc.Apparently, the TMJ has the capacity to adapt tochanging functional demands. Degradation andloss of articular cartilage may lead to subsequentreduced smoothness of the articular surfaces and ifsurface irregularities have developed, joint noises(crepitation) may become present. It is highlyunlikely that disc displacement is a prerequisitefor osteoarthritis to occur. It is incorrect to assume(but nevertheless this view is still widely held)that a disc displacement would inevitably pro-gress to degenerative joint disease.

Fig. 17 Disc displacement without reduction. (1) Thearticular disc is anteriorly displaced relative to the head ofthe condyle when the mouth is fully closed. (2, 3, 4) As themouth begins to open, the articular disc is unable to resumeits original position on the condylar head. (5) Mouth

opening is limited as the anteriorly displaced articulardisc prevents the condyle from fully translating. (6, 7, 8)The anteriorly displaced disc remains as the mouth beginsto close (Original drawing by Dr Hala Al Janaby, Perth,WA, Australia)



Adherences occur when the TMJ is subject toprolonged static loading. They result in a tempo-rary hypomobilty, and oftentimes can be releasedby the patient through manipulation of the jaw.The release is usually accompanied by a loudnoise, upon which mobility is restored.

Adhesions are the result of the development offibrotic connective tissue between the articularsurfaces after damage to the joint. The fibroticconnective tissue lines the original synovial sur-faces and may result in adhesions. If the connec-tive tissue can organize itself, for example in thecase of a prolonged fixation of the joint (e.g., afterintermaxillary fixation due to orthognathic sur-gery) it may lead to capsular fibrosis. In moreextreme cases, especially after intra-articularbleeding more advanced fibrosis may occur.Ankylosis is a fibrotic or bony connectionbetween the articular surfaces, which may leadto a persistent intra-articular hypomobility. Clini-cally, the result is a permanently reduced mouthopening. Ankylosis after a condylar fracture injuveniles may lead to growth disturbances of thelower face (retrognathia).


Hypermobility or subluxation should be regardedas a nonpathologic condition. As in a hypermobilejoint, the ligaments are loose and the condyle canmove beyond the crest of the articular eminence, itappears to jump forward into a more wide openposition (Gutierrez et al. 2011). Complaints usu-ally occur due to overextension of the muscles andsome discomfort of temporarily not being able toclose the mouth. In unilateral dislocation, themandible deviates toward the healthy side, whilein bilateral dislocation, the mandible slides for-ward in a gaping mouth opening.

Fractures

As the forces generated by trauma are transmittedto the articular surfaces in the TMJ, an

inflammatory response occurs in the synovial lin-ing. Proliferation of surface cells, increased vas-cularity, and fibrosis of the subsynovial tissuesoccur and erythrocytes extravasate. A prolifera-tive synovitis ensues. Despite the damage, thepotential for repair is high. The subsynovial tis-sues have a rich vascularity and their regenerativeabilities are excellent. It has been reported that,within weeks of a trauma, the injured synovialtissues are indistinguishable from normal tissues.

The potential for repair after trauma is high butis incomparable to an inflammatory disorder, suchas osteoarthritis (see below). The latter disordersheal slowly and usually coincide with far moresymptoms than fractures.

Arthralgia

The auriculotemporal nerve innervates the TMJ.The nociceptors within the joint have a highthreshold and only react to serious overloadingof the capsule. In case of an inflammation of thejoint, the threshold of the nociceptors is loweredand as a result normal movements of the jointbecome painful. Inflammatory exudate (hydrops)in the joint build up some pressure in the joint andmay elucidate a pain reaction on palpation of thejoint or during its movements (Kothari et al.2015).

Pain in the joint may result in co-contraction ofthe masticatory muscles (muscular splinting),which in turn can become painful (Okeson2013). Arthralgia of the TMJ can be due to aninflammation of the synovial membrane (synovi-tis) or can be due to an inflammation of the cap-sule (capsulitis) or a combination of latter causes(Kalladka et al. 2014).

Osteoarthritis

Osteoarthritis involves degeneration and inflam-mation and may be considered as a maladaptiveresponse. It involves replacement of the originaltissue structure by a tissue of inferior quality andon a cellular level, in addition to adaptiveresponses, necrosis is present. Normal tissue


turnover involves synthesis and breakdown in awell-regulated balance, but a relative increase ofbreakdown, such as that caused by degenerativeactivity, leads to accumulation of degradativeproducts. At first, an adaptive increase in phago-cytic activity of the synovial membrane starts, butwhen the levels of degenerative products exceedthe clearing capacity of the synovial tissues, aninflammatory response is initiated. The inflamma-tory reaction reflects increased degenerative activ-ity and is core of the disease process. Chondrocytemetabolism is very sensitive to its environmentand cartilage breakdown may reflect decreasedsynthesis of new matrices, increased breakdownof existing matrices, or both. Although osteoar-thritis is considered a degenerative process, pri-marily affecting the articular tissues andeventually leading to destruction of cartilage andthe subchondral bone, the secondary inflamma-tory components account for many of its clinicalsymptoms, named arthralgia. It is known that thesynovial fluid of affected joints is less viscousthan that of healthy joints. This is due to a lowerquality of the highly viscous hyaluronic acid thatacts as a boundary lubricant for soft tissues. As aresult, the synovial fluid has reduced protectivelubricating ability. This reduced protection,together with the impaired joint mobility, isthought to trigger a sequence of events that ham-per the transsynovial flow and subsequently themetabolic and rheological homeostasis of thejoint. It has been suggested that free radicalscould act as a potential mechanism for the initia-tion of the molecular events in osteoarthritis(Sheets et al. 2006). Normally, accumulation offree radicals is prevented by endogenous freeradical–scavenging mechanisms, but the scaveng-ing capacity is probably exceeded by an over-whelming production of free radicals. Freeradicals may be produced by direct mechanicaltrauma as well as by several other mechanisms. Ithas been thought that an increased intra-articularpressure in joints might evoke a period of hyp-oxia. By alterations in the metabolism on reperfu-sion, cells may generate free radicals. Thismechanism is termed hypoxia-reperfusion injury.Currently, there is however no evidence to corrob-orate the hypothesis that hypoxia-reperfusion

occurs in patients with osteoarthritis in the TMJ(Vos et al. 2012). Nevertheless, damage evokedby the accumulation of free radicals in affectedjoint tissues can be expanded by the production ofextracellular matrix degradation products, by acti-vation of inflammatory cells to synthesize andsecrete cytokines, and by the generation of pro-inflammatory molecules (e.g., prostaglandins,bradykinin, and histamine). The ensuing collagenbreakdown causes disruption of the collagenousnetwork. As a result, the tissue swells and softens(termed chondromalacia). The increase of break-down products in the synovial fluid may result inan inflammatory response in the synovial mem-brane, which may produce an appearance of jointeffusion on MRI (Fig. 18), probably representingtissue edema rather than increased fluid produc-tion. Joint “effusion” on the MRI is a sign of bonemarrow edema and has been shown to be presentin 80% of painful joints (Takahashi et al. 1999).Bone marrow edema is a significant pain genera-tor and may be a primary contributor to disease(Eustace et al. 2001; Hofmann et al. 2004).Because of the above-mentioned changes of thearticular surfaces, adaptive and compensatorychanges (e.g., muscular responses, changes withinthe capsule, retrodiscal tissue and subchondralbone) or decompensation (e.g., erosions, perfora-tions) occur. Over time, this may lead to (mechan-ical) changes of the associated tissues.Radiographic changes are the vast reminder ofthese processes. Interestingly, about 50–90% ofsymptom-free individuals have been shown tohave radiographically visible changes probablydue to osteoarthritis. This may reflect the tendencyof clinical symptoms of osteoarthritis to subsidewith time, but radiographic changes may also bethe result of remodeling that is associated withgrowth and recovery or repair, which results inadaptation and normalization of function. It isessential to understand that osteoarthritis is a dis-order that occurs in joints regardless of the posi-tion of the articular disc and is characterized bytwo basic pathologic mechanisms: degenerationand inflammation. It is highly unlikely that discdisplacement is a prerequisite for osteoarthritis tooccur. Often, however the term “internal derange-ment” has become a false diagnostic description


in patients with symptoms such as pain, clicking,and restriction of mouth opening.

Rheumatoid Arthritis

Rheumatoid arthritis is a chronic inflammatorydisease that primarily affects the periarticularstructures such the capsule, tendons, and liga-ments. It secondarily involves the articular carti-lage and subchondral bone. Approximately50–70% of patients with rheumatoid arthritishave involvement of the TMJ. It is bilateral inabout half of the patients. Mandibular movementmay be severely limited in the late stages of thedisease, often through stiffening of the joint.Often an anterior open bite is seen, due to destruc-tion of the joints. In young patients, under16 years of age, a distinct form named juvenilerheumatoid arthritis also called juvenile idiopathicor chronic arthritis exists. In an estimated 45–75%of children with this disease, the TMJ is involved,

with significant adverse effects on dental occlu-sion, oral health, and in particular facial growth(Twilt et al. 2004; Billiau et al. 2007; Weisset al. 2008).

Spondyloarthritides

Ankylosing spondylitis is a rheumatic diseasecharacterized by inflammatory stiffening of thespine and sacroiliac joints. The primary patho-logic site is not the synovium, but rather the liga-ments and the surrounding joint capsule. Thedisease is characterized by fibrosis and ossifica-tion rather than joint degeneration. The TMJ maybe involved in the disease (Wenneberg 1983).

Psoriatic arthritis is an inflammatory arthritisassociated with psoriasis. Although most patientswith psoriasis have a benign course, a subgrouphas a more severe course, including arthritis. Pain,swelling, or stiffness in one or more joints iscommonly present in psoriatic arthritis. Affected

Fig. 18 Fat-saturation T2 oblique sagittal MRI scans ofthe left TMJ in two patients with internal derangement andpain. (a) A moderate sized, hyperintense (“bright”) effu-sion is present in the anterior recess of the upper joint spacewith a small effusion in anterior recess of the inferior jointspace (white dotted arrows). Synovitis is also hyperintense(white arrows) but the signal is lower than that of jointfluid. The condyle is remodelled with focal subarticular

reactive marrow change (white dotted oval). (b) There is alarge, hyperintense effusion in the anterior recess of theupper joint space (white dotted arrow). Marked synovitisaround the bilaminar zone (white arrows) and inferior jointspace with extensive condylar erosion and resorption(white open arrow) in a young female adult with ICR(Images courtesy of Clinical Professor Andy Whyte,Perth Radiological Clinic, Perth, WA, Australia)


joints are generally red or warm. Most often thejoints of the hands and wrists are affected, but inselected cases the TMJ can also be affected. Alongwith the above noted pain and inflammation, thereis extreme exhaustion that does not subside withadequate rest (Lee et al. 2010). The exhaustionmay last for days or weeks without abatement.Psoriatic arthritis may remain mild, or may pro-gress to more destructive joint disease. Periods ofactive disease, or flares, will typically alternatewith periods of remission. Because prolongedinflammation can lead to joint damage, early diag-nosis and treatment to slow or prevent joint dam-age is recommended.

Reiter syndrome or reactive arthritis can bedefined as aseptic arthritis triggered by an infec-tious agent not present in the joint itself. It usuallyincludes a combination of urethritis, arthritis, andconjunctivitis (Stavropoulos et al. 2015). Theexact pathogenesis is unknown, but several infec-tive agents and a specific genetic (HLA-B27)background are recognized. The TMJ can beinvolved in patients who suffer from Reiter Syn-drome (Könönen et al. 1992).

Crystal Deposition Diseases

Gout is a disorder of purine metabolism, andoccurs when its end product, uric acid, crystal-lizes, precipitates, and forms deposits (tophi) injoints, on tendons, and even in the surroundingtissues. Microscopic tophi may be walled off by aring of proteins, which blocks interaction of thecrystals with cells, and therefore avoids inflam-mation. Unprotected crystals may break out due tominor physical trauma to the joint, surgical stress,or rapid changes in uric acid levels and as a resulttrigger an inflammatory reaction. The triggers forprecipitation of uric acid are not well understood(Larsen et al. 2015). While it may crystallize atnormal levels, it is more likely to do so as levelsincrease (Zhu et al. 2017). Other factors believedto be important in triggering an acute episode ofarthritis include cool temperatures, rapid changesin uric acid levels, acidosis, articular hydration,and extracellular matrix proteins, such as

proteoglycans, collagens, and chondroitin sulfate(Schlee et al. 2017). Blood uric acid levels may benormal during an attack. Calcium pyrophosphatedihydrate (CPPD) crystals are predominantlyfound in articular cartilage and meniscus, but arealso found in the membrane, joint capsule ten-dons, ligaments, and blood vessels. The pathogen-esis of CPPD crystal formation is still unclear(Abhishek and Doherty 2016). CPPD crystal for-mation may result from the presence or exposureof nucleating factors or the absence of inhibitorsfor precipitating factors. Crystal nucleation maybe predisposed by changes in the matrix, such ascollagen fibril fragmentation and changed compo-sition of glycosaminoglycans or proteoglycans(Abhishek and Doherty 2016). It is still unknownwhether crystal deposition is a result of or a con-tributing factor to osteoarthritis, but based on thefindings of intracellular CPPD crystals, it wassuggested that an intracellular pathway of CPPDcrystal formation could exist (Sheets et al. 2006).

Hyperplasia

The direct consequence of condylar hyperplasia isasymmetric facial deformity, by which the man-dible displaces to the nonactive side. The occlusalplane is also displaced and an open bite occurs(Fig. 14). The result is an enlarged condylar headand elongated mandibular collum. Often the openbite is compensated for by eruption of the teeth.Sometimes, a unilateral cross-bite on the non-active side occurs, which is the result of the rota-tional growth process (Olate et al. 2013; Portelliet al. 2015).

Hypoplasia

In most cases, condylar hypoplasia is unilateraland is often noticed as a facial asymmetry. Often,there is a unilateral impairment of the slidingmotion of the joint. Further, the antogonal notchis more prominent. Bilateral hypoplasia isobserved as a mandibular retrognathia, sometimeswith a frontal open bite.


Clinical–Pathological Features

Disc Derangements

The clinical features of disc derangements dependon the mobility of the displaced disc, the lubrica-tion of the joint, and the extent of displacement. Adisc displacement with reduction (Fig. 16) is oftencharacterized by reciprocal clicking, meaning thata clicking, popping, or snapping sound or sensa-tion can be heard/felt on opening as well as onclosing the mouth. In the closed mouth position,the disc is typically displaced in an anterior, ante-romedial or anterolateral position. On opening thecondyle pushes the disc forward until there isenough pressure that the condyle can “jump”past the posterior band of the disc and assume itsposition under the intermediate zone of the disc.The “jump” is heard or felt as a click, pop or snap.Before the disc reduces on opening, one mayobserve a deviation of the jaw to the ipsilateralside due to the disc obstructing smooth move-ment. On closing, the disc presumably slips backoff the condylar head, giving rise to another jointsound (Huddleston Slater et al. 2002). This con-dition is frequently asymptomatic and pain free.

A disc derangement with intermittent lockingis characterized by an intermittent inability tofully open the mouth. In this condition, the con-dyle transiently cannot clear the posterior band ofthe disc, resulting in limited translational move-ment. Clinically, the mouth opening is limited,and, if unilateral, the jaw typically deflects to theipsilateral side on opening and protrusion. Thiscondition is also called acute closed lock. Theclicking sound is absent during the period ofacute locking. A person with this condition maybe able to unlock his/her jaw and the jaw mayresume with the features of a disc displacementwith reduction. Sometimes the help of a clinicianis needed to unlock the jaw.

A disc derangement without reduction is char-acterized by a sudden closed lock as describedabove; however, in this case the disc is perma-nently displaced in anterior, anteromedial, or ante-rolateral position. The displaced disc interfereswith the patient’s ability to open the mouth fully,

and as a result the mouth opening is limited and, ifthe condition occurs unilaterally, the jaw often-times deflects to the ipsilateral side on openingand protrusion (Fig. 17). If the disc is displacedanteriorly, anteromedially, or anterolaterally,movement of the jaw to the contralateral sidemay be limited due to the disc barricading theforward and medial movements of the condyle.This condition frequently prompts a patient toseek help, not only because of the inability toopen the mouth but because this condition isoften associated with pain. Posterior disc dis-placement without reduction is described as apainful inability to maximally occlude the teethtogether. The displaced disc interferes with theability of the condyle to seat in its normal position,causing the condyle to be seated downward andforward, and resulting in an ipsilateral posterioropen bite. Posterior disc displacement with reduc-tion is characterized by a click on closing. Whenthe patient attempts to occlude, the disc assumesits normal position on the condyle. A snapping orclicking sound can be appreciated when the con-dyle passes the anterior band of the disc(Huddleston Slater et al. 2005).


Adherences cause a similar clinical picture to ananterior disc displacement without reduction.When the condition occurs unilaterally, the clini-cal picture shows limited mouth opening anddeflection to the ipsilateral side on opening andprotrusion. When this condition occurs bilaterally,the limited mouth opening will be the only clinicalfinding. Depending on where the adherence islocated, the patient’s mouth opening will bemore or less limited. If the adherence occurs inthe lower joint compartment, the rotation of thejoint is compromised, but the translational capac-ity is intact. If the adherence occurs in the upperjoint compartment, the translation of the joint iscompromised but the rotational capacity remainsintact. The latter condition will result in lessmobility than the former condition. A patientwith this condition will relate that the jaw


sometimes gets locked and that s/he is able tomove the jaw smoothly again after a loud snap-ping, popping, or cracking sound as occurred.This condition often occurs after a period ofimmobility or clenching. Patients with adherenceswill describe their condition as an occasional lim-itation of mouth opening relieved by a single loudsound, whereas a patient with a disc displacementwith reduction will describe the condition withmore consistent and frequent joint sounds, i.e.,“every time I chew or open my mouth”.

Adhesions also cause a similar clinical pictureto a disc displacement without reduction andadherences: limited mouth opening, and deflec-tion on opening or protrusion to the ipsilateralside. The difference between this and the othertwo conditions is that in the case of adhesions thelimitation occurs more gradually. Adhesions aremore frequent in the advanced stages of internalderangement and osteoarthritis (Zhang et al. 2009;Millon-Cruz et al. 2015).

Impedance of the coronoid process is charac-terized by a slowly progressive limitation of jawmovements. The condition is often bilateral, andthe patient will report a slowly progressing limi-tation of jaw movements in all directions. Whenthe condition occurs unilaterally, there is deflec-tion to the ipsilateral side and limited movementto the contralateral side. This condition is typi-cally pain free, but normal mouth functions, suchas opening and eating, and dental procedures willbecome increasingly hampered. Computerizedtomography with open mouth images showimpact of the coronoid process against thezygomatic bone.


Subluxation or luxation of the jaw is characterizedby the inability of the patient to close the mouthafter wide opening without a specific maneuverperformed either by the patient or a clinician.Consequently, the patient will be unable to bringthe teeth in occlusion. If the condition is unilat-eral, the jaw will deflect to the contralateral side.This condition is frequently associated with

significant pain and distress. Pain may eitherresult from strain of the joint which may result ininflammation, or from overextension of the mus-cles. Thus, pain may linger or persist after theluxation has been salvaged. On clinical examina-tion, pain to palpation of the muscles and affectedjoint(s) may be noted. A preauricular depressionmay be noted in the presence of the open lock(Fig. 19). In case of bilateral joint dislocations, thepatient may appear prognathic or show elongationof the lower third of the face. Radiographically,the condyle is positioned in front of the eminenceand the fossa is empty (Guttierrez et al. 2011)(Fig. 20).

Fractures

Fractures of the condylar head or neck may resultin limited mouth opening, malocclusion, swell-ing, pain, deflection on opening and protrusion,and facial asymmetry. Both acute displaced andnondisplaced fractures may present with thesefeatures depending on the severity of the respon-sible insult. These characteristics may be tempo-rary when left untreated in nondisplaced fractures,but some of these may remain in untreated

Fig. 19 Preauricular depression (arrow) in the presence ofthe open lock. The condyle is located anterior to the emi-nence creating a marked prominence (C). C condyle(Image courtesy of Dr. Pratishtha Mishra, University ofKentucky, Lexington, KY, USA)


displaced fractures. About 1–2% of condylar frac-tures result in ankylosis (Anyanechi 2015).

Arthralgia and Osteoarthritis

Arthralgia is characterized by report of pain felt inthe preauricular area or in the ear on jaw move-ment and/or jaw function. If the condition isaccompanied by significant inflammation, a mal-occlusion may be reported by the patient. Due toinflammation, effusion, or swelling of theintraarticular tissues, the patient may not be ableto bring the teeth into occlusion on the ipsilateralside, clinically detectable as a posterior open bite.Attempting to bring the teeth in occlusion mayresult in increased pain. The patient may alsoreport limited mouth opening due to pain. Palpa-tion of the area or manipulation/compression ofthe affected side results in an increase of thefamiliar pain. The clinical characteristics of oste-oarthritis are similar to those of arthralgia. How-ever, depending on the extent of degenerativechanges, the patient may report a malocclusionwith the sense of a heavier occlusion on the ipsi-lateral side, or the inability to bring the molars inocclusion on the contralateral side. Manualmanipulation of the mandible in an attempt toseat the condyle in its musculoskeletal supportedposition may unveil a discrepancy between this

position and habitual occlusion. In case of bilat-eral degenerative changes, an anterior open bitemay result (Fig. 21).

Crystal Deposit Diseases

Gout and CPPD are characterized by acute pain,redness, and swelling due to intense inflammationin the joint. The clinical characteristics, therefore,are the same as those for arthralgia.

Synovial (osteo)chondromatosis of the TMJ ischaracterized by progressive swelling and painand may be accompanied by intermittent orlong-lasting malocclusion and limitation of move-ment. The malocclusion and limitation can beintermittent due to free-floating osteocartilaginousbodies interfering with smooth movement of thejoint. When more severe, the limitation and/ormalocclusion may be more permanent. Jointnoises are frequently present, but in some cases,the disease is asymptomatic.

Hyperplasia

Condylar hyperplasia is an uncommon idiopathicunilateral disorder of jaw growth consistent withexuberant or persistent activity of the condylenucleus. Hyperplasia of the TMJ or of the

Fig. 20 Hypermobility of the right TMJ. The right TMJ islocated in front of the eminence, and the left TMJ remainsin the fossa (arrows). C condyle (Image courtesy of

Dr. Jeffrey P. Okeson, University of Kentucky, Lexington,KY, USA)


mandible is characterized by a slowly increasingfacial asymmetry with chin point deviation to thecontralateral side, and may be accompanied bymalocclusion. The condition is typically not asso-ciated with pain, and the patient’s concern is usu-ally the increasing facial asymmetry. Onexamination, facial asymmetry, chin point devia-tion, and canting of the occlusal plane are evident.This is best observed when the head is bend back-ward. On opening and protrusion, the jaw willdeflect to the contralateral side. A cross-bite mayalso be observed (Olate et al. 2013). Radiographicimaging can be used to confirm the diagnosis andthe extent of the excessive growth (Fig. 22). In

addition, isotope bone scan with SPECT imagingcan be used to determine whether the process isstill active (Fig. 23).

Hypoplasia

Hypoplasia of the condyle or the mandible is alsocharacterized by a slowly increasing facial asym-metry. Lack of mandibular and/or condylargrowth will result in facial asymmetry, occlusalcanting, malocclusion, and chin point deviation tothe affected side (Fig. 15). On opening and pro-trusion, the jaw will deflect to the ipsilateral side.A cross-bite may also be observed. If the condi-tion is bilateral, micrognathia will ensue. Radio-graphic imaging can be used to confirm thediagnosis and the extent of deficiency.

Patient Management

Disc Derangements

Depending on the type of derangement, and theimpact a disc derangement has on a person’s qual-ity of life, and the preference of the clinician,treatment can vary from reassurance and educa-tion to surgical interventions. Literature suggeststhat disc displacement with reduction may persistfor many years without progression causing min-imal to no discomfort to the patient (Greene andLaskin 1988; de Leeuw et al. 1994). It is alsoknown that little to no degenerative changesoccur when a disc displacement with reductionpersists for many years (de Leeuw 1995a). Thus,common sense would indicate that the patientshould be educated about the condition and itslong-term prognosis, and that invasive or aggres-sive methods to restore the position of the discshould be avoided. If there is pain involved, thenthe clinician should focus on reducing and elimi-nating the pain. This can be achieved by control-ling contributing and perpetuating factors such asunnecessary loading or relative overloading of thejoint and using supportive non-pharmacologicalor pharmacological management strategies. Theconcepts of self-awareness of jaw use and

Fig. 21 Open bite due to bilateral (juvenile) osteoarthritis.Frontal (a) and lateral views (b and c). Note the physio-logical attrition of the cusps of the molars


overuse, and employing therapies such as soft dietand habit reversal techniques should be intro-duced to the patient and subsequently reinforced.

Soft diet suggestions would include anything thepatient can eat within pain free limits, i.e., any-thing that does not aggravate the pain. Habit

Fig. 22 Mandibular hyperplasia of the right mandible andtilted occlusal plane. The dotted line indicates the

difference in height between the left and right ramus, andthe dashed line shows the tilted occlusal plane

Fig. 23 Twenty-one-year-old male with right condylarhyperplasia. An isotopebone scan with SPECT wasperformed to determine ifthere was persistentabnormal growth in theright condyle to aid timingof orthognathic surgery.The study demonstratesasymmetric and abnormalisotope uptake (metabolicactivity) in the right condyle(black dotted arrow).Uptake in the condyles canbe quantitated bycomparison with uptake inthe clivus (central skullbase): a + b, or the L4vertebral body: c (Imagescourtesy of ClinicalProfessor Andy Whyte,Perth Radiological Clinic,Perth, WA, Australia)


reversal techniques include methods to increaseawareness of adverse habits and to train thepatient to check periodically for such habits espe-cially during circumstances and activities whichhave been identified to likely trigger the adversehabit, and implement relaxation techniques aimedat keeping the teeth and lips slightly apart. Sup-portive pharmacological treatment can includeshort-term use of nonsteroidal anti-inflammatorymedications or other mild analgesics, such asacetaminophen, or in acute and severe cases ashort course of glucocorticoids. Non-pharmacological treatment can include moistheat and jaw relaxation exercises. When there issignificant joint pain on awakening, a maxillary,hard acrylic full coverage stabilization appliancemay be indicated (Fig. 24).

When the patient is diagnosed with disc dis-placement with intermittent locking, especiallywith the locking occurring on awakening, an ante-rior repositioning appliance may be indicated(Fig. 25). This appliance will keep the disc onthe condyle during the night and relieves pressureon the retrodiscal tissue allowing this tissue toheal. The purpose of the appliance is not to elim-inate the clicking but rather to bring the patientback to pain free clicking. The appliance shouldbe worn only at night in order to avoid occlusalchanges. In case of an acute closed lock, theclinician should attempt to unlock the jaw. If theattempt is successful, but the patient’s jaw locksimmediately again upon closing, an anteriorrepositioning appliance should be fabricated tokeep the jaw from locking. In this case, the patientis advised to wear the appliance full time for no

Fig. 24 (a) Frontal view of a full coverage of maxillaryhard acrylic stabilization appliance. (b) Frontal view of a

full coverage maxillary hard acrylic stabilization appliancein place

Fig. 25 (a) Frontal view of anterior repositioning appli-ance (b) Lateral view of anterior repositioning appliance

(Images courtesy of Dr. Jeffrey P. Okeson, University ofKentucky, Lexington, KY, USA)


longer than 5 days in order to avoid permanentocclusal changes. After that time, the patientshould wean off the use during the day to useonly at night, if there is still a need for nighttimeuse.

When a patient presents with a disc displace-ment without reduction, treatment should initiallyaim at reducing pain and discomfort, which can bedone as described above for disc displacementwith reduction, and then followed by jaw exer-cises aimed at increasing the mouth opening.Exercises can be performed by the patient bymeans of slowly stretching the jaw open bystacking tongue blades between the teeth, or bypushing with the thumb on the maxillary incisorsand with a finger on the mandibular incisors. Apassive motion device such as the Therabite(Fig. 26) can also be used. The exercises shouldbe performed within pain-free limits to avoidinflammation. Jaw stretching manipulation canalso be performed by physical therapists (seebelow). Studies have shown that with no (Satoet al. 1998; Sato et al. 2002) or minimal (Rasmus-sen 1981; de Leeuw et al. 1994) treatment, symp-toms and signs of pain and limited jawmovements gradually improve. However, withtreatment, signs and symptoms improve faster(Kai et al. 1998; Minakuchi et al. 2001; Murakamiet al. 2002). A recent systematic review and meta-analysis on the effectiveness of manual therapyand therapeutic exercises for temporomandibulardisorders (Armijo-Olivo et al. 2016) concludedthat there was only a slight trend toward betterpain reduction and increased mouth opening withexercises compared to education, splint therapy,or a control group. However, two recent reviewsfound that manual therapy (Martins et al. 2016) ormanual therapy in combination with exercises(Armijo-Olivo et al. 2016) was superior to splint

therapy, self-care, or pharmacological manage-ment with regard to reducing pain and increasingmouth opening. Manual therapy can involve jointmobilization, manipulation, or soft tissue treat-ment. A recent systematic review (Goiato et al.2016) investigating the benefits of intraarticularinjections of hyaluronic acid included two articleswith a total of 118 patients with internal derange-ments. This review showed a significant reductionin pain in one of the studies at 1 week and 6 weeksfor hyaluronic acid compared to saline and corti-costeroid or tenoxicam injections, while the sec-ond included study found no significant effect ofintraarticular injections of either hyaluronic acidor tenoxicam up to 3 months (Goiato et al. 2016).

Clinical Practice Guidelines for Oral and Max-illofacial Surgery of the American Association ofOral and Maxillofacial Surgeons (Bouloux et al.2017) state that surgical interventions for internalderangement should only be attempted after non-surgical treatments have proven ineffective andpain or dysfunction is moderate to severe. Theyspecifically state that surgery is not indicated forpreventive reasons or for asymptomatic or mini-mally symptomatic cases. The surgical optionsthat are available vary from arthrocentesis to fulljoint replacements.

Arthrocentesis is a simplified arthroscopy sur-gery without the use of a camera and intra-articular instruments and is rapid, minimally inva-sive, and safe. Arthrocentesis can be performedunder local anesthesia either with or without intra-venous sedation. Typically, after disinfection andpreparation of the surgical area, the area is anes-thetized with an auriculotemporal nerve block.Then, a 19 gauge needle is introduced into theupper joint compartment and 1–2 ml of lactatedRinger’s solution is introduced into the joint todistend the joint slightly after which in the case ofrestricted mouth opening, the mandible is manip-ulated in an attempt to improve joint mobility.Subsequently, a second 19-gauge needle is intro-duced into the upper joint compartment near theeminence. This needle serves as an outlet for thesaline solution. Subsequently, 200–300 ml of lac-tated Ringer’s solution is flushed through the jointover a period of about 15 minutes (Nitzan et al.1991). Some surgeons prefer to end the procedure

Fig. 26 Therabite®


by leaving steroids in the joint, while otherschoose to use hyaluronic acid. At this time, thereis no clear indication that one method is betterthan the other (Goiato et al. 2016). As with anyinvasive procedure, there is a risk of bleeding,bruising, infection, soreness at the injection site,transient paralysis of the facial nerve, transientmalocclusion, and a chance that the proceduredoes not provide relief. A meta-analysis includingthree studies with patients diagnosed with discdisplacement showed that arthrocentesis washighly successful for these patients (Reston andTurkelson 2003). Arthrocentesis is the least inva-sive type of surgical intervention with good out-comes in patients with closed lock. Even in theabsence of correction of the disc-condyle relation-ship, the improvement of dysfunction and mouthopening can be achieved (Al-Belasy and Dolwick2007).

Surgical procedures, including discoplasty,disc repositioning techniques, and modifiedcondylotomy (Hall et al. 2000), typically aim toimprove the disc condyle relationship.Discectomy either with or without replacementof the removed disc has also been used withvarying degrees of success (Bjornland andLarheim 2003; Nyberg et al. 2004; Dimitroulis2005; Holmlund et al. 2013). Discectomy proce-dures with alloplastic implants (silastic or pro-plast) have shown less favorable results thandiscectomy without replacement or nonsurgicaltreatment (Fricton et al. 2002). Patients whoreceived discectomy with dermis graft replace-ments (Dimitroulis 2005) or no replacements(Bjornland and Larheim 2003; Miloro andHenriksen 2010; Holmlund et al. 2013) seemedto improve in mandibular function, however thestudies cited did not use a comparison group.Replacements with ear cartilage or free fat havebeen performed as well. While ear cartilage has atendency to fragment or proliferate, free-fat grafts,while quickly shrinking in volume after transplan-tation, may minimize intraarticular scar forma-tion. While temporalis flaps have enjoyedpopularity as interpositional grafts, no random-ized controlled studies are available to demon-strate their effectiveness (Dimitroulis 2011).

Adherences

Adherences can be treated by arthrocentesis orarthroscopic lysis and lavage, and further pre-vented by avoiding continuous or prolonged load-ing of the joints. This can be accomplished byeducation regarding, and avoidance of contribut-ing factors such as awake clenching the teeth, andin case of sleep bruxism, an interocclusal appli-ance (Nitzan et al. 1997). While there is no con-sensus regarding the mechanism of action ofinterocclusal appliances, it is widely acknowl-edged that they redirect the force from sleepbruxism.

Adhesions

Adhesions cannot be managed in a conservativeway. If a patient has a limited mouth opening as aresult of adhesions and is otherwise asymptom-atic, and the patient claims the limitation in mouthopening does not result in unacceptable reductionin quality of life, one could opt to observe forclinical progression rather than intervening. Oth-erwise, adhesions are treated with arthroscopiclysis and lavage to break down and remove theadhesions and smoothen the articular surfaces.These procedures result in increased mouth open-ing, improved jaw function, and reduced pain(Zhang et al. 2011a; Leibur et al. 2010). Adhe-sions are more common in joints with moreadvanced stages of internal derangement(Millon-Cruz et al. 2015).


Mechanical hypermobility disorders are first andforemost treated by helping the patient understandthe underlying mechanics so that the patient canlearn to avoid the occurrence of (sub-)luxationsand learn to self-manipulate the jaw throughbimanual intraoral traction should additional sub-luxations occur. The technique can be appliedwith the patient sitting or in supine position.Some authors claim the supine position is betterbecause it allows the clinician a better view of the


dental arches and dynamic occlusion, is faster andless painful (Xu et al. 2016). Initiating a gag reflexas well as yawning have been described as self-reducing techniques as well (Liddell and Perez2015). In patients with a history of habitual TMJluxation, the mandible should be supported duringan extraction or other lengthy oral surgery ordental procedures, and the patient should if possi-ble avoid opening their mouth excessively. In caseof persistent dislocation, the patient may be needto be sedated in order to unlock the jaw, andintermaxillary fixation is often needed to avoidrelapse due to muscle memory. Recurrent luxa-tions have been managed by injecting autologousblood or sclerosing agents in the joint and sur-rounding tissues. The procedures will cause scar-ring, fibrosis, and/or adhesions which will reducemobility. Risks of these procedures include theinability to predict the extent of scarring andfibrosis (Machon et al. 2009). Chewing efficiencyis reported to improve and maximummouth open-ing to decrease with treatment with autologousblood. Success rates range from 64% to 73%after one treatment (Machon et al. 2009; Coseret al. 2015). Treatment with dextrose prolotherapydoes not appear to be more beneficial than placebo(Cömert Kiliç and Güngörmüş 2016). Treatmentprotocols such as number of injection sites andnumber of sessions vary. Surgical methods suchas flattening the eminence, adding a barricade, orlimiting the mobility by means of downfracturingthe eminence or zygomatic arch, placement ofminiplates, or sutures and mini anchors havealso been proposed (Liddell and Perez 2015). Arecent systematic review showed that there is noconsensus with regard to the most effective treat-ment for recurrent joint luxation, but thateminectomy was resorted to whenever other sur-geries failed or a relapse occurred, leading theauthors to believe that eminectomy is still thestandard of care (de Almeida et al. 2016). If thecause of the luxation is due to dystonia, dyskine-sia, or spasm of the inferior lateral pterygoid mus-cle, injection with botulinum toxin may beindicated (Liddell and Perez 2015). This treatmentmay also be indicated to reduce the force of trans-lation of the inferior lateral pterygoid muscle and

is intended to decrease the risk of additional lux-ations (Liddell and Perez 2015). Likewise, weak-ening the elevator muscles may increase the easeand effectiveness of the traction maneuverbecause it reduces the amount of resistance pro-vided by these muscles. The inferior lateral pter-ygoid muscle can be approached through anintraoral as well as extraoral approach. Bothapproaches should be carried out under electro-myographic guidance. Typically, a dose of25–50 units of onabotulinum toxin A is used forthe masticatory muscles. Effects should be notice-able in about a week and usually last between2 and 3 months (Clark 2003). If myospasm ofthe inferior lateral pterygoid is a repeat offendercausing frequent and debilitating luxations, strip-ping of the lateral pterygoid may be indicated(Liddell and Perez 2015).

Fractures

Much debate exists about whether displaced con-dylar fractures should be treated with open orclosed reduction. A recent study with 50 patientsindicated that both methods yielded similar resultswith the exception of deflection on opening,which was present only in the group that receivedclosed reduction of the fracture (Rastogi et al.2015). A meta-analysis comparing surgical tononsurgical treatment methods including 26 stud-ies found that surgical approaches yielded betterresults with regard to malocclusion and deflectionon opening and that nonsurgical approachesyielded better results with regard to infection.Surgical procedures also yielded better resultswith regard to lateral movements and protrusion,but no differences were found with regard to max-imal mouth opening. In addition, no differenceswere found with regard to TMJ pain or noise(Chrcanovic 2015).

Arthralgia and Osteoarthritis

Management of arthralgia and osteoarthritis of theTMJ should aim at decreasing the loading to the


joint as best as possible. This can be accomplishedby controlling contributing and perpetuating fac-tors such as unnecessary loading or relative over-loading of the joint and using supportivenon-pharmacological or pharmacological man-agement. The concepts of self-awareness of jawuse and overuse, and employing therapies such assoft diet and habit reversal techniques should beintroduced to the patient and subsequentlyreinforced. Soft diet suggestions would includeanything the patient can eat within pain free limits,i.e., anything that does not aggravate the pain.Habit reversal techniques include methods toincrease awareness of adverse habits and to trainthe patient to check periodically for such habitsespecially during circumstances and activitieswhich have been identified to likely trigger theadverse habit, and implement relaxation tech-niques aimed at keeping the teeth and lips slightlyapart instead. Supportive pharmacological treat-ment includes the short-term use of nonsteroidalanti-inflammatories or other mild analgesics orin acute and severe cases, a short course ofglucocorticoids. Generally, there is limited sup-port for the use of intraarticular corticosteroidinjections or steroid for treatment of TMJarthralgia (Stoustrup et al. 2013; Gencer et al.2014). Concerns remain with regard to potentialdamage to the articular cartilage and particu-larly in children with regard to interferencewith mandibular growth (Stoustrup et al.2013). Nonpharmacological treatment caninclude application of moist heat and jaw relax-ation exercises. A systematic review examiningthe differences in outcome between lavage andnonsurgical treatment (Vos et al. 2013a) onlyslightly favored lavage for pain intensity butno differences were found between the modali-ties as far as mouth opening was concerned.Another systematic review (Goiato et al. 2016)investigating the efficacy of intraarticular injec-tions of hyaluronic acid, including six studieswith a total of 234 patients with arthritis orarthralgia, found no superiority of this productover injections with corticosteroids in theseconditions.

Crystal Deposit Diseases

Treatment of acute gout and CPPD is aimed atsymptom reduction and includes cold packs, rest,and use of anti-inflammatory medications such asnonsteroidal anti-inflammatory medications orglucocorticoids. For chronic conditions,low-dose nonsteroidal anti-inflammatories withgastroprotection or low-dose colchicine are indi-cated (Zhang et al. 2011b). For gout, diet and uratelowering medications such as allopurinol,febuxostat, or probenecid can be used, althoughevidence suggests that the beneficial effects ofthese medications takes about 1 year (Shekelleet al. 2016).

Hyperplasia

Some cases of TMJ hyperplasia are subtle. If thepatient is not symptomatic and the quality of life isnot affected or the patient is not bothered by facialasymmetry, and if there is no indication of activegrowth, no treatment is required. However, ifactive growth is suspected, further investigationis warranted. Scintigraphic (technetium-99 m)imaging (bone SPECT) can be used to determinewhether the process is still active or not. BoneSPECT detects well focused (99 m) Tc-MDPuptake in the TMJ, and thus allows to achievenoninvasively the final diagnosis of primary con-dylar hyperplasia. The sensitivity of this proce-dure is claimed to be 88%, whereas the specificityis about 70% (Rushinek et al. 2016). Consensuson best timing and therapeutic approaches forcondylar hyperplasia are yet to be reached, but ifactive growth is established, surgical correctionshould be postponed. Otherwise, the treatment offacial asymmetry consists of high condylectomyor orthodontic and orthognathic correction once ithas been established that the growth has ceased(Mouallem et al. 2017).

Hypoplasia

Similar to mandibular or condylar hyperplasia, thecondition can be asymptomatic and facial a


symmetry can be subtle. If both are the case, thepatient may opt not to be treated. Otherwise, man-dibular hypoplasia can be treated with functionalappliances in growing patients. Mandibular dis-traction osteogenesis and surgical reconstructionare other options. In mild cases, genioplasty canbe an alternative option to improve the asymme-try. Most often the patient also requires orthodon-tic treatment in conjunction with orthognathicsurgery (Arun et al. 2002).

Conclusions and Future Directions

Numerous conditions can interfere with thesmooth movement of the TMJ as evidencedabove. The symptoms of some conditions maybe minimal without any impact on the patient’squality of life and may not require treatment whileothers may cause major disturbances for whichpervasive interventions are necessary. Conserva-tive treatment is still the mainstay for the manage-ment of disc derangements, arthralgia,osteoarthritis, and adherences although minimallyinvasive procedures such as lysis and lavage(arthrocentesis) are frequently used early on inthe care of the patient. The TMJ has a remarkablecapacity to adapt to changing functional demands.In most, but not all, cases, internal derangementsdo not warrant treatment. In general, limited datais available for evidence-based effective treat-ments for internal derangements, and moreresearch is needed in several areas using soundmethodology and large populations.

There is a growing interest in markers for car-tilage degradation in synovial joints because oftheir potential diagnostic and prognostic value.Recently, it was found that the concentrations ofcarboxyterminal telopeptide type II (CTX-II)were unexpectedly high in patients with arthritisas compared to healthy controls. This suggeststhat this marker may in the future be useful toquantify cartilage degradation in the TMJ (Voset al. 2013b). Conservative treatment for degen-erative joint disorders is often time-consumingand has unpredictable success rates. Earlier indi-cation of arthrocentesis may cease further degen-eration of the articular tissues. Repeated

intraarticular injections of hyaluronic acid (2–5times) may replenish the cartilage with protectivehyaluronic acid. A review showed a significantreduction in pain in one of the studies at 1 weekand 6 weeks for hyaluronic acid compared tosaline and corticosteroid or tenoxicam injections,while the other included study found no signifi-cant effect of intraarticular injections of eitherhyaluronic acid or tenoxicam up to 3 months(Goiato et al. 2016).

While it should be noted that the position of thedisc or even the presence of a disc does not seemto be a major factor in the prognosis of thepatient’s condition, future directions include tis-sue engineering efforts to create viable biologicalfunctional implants to replace damaged discs(Emans et al. 2005; Shu et al. 2015).

Depending on the severity of the condition andthe impact it has on the patient’s life, condylar andmandibular hyperplasia and hypoplasia are treatedwith a combination of orthodontic therapy andmaxillofacial surgery. New and exciting technol-ogies for these conditions include the integrationof 3-D surgical and orthodontic approaches tocorrect facial asymmetries due to condylar hyper-plasia or hypoplasia (Janakiraman et al. 2015).3-D technologies can also be used in the designof full joint replacements.

Cross-References

▶Arthritic Conditions Affecting the Temporo-mandibular Joint

▶Classification of Orofacial Pain▶Clinical Evaluation of Oral Diseases▶Clinical Evaluation of Orofacial Pain▶Diagnostic Imaging Principles and Applica-tions in Head and Neck Pathology

▶ Sleep Bruxism

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Internal Derangements of the Temporomandibular Joint · Cross-References ..... 32 References ........

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Transcript of Internal Derangements of the Temporomandibular Joint · Cross-References ..... 32 References ........