Internal Derangement of the Temporomandibular Joint · Internal Derangement of the Temporomandibular ... the joint? Is there a systemic disorder that is ... Internal derangement of

Internal Derangement ofthe Temporomandibular
JointNew Perspectives on an Old Problem
Howard A. Israel, DDS*

KEYWORDS

� Temporomandibular joint � Internal derangement � Classification system � Cause � Synovitis� Osteoarthritis � Arthroscopy

KEY POINTS

� Internal derangement of the temporomandibular joint is not a disease, but a nonspecific sign of tis-sue failure leading to biomechanical dysfunction of the joint.

� Establishing the cause of the internal derangement is essential, because successful managementmust be based on the underlying cause of the pathologic process.

� Major categories of disease that cause temporomandibular joint internal derangement include in-flammatory/degenerative arthropathy caused by joint overload, systemic arthropathy making thejoint susceptible to tissue failure, atypical localized arthropathy (disorder localized to 1 temporo-mandibular joint), and false arthropathy (signs and symptoms that simulate internal derangementbut are caused by extra-articular disorders).

� Minimally invasive operative arthroscopy is indicated when signs and symptoms persist, and oftenprovides essential information on the cause of disease.

� Arthroscopic temporomandibular joint surgery permits biopsy of intra-articular disorders and issuccessful in reducing pain, increasing range of motion, and improving mandibular function, partic-ularly in patients with inflammatory/degenerative arthropathies.

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INTRODUCTION

Internal derangement of a synovial joint is not adisease. The biomechanical joint dysfunction thatis associated with internal derangement repre-sents a failure of the intra-articular tissues causedby the loss of the structure and function. Identi-fying the cause of the breakdown of the tis-sues within a synovial joint that leads to internalderangement is an important component of suc-cessful treatment. Clinicians must ask what dis-ease process is causing the tissue breakdown. Is

Disclosure: Dr H.A. Israel is the owner of Therapeutic MobiE-Z Flex II, a passive-motion jaw exerciser.Division of Oral & Maxillofacial Surgery, Weill-Cornell MeF2132, New York, NY 10065, USA* 12 Bond Street, Great Neck, NY 11021.E-mail address: [email protected]

Oral Maxillofacial Surg Clin N Am 28 (2016) 313–333http://dx.doi.org/10.1016/j.coms.2016.03.0091042-3699/16/$ – see front matter � 2016 Elsevier Inc. All

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there a history of acute or chronic trauma tothe joint? Is there a systemic disorder that iscontributing to the breakdown of connective tis-sues? Is there an infection or a tumor presentthat is causing the nonspecific symptoms of inter-nal derangement? A clear understanding of thisconcept by clinicians is essential and has signifi-cant implications on patient management andthe outcome of therapy.

On reviewof the literature on temporomandibularjoint disorders over the past 35 years, the problemof internal derangement of the temporomandibular

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joint is often the central focus of the diagnosis andmanagement of patientswith orofacial pain causedby temporomandibular disorders (TMDs). Clearguidelines for diagnosis and management of inter-nal derangement of the temporomandibular jointare often elusive, although there has been muchexcellent researchon thevalidationof classificationsystems, such as the Research Diagnostic Criteriafor TMDs1 (more recently updated to theDiagnosticCriteria [DC] for TMDs)2,3 and the Wilkes StagingSystem4 for temporomandibular joint disorders.For any given diagnosis, there are multiple man-agement options that have been recommended,including no treatment, nonsurgical therapies,minimally invasive surgical procedures (arthrocent-esis, arthroscopy), arthroplasty (repair of intra-articular tissues), discectomy, and total jointreplacement. The main focus of this article theconcept of internal derangement and temporo-mandibular joint disorders from a new perspective,based on clinical research, basic science researchon synovial joint pathophysiology, and the prin-ciples of diagnosis and management from theperspective of the specialties of rheumatologyand orthopaedics. This information ultimately leadsto new concepts in the classification of internalderangement based on cause and pathophysi-ology, and leads to new perspectives on the man-agement and treatment of internal derangementof the temporomandibular joint.

CURRENT CLASSIFICATION SYSTEMS FORTEMPOROMANDIBULAR JOINT DISORDERS

The Research Diagnostic Criteria (RDC) for TMDs,1

published in 1992, was an excellent first step inhelping to standardize diagnostic categories ofTMDs. The RDC have undergone extensive testingand much research has led toward validating thisclassification system for TMDs to enable clinical

Fig. 1. AAOP taxonomic classification and DC for TMDs.

research investigators to use the same system.This progress has improved the overall ability todevelop further insights into epidemiology, diag-nostic categories, causes, and ultimately treat-ment/management of these disorders. The originalinvestigators recognized that many of these pa-tients had high levels of psychosocial stress alongwith the physical aspects of their disease, and sothis diagnostic system included AXIS I, a classifica-tion systemof the physical categories of TMDs, andAXIS II, a classification system of the psychosocialbehavioral aspects of patients who develop thesedisorders. Following years of research involving val-idity testing of the RDC, more recently it becameapparent that updates were necessary in this sys-tem to include a larger variety of disorders of thetemporomandibular joint and surrounding struc-tures. Thus recent changes in this classification sys-temhavebeenmade,ultimately combining theRDC(recently changed toDC for TMD)with theAmericanAssociation of Orofacial Pain (AAOP) TaxonomicClassification, which encompasses a larger andmore accurate description of the variety of diseasesaffecting the temporomandibular joint and sur-rounding structures.3 Although it is beyond thescope of this article to review the details of themost current DC/TMDandAAOP taxonomic classi-fication systems (Fig. 1), many of the classificationcategories describe nonspecific signs and symp-toms, and not a disease process.TheWilkes Staging System4 for internal derange-

ment is frequently used by oral and maxillofacialsurgeons andhelps to provide a guide for treatmentbasedon theseverityof thedamage to the joint. Thissystem includes 5 stages with stage I being apainless disc displacement with reduction andstage V being an advanced disc displacementwith severe degenerative changes, adhesions, sub-chondral bone changes, and disc perforation(Box 1). Because the main focus of the Wilkes

Box 1Wilkes staging of internal derangements

Stage I: early

Painless clicking, anterior disc displacement with reduction

Stage II: early/intermediate

Clicking with intermittent pain and locking, anterior disc displacement with reduction

Stage III: intermediate

Pain, joint tenderness, frequent andprolonged locking, restrictedmotion, anterior disc displacementwithor without reduction, no degenerative changes

Stage IV: intermediate/late

Chronic pain, restricted motion, no clicking, anterior disc displacement without reduction, degenerativebony changes, adhesions

Stage V: late

Variable pain, painful/reduced function, crepitus, anterior disc displacementwithout reduction, advanceddegenerative bony changes, gross disc deformity and/or perforation, advanced adhesions

Adapted from American Society of Temporomandibular Joint Surgeons. Guidelines for diagnosis and management ofdisorders involving the temporomandibular joint and related musculoskeletal structures. 2001.

Internal Derangement of the Temporomandibular Joint 315

system involves categorizing the extent of damagethere is to joint tissues, it is useful to oral andmaxil-lofacial surgeons in planning the operative proce-dure that they perceive will best treat the patient.However, in spite of the precise description of thevarious stages described for internal derangement,there is no corresponding information on the causaldiagnosis associated with these stages.

From the standpoint of treating clinicians, thereare flaws in these current classification systemsthat may further confuse diagnosis, cause, andultimately treatment and management of thesepatients. For the most part, both of these systemsare descriptive of a compilation of signs and symp-toms and there is no useful categorization of causeand pathogenesis. For example, merely categoriz-ing a patient with a disc displacement with orwithout reductiondescribes a signof a diseasepro-cess without any information as to the cause of thecondition. The importance of this cannot be over-stated, because many treatments over the past35 years have focused on trying to recapture thedisc. Oral repositioning appliances, mandibularmanipulation, disc repositioning surgery, and discreplacement surgery have been the focus ofmost treatments for internal derangement. Withoutknowledge of the underlying cause, these treat-ments often fail, because causative factors persist.For example, if a patient has internal derangementassociated with a systemic arthropathy, failureto treat and manage the systemic disorder is likelyto result in persistent symptoms and treatmentfailure. Patients with excessive joint overload from

mandibular parafunction ultimately fail disc repo-sitioning treatment because of the physiologiceffects of joint overload on the intra-articulartissues. Further detailed discussion on the impor-tance of identification and categorization of causalfactors is provided later in this article.

Another intriguing factor in the development ofthe RDC for TMD is AXIS II, which is an essentialcomponent of the diagnosis. Clinicians must askwhether there is something unique about thetemporomandibular joint that makes a psychoso-cial categorization model a component of thediagnosis. Do diagnostic classification systemsfor other synovial joints and musculoskeletal con-ditions include a psychosocial component as anintegral part of the diagnosis?

A literature search of the orthopaedic and rheu-matologic literature on diagnostic systems failedto find that AXIS II psychosocial classification isan integral part of disorders of the knee, hip, shoul-der, patella-femoral pain and dysfunction, cervicalspine, and lower back. The American College ofRheumatology has classification systems for oste-oarthritis, systemic sclerosis, and other rheumato-logic diseases5,6 and a psychosocial component isnot part of the diagnostic categorization of theseconditions.

This is not to suggest that the psychosocialaspects of these diseases are not important.All chronic pain conditions have accompanyingAXIS II diagnoses because chronic pain and lossof function affect quality of life. The impact of thedisease and associated pain with loss of normal

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function must be an essential factor for cliniciansto consider in the overall management of the pa-tient. Perhaps the failures in appropriately andsuccessfully treating many TMDs has led to pa-tients with chronic pain, loss of function, and frus-tration because failed treatments have a profoundeffect on quality of life and result in psychologicalconditions such as depression and anxiety, whichare common in those patients who seek treatmentof TMDs. Regardless of whether preexisting psy-chosocial factors play an important role in causingthe symptoms associated with TMDs or whetherthey are the result of the disease process itself,psychosocial factors must be addressed whenconsidering the overall management of the patient.However, because psychosocial issues play animportant role in most chronic disease entities,there is the need for primary treating clinicians toassess whether appropriate referral to specialistsin psychology, psychiatry, and stress manage-ment is indicated.

INTERNAL DERANGEMENT OF THETEMPOROMANDIBULAR JOINT: DEFINITIONFROM AN ORTHOPAEDIC PERSPECTIVE

The most popular definition of internal derange-ment of the temporomandibular joint has generallyalluded to joint dysfunction associated with anabnormal disc position. The Merck Manual7 de-scribes internal derangement of the temporoman-dibular joint as a condition with damage to theinternal structures of the joint and “the mostcommon form of internal temporomandibular jointderangement is anterior misalignment or displace-ment of the articular disc above the condyle.” Moli-nari and colleagues8 defined internal derangementas follows: “the term derangement refers to analteration in the normal pathways of motion of theTMJ [temporomandibular joint] that largely involvesthe function of the articular disc.” A definition of in-ternal derangement of the temporomandibular jointthat has been widely used by the dental professionfor the past 4 decades describes a disruption of theinternal aspects of the joint involving displacementof the disc froma normal functional relationship be-tween the condyle of themandible and the articulareminence of the temporal bone.9 This definition hasbeen widely accepted in the dental profession, butperhapswould not be accepted if temporomandib-ular joint disorders were treated by specialists inorthopaedics or rheumatology.The specialties of orthopaedics and rheuma-

tology have a much broader definition for internalderangement of a synovial joint. For example, thesespecialties describe knee internal derangement asan intra-articular disorder caused by damage to

internal structures within the joint. These conditionsare usually caused by trauma and result in ongoingsignsandsymptomsof pain, instability, or abnormalmobility. Internal derangement is an old term thatis nonspecific and requires a detailed history, phys-ical examination, and diagnostic images to moreclearlydiagnose thecondition. Theclassic textbookCampbell’sOperativeOrthopaedics, 12thEdition,10

defines internal derangement of thekneeas follows:

The term internal derangement.looselyapplied to a variety of intra-articular andextra-articular disturbances, usually of trau-matic origin, that interfere with the functionof the joint.

I choose to use a more orthopaedic andrheumatologic approach to the term, and thus allreferences to internal derangement of the tempo-romandibular joint in this article use the followingdefinition.A condition in which there are damaged intra-

articular tissues leading to disturbances in thebiomechanical functioning of the temporomandib-ular joint.Based on this broader definition, anterior disc

displacement is considered one type of internalderangement without exclusivity. Thus, a patientwho has severely limited opening with decreasedtranslation of the temporomandibular joint causedby adhesions, osteoarthritis, synovial inflamma-tion, disc displacement, or other intra-articular dis-order is also considered to have the clinical signsand symptoms of internal derangement.

IS INTERNAL DERANGEMENT A DISEASE?

Mosby’s Dictionary of Medicine, Nursing & HealthProfessions, Ninth Edition, defines the term dis-ease as follows: “a specific illness or disordercharacterized by a recognizable set of signs andsymptoms attributable to heredity, infection, dietor environment.” A key aspect of this definition ofdisease is that there is an abnormal function orprocess involving an organ and/or system withcharacteristic symptoms that have a specificcause. Internal derangement of the temporoman-dibular joint represents signs and symptoms ofaltered biomechanical function (failure of transla-tion, locking, intermittent locking, clicking) withdamaged intra-articular tissues without alludingto a specific cause. The signs and symptomsassociated with internal derangement are nonspe-cific and can be caused by a multitude of dis-ease conditions. Therefore, internal derangementshould not, by itself, be considered a disease,but should be considered a manifestation of a pro-cess in which there is damage to intra-articular


tissues from a specific cause that must be identi-fied by the clinician. The variety of disease cate-gories that commonly cause internalderangement is further described later in thisarticle.

Further complicating the understanding of inter-nal derangement are the current diagnostic classi-fication systems that are used in the staging oftemporomandibular joint disorders. The DC/TMDclassification system2,3 uses physical diagnosisto further subclassify temporomandibular diseaseinto muscle disorders, disc disorders, arthritic dis-orders, hypermobility disorders, and tension head-aches. However, these disorders mostly representsigns and symptoms that are nonspecific and arenot mutually exclusive.

The Wilkes classification system4 also focuseson the progressive stages of internal derange-ment, ultimately leading to failure of normal jointfunction. These progressive changes leading toloss of the structure and function of the cartilage,synovium, and subchondral bone represent theend result of a disease process. Both of theseclassification systems are not based on the causalconditions that lead to failure of the joint tissuesand loss of normal joint function.

Understanding the true cause of failure of thejoint tissues is essential for proper treatment,prevention, and/or delay in the progression ofjoint disease. Stegenga11 recognized this defi-ciency in the current classification of temporo-mandibular joint disorders and proposed asystem based on the pathologic process thatis causing the structural failure of the joint tis-sues. This proposed change in nomenclatureemphasizes the importance of the diagnosis inproviding the basis for treatment. Therefore, theauthor proposes control of risk factors that leadto pathologic intra-articular structural changes,reducing pain and improving function ratherthan attempting to control the position of thedisc, as essential components of patient man-agement. For clinicians to truly understand andmanage the variety of disease conditions thataffect the temporomandibular joint, it is impor-tant to understand that our current classificationsystems describe nonspecific stages of a dis-ease process, without being specific for thetrue diagnosis that is responsible for the failureof the joint tissues.

The detailed review of the problem of internalderangement of the temporomandibular joint laterin this article clearly shows that internal derange-ment is not a disease, but represents a variety ofstages of biomechanical failure of the joint tissues,which can be caused by several specific diseaseentities.

DOES INTERNAL DERANGEMENT REQUIRETREATMENT?Historical Perspectives

A review of the history of treatment of internalderangement of the temporomandibular joint re-veals changing perspectives on management. Inthe 1970s and 1980s, internal derangementwas viewed as a mechanical problem, resultingin mechanical attempts at repositioning orreplacing the disc. In 1979, McCarty and Farrar9

published an article in the Journal of Prostho-dontics that emphasized the importance of discdisplacement as a major disorder of the tempo-romandibular joint. It was thought that the failureto have the disc in the proper position betweenthe condyle and the articular eminence inevitablyleads to severe degenerative joint disease. Thus,repositioning the disc became a central focus formany clinicians in the dental profession.Oral appliances designed to reposition the disc,as well as mandibular manipulations, wereconsidered mainstays of conservative therapy.Patients who had persistent symptoms andinternal derangement were often referred tooral and maxillofacial surgeons and there werea variety of surgeries designed to solve theproblem of internal derangement of the temporo-mandibular joint. Discoplasty, involving discrepositioning surgery, was a common surgicalprocedure. Discectomy was often performedif there was a perforation in the disc. A varietyof tissues were used for disc replacement,including ear cartilage, temporalis muscle,temporalis fascia, Silastic, and Proplast-Teflon.However, the use of Proplast-Teflon led toforeign body reaction and destruction of articulartissues.12–14

In the 1990s, the realization that arthroplastywith disc repositioning or disc replacement oftenresulted in degenerative changes and fibrosisand did not reliably maintain a repositioneddisc15 resulted in a significant change in the sur-gical management of patients with severe symp-toms and internal derangement. Arthroscopictemporomandibular joint surgery was shown tobe a safe and effective alternative to arthro-plasty, which reliably reduced pain and improvedmaximum interincisal opening distance.16–27

Excellent results were achieved with arthro-scopic surgery without changing disc position.MRI studies28–31 have shown a high percentageof disc displacement in asymptomatic patients(32%–38%) and this has raised further questionsabout the importance of internal derangement inpatients with symptomatic temporomandibularjoint disease.

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Arthrocentesis32–35 was introduced as anotherminimally invasive treatment of internal derange-ment and has been shown to be safe and effective.A major advance in the understanding of thepathogenesis of temporomandibular joint diseaseoccurred as a result of arthroscopy and arthro-centesis and resulted in research on biochemicalmediators in the synovial fluid. Mediators of inflam-mation, cartilage degradation, and adhesion for-mation have been identified, which represent thebiochemical basis for destruction of joint tissuesleading to internal derangement.36–49 Synovialfluid research has continued since the 1990s andhas offered promising strategies for the identifica-tion of biochemical markers of disease and the po-tential for new therapies designed to alter or blockpathogenic mechanisms.

Internal Derangement Treatment: ClinicalResearch Results

Clinical research on the natural course of internalderangement without treatment50–52 has shownthe following:

� Most patients improve without any treatment� The length of time for symptoms to resolve isvariable, but generally a minimum of 1 year

� A percentage (25%–33%) of patients do notimprove

� Older patients and those with MRI evidence ofmore advanced disease (osteoarthritis andadvanced internal derangement) are at higherrisk for not improving spontaneously

There have been a variety of good evidence-based literature reviews and studies53–58 thatcompared the results of nonsurgical treatmentsof internal derangement. Nonsurgical therapiesthat have been studied include patient education,nonsteroidal antiinflammatory drugs (NSAIDs),muscle relaxants, hot/cold packs, mouth openingexercises, softer diet, and occlusal appliances.Because appliance therapy is often the initial

treatment intervention for patients who developtemporomandibular joint symptoms, knowledgeof the evidence-based literature on occlusal ap-pliances is necessary for clinicians. Lundh andcolleagues55 compared treatment outcomes onpatients with anterior disc displacement withoutreduction who were placed into one of 2 groups.The first group was treated with an occlusalsplint and the second group had no treatment.The results of treatment after 12 months were asfollows:

� Pain disappeared in approximately 33% ofpatients in both groups

� Increased joint pain was experienced by 40%of the occlusal splint group, and16% of theno-treatment group after 12 months

The investigators concluded that there wasno significant benefit in occlusal splint therapycompared with no treatment.Truelove and colleagues56 evaluated treatment

outcomes in 200 patients with anterior discdisplacement with reduction, arthralgia, andmyalgia. The patients were randomly assigned toone of 3 treatment groups:

� Usual treatment, which included self-care, ed-ucation, NSAIDs, hot/cold packs, and passivestretching

� Hard flat plane splint and usual treatment (asdescribed earlier)

� Soft splint and usual treatment

Treatment outcomeswere evaluated at 3monthsand12months,which revealednosignificant differ-ence in all 3 groups. The investigators concludedthat self-care, low-cost therapy is as effective asocclusal splint therapy.Clark and Minakuchi57 provided an excellent re-

view of the evidence-based literature on appliancetherapy and their conclusions on occlusal stabili-zation appliances were:

� Occlusal stabilization appliances decreasesymptoms of myalgia and arthralgia

� They protect the dentition from wear causedby parafunctional habits

� They are low risk as long as they are not worn24 hours a day

� They do not change disc position

Clark and Minakuchi57 also concluded thatappliances that are designed to reposition themandible do not change disc position.Based on current research, clinicians should

follow a common-sense approach concerningappliance therapy. Appliances should be designedto provide a buffer between the maxilla and themandible, in theory to offset the forces of mandib-ular parafunction and to reduce the load onthe temporomandibular joints. Therefore, occlusalstabilization appliances that equally distributethese forces throughout the arch should beconsidered as an appropriate initial treatment ofmyalgia and arthralgia. However, clinicians mustcontinuously evaluate the patient’s response totreatment. Some patients with a significant paraf-unctional habit develop increased parafunctionwith an appliance. Patients often tell cliniciansthat they find themselves clenching on the appli-ance and that their jaw muscles are more sore in


the morning, following the nighttime use of anocclusal stabilization appliance. For patients withdaytime clenching, an appliance can be used for1 minute, to assist in self-awareness with thegoal of breaking the habit. Continuous and/orexcessive use of an appliance can contribute tothe development of a malocclusion and must beavoided, particularly for appliances that providepartial coverage of the dentition, and thus theseappliances are to be avoided. In addition, appli-ances that reposition the mandible in an attemptto recapture the disc in patients with arthralgiaand/or internal derangement should be avoided,because the scientific literature does not supportthis. Most importantly, patients treated with appli-ance therapy must continuously be evaluated todetermine whether the appliance is effective inreducing myalgia and arthralgia. If appliance ther-apy is not effective in reducing symptoms, theclinician must reevaluate the diagnosis and alterthe therapeutic regimen.

Further complicating the understanding ofresponse to treatment is the placebo effect ofall therapeutic interventions. Greene and col-leagues59 studied placebo responses to orofacialpain and reported that “present knowledge sug-gests that every treatment for pain contains a pla-cebo component, which sometimes is as powerfulas the so-called active counterpart.” A summaryof the results of evidence-based studies onnonsurgical therapy for internal derangement islisted here53–59:

� Most patients have improvement in signs andsymptoms with time

� No significant differences between treatmentand nontreatment groups

� Palliative care (NSAIDs, education, diet modi-fication, exercises) seem to be as effective asmore costly appliance therapy

� Occlusal appliances do not change discposition

� Occlusal stabilization appliances may reducemyalgia and arthralgia

� Although patients with internal derangementimprove with time, the length of time for symp-toms to improve is not clearly identified

� All treatments have a powerful placebo effect

Patients with internal derangement with severesymptoms of pain and dysfunction who have failednonsurgical therapy are often candidates for surgi-cal treatment. Laskin60 provided an excellentreview of evidence-based research on the surgicalmanagement of internal derangement. Clinicalresearch on the results of surgical treatment ofinternal derangement is summarized here:

� There are no prospective, randomizedcontrolled, double-blinded trials; only caseseries, and comparison of preoperative andpostoperative signs and symptoms

� Arthroscopy, arthrocentesis, discoplasty, anddiscectomy have all been reported to havereasonably good success with reduction insigns and symptoms in the range of 80% to90%

� Surgical success is highest with the first sur-gery, and each surgical procedure reducesthe success rate

� Surgical failure is often caused by lack of con-trol of causal factors such as joint overload

� When surgery is indicated, the least invasiveapproach is recommended

Because of the lack of randomized controlledstudies on surgical management of internalderangement, Reston and Turkelson25 performeda meta-analysis of the results of surgical treat-ment of disc displacement without reduction. Thisbiostatistical approach studied many reportedsurgical trials to help compensate for the lackof parallel control groups. The investigatorsconcluded that only arthroscopic surgery andarthrocentesis showed effectiveness significantlygreater than all assumed control group improve-ment rates. Al-Moraissi27 performed a systematicreview and meta-analysis comparing arthros-copy and arthrocentesis for management of inter-nal derangement. The results suggested thatarthroscopy yielded superior efficacy to arthro-centesis in increasing joint movement anddecreasing pain.

Does Any Surgical Procedure Reposition andMaintain a Normal Disc Position?

The literature on surgical outcomes assess pain re-lief, improved function, and increased interincisalopening distance, but do not show the mainte-nance of normal disc position.60–64 Zhang and col-leagues65 assessed thepostoperativediscpositionfollowing discoplasty and disc stabilization withbone anchors. The investigators reported 96%successful disc repositioning based on MRI scanstaken 7 days postoperatively. However, conclu-sions based on a early postoperative MRI do notprovide information about patients who functionand load their temporomandibular joints. There-fore, based on a review of the literature, theredoes not seem to be any evidence that surgicallyrepositioning a disc maintains the disc in a normalposition; there does not seem to be any evidencethat any procedure, treatment, or appliance reposi-tions and maintains the disc in a normal position.

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Thus the major goals of treatment of internalderangement should not be to reposition the disc,but should be to:

� Establish the diagnosis and the cause of theinternal derangement

� Reduce inflammation� Reduce pain� Reduce joint overload� Improve range of motion� Restore mandibular function� Identify and control causal factors

MANAGEMENT OF TEMPOROMANDIBULARJOINT DISORDER BASED ON DISEASE CAUSE:NEW PERSPECTIVES ON INTERNALDERANGEMENT AS A SIGN OF DISORDER

The DC for TMDs and theWilkes staging of internalderangement are helpful for clinicians in assessingthe extent to which a pathologic process hascaused damage to the intra-articular tissues,resulting in biomechanical failure and/or compro-mise in joint function. However, these classifi-cation systems do not provide information onfactors that cause damage and dysfunction of jointtissues leading to internal derangement. Thus,merely repositioning a disc ultimately leads to jointfailure if the causal factors are not recognizedand managed. The classification of intra-articulartemporomandibular joint disease based on causalfactors is discussed here, and is intended to pro-vide clinicians with a different perspective in themanagement of temporomandibular joint internalderangements. Internal derangement should beviewed by clinicians as a sign of a disease processleading to biomechanical compromise or failureof the temporomandibular joint. The challenge forclinicians is to diagnose the condition that is

Fig. 2. Major categories of temporomandibular joint (TM

causing the internal derangement. Once identified,the basis for treatment is to reduce the patient’ssymptoms while simultaneously identifying andmanaging the disease process. The followingmajor categories of disease can cause internalderangement of the temporomandibular joint(Fig. 2):

1. Inflammatory/degenerative arthropathy: jointoverload (acute and/or chronic) leading toinflammation and degeneration of intra-articulartissues

2. Systemicarthropathy: systemicdisordercausingtemporomandibular joint disease

3. Localized atypical arthropathy: intra-articulartemporomandibular joint disorder that is atyp-ical and not caused by joint overload

4. False arthropathy: extra-articular disorder simu-lating and/or causing temporomandibular jointsymptoms

Inflammatory/Degenerative Arthropathy:Pathogenesis

Chronic joint overload is the most common causeof internal derangement of the temporomandib-ular joint. There is a significant body of researchon temporomandibular joint synovial fluids andarthroscopic tissue morphology, which has shownthat synovitis, osteoarthritis, and adhesions arethe major tissue changes that occur in symptom-atic patients requiring arthroscopic surgery.36–49

Chronic joint overload, often caused by mandib-ular parafunction, results in a change in articularcartilage metabolism, with degradation of thecartilaginous matrix exceeding production. Thisoverload of the cartilage upsets the balance be-tween the buildup and degradation of the cartilagematrix, ultimately resulting in a breakdown of

J) disease based on cause.


the cartilaginous surfaces. In the earliest stages ofthis pathologic process, fibrillation of articularcartilage is seen arthroscopically (Fig. 3). Thisfibrillation ultimately results in biomechanical fail-ure impairing the sliding of articular surfaces. Theclinical correlation with this early failure of articularcartilage is joint noise (clicking and/or crepitus).Tissue changes that occur in the cartilage impairthe sliding ability of the joint, often resulting in achange in disc position (see Fig. 3). These earlydegenerative changes do not necessarily causepain. If there is no associated inflammation, thepatient may function with a clicking joint and nomajor functional disability. This possibility mayexplain why a significant percentage of the popu-lation (32%–38%) who are without complaintsand totally functional have disc displacement,which can be seen on MRI.28–31

Individuals who have severe and persistentmandibular parafunction continue to load theintra-articular tissues beyond their adaptive capac-ity, leading to further changes in the structure andfunction of these tissues. Continued cartilagedegradation results in significant osteoarthritis andcan ultimately lead to a disc perforation (Fig. 4).The alteration in joint biomechanics often leads toloading of the synovial tissues, which is not whatthe synovium normally experiences. The synoviumis a connective tissue that is very vascular and iswell innervated, unlike articular cartilage. The majorfunction of synovium is the production of synovialfluid, which is necessary for joint lubrication andalso for nutrition of chondrocytes in the articularcartilage, which does not have a blood supply.Thus, loading of the synovial tissues results in asignificant escalation in symptoms because:

1. The synovial membrane becomes inflamed,erythematous, and edematous, which resultsin the clinical appearance of synovitis (Fig. 5)

Fig. 3. Chronic joint overload: degradation exceeds repair

2. The abnormal loading of the synovial tissuescauses pain, because this tissue has a nervesupply and does not normally undergo loading

3. Inflamed synovium impairs production of syno-vial fluid, impairing lubrication of the joint, furtheraltering the biomechanics of the joint andreducing the ability of the temporomandibularjoint to slide

4. Once synovitis develops in the temporomandib-ular joint, it is difficult to resolve, because thisjoint is constantly being used, resulting in furtherloading and further synovial inflammation

With the onset of an acute synovitis, patientshave a noticeable increase in temporomandibularjoint symptoms:

1. Acute pain localized to the temporomandibularjoint

2. Reduced translation of the affected joint withlimited maximum interincisal opening distance,deviation of the mandible to the affected sidewith opening, and reduced lateral excursion tothe contralateral side

3. If there is significant intra-articular swellingassociated with the synovitis, there may be analteration in theocclusionwithan ipsilateral pos-terior open bite and deviation of the mandibularmidline to the contralateral side at rest

4. Myospasmof the surroundingmusclesofmasti-cation (masseter and temporalis become signif-icantly tender to palpation) as thebody attemptsto splint the injured joint

5. MRI shows a synovial effusion best seen on theT2 images and anterior disc position (Fig. 6)

Patients who develop acute synovitis ofthe temporomandibular joint that does notresolve with nonsurgical therapies such as jointunloading (oral appliances, diet modification),anti-inflammatory medications, and muscle

.

Fig. 4. Arthroscopic view of leftTMJ in patient with severe masti-catory parafunction. Osteoarthritiswith disc perforation and exposedcondyle. Black arrow indicates discperforation.

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relaxant medications often transition to a chronicsynovitis of the temporomandibular joint. Thecontinued loading of inflamed synovial tissuescombined with reduced mobilization often resultsin adhesions, which also affects the ability of themandible to translate. Patients with chronic syno-vitis of the temporomandibular joint often presentwith a history of acute locking and pain, followedby a period of gradual reduction in pain and a slightincrease in the maximum interincisal opening dis-tance over several months. However, thesechronic changes occur at the expense of greatlyreduced masticatory function. Patients complainthat they cannot open their mouths widely andthey can only eat soft foods. If these patientsdo not pursue surgical treatment designed toreduce inflammation, remove adhesions, and in-crease mandibular mobility, they may eventuallydevelop less pain, with reduced synovial inflam-mation, with persistent reduction in mandibularrange of motion because of adhesions (Fig. 7).

Fig. 5. The synovial membrane becomes inflamed, erytheappearance of synovitis.

The simultaneous occurrence of synovitis andreduced mobility leads to the development of ad-hesions in the synovial joint.66 If the pathologicprocess continues with persistence of synovitis,cartilage degradation, reduced mobility, andadhesion formation, ultimately this may lead to afibrous and/or bony ankylosis.There are some patients with synovitis and inter-

nal derangement of the temporomandibular jointwho do not progress to further joint disease andeventually return to normal masticatory function.However, clinicians do not have the capacity topredict which patients are likely to have a returnto asymptomatic function and it is not clear whysome patients have this healing capacity. Clini-cians can speculate on those factors that maylead to a resolution of symptoms. Theoretically, ifthe clinician is successful in reducing joint over-load, maximizing joint mobility, and reducinginflammation, this may create an intra-articularenvironment that is more likely to heal, given

matous, and edematous, which results in the clinical

Fig. 6. MRI T2 images showing anterior disc positionand a synovial effusion of the superior joint space.This important finding is consistent with synovitis.


enough time. Clinical arthroscopic observationshave shown that some joints with anterior discdisplacement have remodeled retrodiscal tissuethat has the white appearance of cartilage butclearly is not disc, because of the presence ofblood vessels that can be seen in the tissue(Fig. 8). Recent research showed that increasedmechanical loading on the disc increased proteinlevels and proteoglycan messenger RNA expres-sion in temporomandibular joint discs in a ratmodel.67 It is likely that functional loading of theretrodiscal synovial tissues has the capacity toresult in stimulation of the production of proteogly-cans, leading to the formation of tissue that has theappearance and function of cartilage.

In patients with internal derangement caused byoverload associated with a chronic inflammatory/degenerative arthropathy, it is also important torealize that the maintenance of the structure andfunction of synovial and cartilaginous tissues is

Fig. 7. Synovitis and adhesions in the posterior recess of tjoint.

interdependent. Inflamed synovial tissues and ad-hesions lead to reduced joint motion, decreasedpumping action of the synovial fluid, and adecrease in the nutrition of chondrocytes. Failureto maintain the viability and function of chondro-cytes results in the loss of the matrix of the carti-lage (collagen and proteoglycans), resulting infurther cartilage degradation. This degradationleads to further progression of degenerative jointdisease (osteoarthritis) within the joint. Jointswith persistent degradation of articular cartilagehave increased levels of degradation products(glycosaminoglycans) in the synovial fluid,39,40,46

which can overwhelm the phagocytic function ofthe synovial membrane and lead to further synovialdysfunction and synovitis. It has been shown thatosteoarthritis and synovitis occur simultaneouslyin symptomatic temporomandibular joints thathave undergone arthroscopic surgery.43 Thus theinflammatory and degenerative processes thatoccur in temporomandibular joints that are chron-ically overloaded occur simultaneously, resultingin the alteration of the intra-articular tissues, lead-ing to biomechanical failure and internal derange-ment (Fig. 9).

Treatment of Inflammatory/DegenerativeArthropathy

A key principle in the management of internalderangement caused by an inflammatory/degen-erative arthropathy is for clinicians to realize thatthe internal derangement is the end result ofdamaged intra-articular tissues usually causedby chronic overload. Therefore, identification andmanagement of factors that contribute to the fail-ure of the synovium and articular cartilage areessential for a favorable outcome. Once the diag-nosis of inflammatory/degenerative arthropathy

he superior joint space in a right temporomandibular

Fig. 8. Retrodiscal and other joint tissues have the capacity to adapt to functional loads.

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with concurrent joint overload is established,essential principles of management include:

1. Reduction of joint loading2. Maximizing joint mobility3. Reduction of inflammation4. Control of pain

Clinicians who treat these patients are wellversed in nonsurgical therapies to accomplishthese goals, including:

1. Diet modification2. Awareness and control of mandibular

parafunction3. Passive-motion exercises4. Physical therapy5. Masticatory muscle massage and heat6. Occlusal stabilization oral appliances (appli-

ances that provide equal distribution of forces

RESOLUTION/REDUCTION IN SYMPTOMS

CHRONIC JOINTNO

l

PERSISTENT INFLAMM• CHRONIC PAIN• LIMITATION OF FUNCT• ALTERED JOINT BIOME

LOAD NOT EXCEEDING ADAPTIVE CAPACITY OF TISSUES LO

Fig. 9. The response (or lack thereof) to nonsurgical mancapacity and dictates future treatment.

throughout the arch and do not attempt toreposition the mandible)

7. Antiinflammatory medications8. Muscle relaxant medications9. Pain management modalities

10. Improving sleep

Patient education is an essential part of man-agement and it is important that these patientsbecome partners in their care, focused on controlof causal factors that are contributing to the dis-ease process.Patients often present to the oral and maxillofa-

cial surgeon with symptoms associated with inter-nal derangement. Clinicians must first approachthese patients with an open mind with the realiza-tion that internal derangement is a nonspecificsign of intra-articular disorder that can have avariety of diagnoses. Thus, establishment of thediagnosis and the cause of the joint disorder is

OVERLOADNSURGICAL MANAGEMENT oad inflamma on mobility

ATION/DEGENERATION & SYMPTOMS:

ION CHANICS

AD EXCEEDING ADAPTIVE CAPACITY OF TISSUES

MALADAPTIVE TISSUE RESPONSES

agement determines whether the joint has adaptive


essential. If the patient has signs and symptomscaused by joint overload (chronic or acute) andif all other causal diagnoses are ruled out, aninflammatory/degenerative arthropathy is likely.These patients are placed on an intense 2-weekto 3-week regimen of nonsurgical therapy asdescribed earlier. If the symptomsbegin to resolve,then nonsurgical management is continued (seeFig. 9). However, if the symptomspersist,minimallyinvasive surgical intervention is often required.

The least invasive procedure that will resolvethe symptoms is the treatment of choice; there-fore, arthroscopic surgery (or arthrocentesis) isperformed.25,27 A major advantage of arthro-scopic surgery compared with arthrocentesis isthe ability to directly see the disorder and toobtain specimens for histopathologic examinationto further confirm the diagnosis. Furthermore,arthroscopic surgery involves the removal ofpathologic tissue, lysis of adhesions, direct injec-tion of medications into the synovium, anddebridement of degenerative articular cartilage.Arthrocentesis requires less surgical skill and isperformed at a lower cost but does not permitdirect visualization and removal of pathologic tis-sue. Patients with symptoms of limited openingfor greater than 3 months often have intra-articular adhesions, and arthrocentesis is not aseffective as arthroscopy, which permits removalof these adhesions.

A major challenge to the specialty of oral andmaxillofacial surgery is to properly train interestedclinicians in the required skills necessary toperform arthroscopic surgery. Failure to train thisspecialty will ultimately prevent these patientsfrom having access to minimally invasive temporo-mandibular joint surgery. Furthermore, clinicians inother fields, without advanced training in oral andmaxillofacial surgery, will attempt to develop theskills for arthroscopic surgery, to the detriment oforal and maxillofacial surgery and of patients.The skills required for arthroscopic surgery areunique and thus it is necessary for experiencedsurgeons to train the next generation of oral andmaxillofacial surgeons. Although many advancededucation programs in oral and maxillofacial sur-gery do not provide training in arthroscopy, thisshould not be a justification for performing moreinvasive surgery when arthroscopy is indicated.Excellent hands-on training courses do exist forthose oral and maxillofacial surgeons who wantto provide arthroscopic temporomandibular jointsurgery as an effective minimally invasive optionfor their patients.68–70

Regardless of which minimally invasive modalityis performed, a postoperative rehabilitationregimen with control of causal factors is essential.

This regimen is the same as the nonsurgicalregimen that was prescribed before the decisionto perform minimally invasive surgery. Aside fromthe reduction of joint loading, it is essential for pa-tients to perform passive-motion exercises severaltimes daily for a minimum of 2 months postopera-tively. Mobilization of the mandible with gentlestretching prevents the formation of adhesions,which are removed during arthroscopic surgery,and helps to stimulate the synovial fluid to providenutrition to articular cartilage chondrocytes. Pas-sive mobilization exercises should be startedwithin 24 hours of surgery and are repeated 3 to4 times daily, with each session lasting 15minutes.Physical therapy can be added to the postopera-tive regimen, but this must not be a replacementfor the daily passive-motion exercises that the pa-tient performs at home.

The treatment of an inflammatory/degenerativetemporomandibular joint arthropathy varies basedon the stage of the internal derangement andthe disease process. The early stages of internalderangement (Wilkes I and II) canoftenbemanagedwith nonsurgical therapy.More advanced stages ofinternal derangementwith persistenceof significantsymptoms, in spite of appropriate nonsurgicaltherapy, are treated with minimally invasive surgery(arthroscopy or arthrocentesis) if diagnostic im-aging confirms the presence of a joint space.Advanced stages of internal derangement leadingto fibrosis and/or ankylosis with loss of joint spacerequire arthrotomy. Fig. 10 shows the treatmentalgorithm used for the various stages of internalderangement caused by inflammatory/degenera-tive arthropathies.

Systemic Arthropathy: Systemic DisordersCausing Temporomandibular Joint Disease

Systemic diseases can often contribute to temporo-mandibular joint disorders. In the case of an in-flammatory/degenerative temporomandibular jointarthropathy, excessive joint loads exceed the adap-tivecapacityof the intra-articular tissues, resulting incartilage degradation and synovial inflammation,which then cause internal derangement. Patientswith a systemic arthropathy are those with jointtissues that will fail with normal joint loads, becausethe systemic disorder affects the structure andfunction of the intra-articular connective tissues.Therefore, internal derangement of the temporo-mandibular joint can be causedby a systemic disor-der and it is essential for oral and maxillofacialsurgeons to be aware of this when considering pa-tient management. Examples of systemic disordersthat can cause internal derangement include rheu-matoid arthritis, psoriatic arthritis, juvenile idiopathic

ADD w REDUCTION CLICKING NO PAIN

ADD w REDUCTION CLICKING, PAIN, OPENING NOT LIMITED

ADD without REDUCTION, PAIN, NO CLICKING, LIMITED OPENING

ADD without REDUCTION, PAIN, CREPITUS, MRI DEGENERATIVE

CHANGES

RULE OUT SYSTEMIC & LOCAL SYNOVIAL JOINT DISORDER

• EDUCATION• IDENTIFICATION &

REDUCTION OF JOINT OVERLOAD FACTORS


• EDUCATION• REDUCE LOAD• CONSERVATIVE REGIMEN

IF SYMPTOMS PERSIST• MRI• CONTINUED

CONSERVATIVE REGIMEN• ARTHROSCOPYa

(or ARTHROCENTESIS)



IF SYMPTOMS PERSIST• MRI• CONTINUED CONSERVATIVE

REGIMEN• ARTHROSCOPYa

(or ARTHROCENTESIS)



IF SYMPTOMS PERSIST• CT• CONTINUED CONSERVATIVE

REGIMEN• ARTHROSCOPY IF JOINT

SPACE• ARTHROTOMY IF ANKYLOSIS

OR TUMOR

Fig. 10. Management of internal derangement caused by inflammatory/degenerative joint disease. a Arthroscopyis the minimally invasive treatment of choice.

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arthritis, Lyme disease, polymyalgia rheumatica,chondrocalcinosis, Ehlers-Danlos syndrome, lupus,and other connective tissue disorders.Arthroscopic surgery is often performed for

obtaining pathologic tissue for diagnostic pur-poses, and is also helpful in managing symptoms.However, management of the systemic disorderis essential for prolonged control of the patient’ssymptoms and this frequently requires coordinationof treatment with a rheumatologist (Figs. 11–13).

Localized Atypical Arthropathy: Intra-Articular Temporomandibular Joint Disorderthat Is Atypical and Not Caused by JointOverload or Systemic Disease

Because the temporomandibular joint is a syno-vial joint, it is subject to the same local disorders

Fig. 11. A 46-year-old woman with systemic lupus erythdegenerative changes involving the left temporomandibthritis and disc perforation. (C) MRI shows degenerative c

as other synovial joints. A localized atypicalarthropathy is uncommon for the temporoman-dibular joint; however, these conditions do occurin clinical practice. These patients haveintra-articular temporomandibular joint disorderthat is localized to 1 joint, and is not caused bysystemic disease or joint overload. Theclinical presentation of this group of disordersis nonspecific, but ultimately the signs andsymptoms (which occur with any internalderangement) include any combination of thefollowing:

1. Joint pain2. Joint noise: clicking and/or crepitus3. Altered mandibular range of motion4. Gross changes in the occlusion

ematosus and synovitis, disc perforation, and severeular joint. (A) Synovitis posterior recess. (B) Osteoar-hanges and anterior disc position.

Fig. 12. A 41-year-old with psoriatic arthritis and severe synovitis left temporomandibular joint. (A) Severeinflammation of the synovial membrane. (B) MRI showing anterior disc position and small synovial effusion ante-rior recess (arrow).


Clinical findings that are suggestive of alocalized atypical arthropathy include a gradualchange in the occlusion, with the developmentof an ipsilateral posterior open bite, and shiftingof the mandibular midline to the contralateralside. An osteochondroma of the condyle is themost common neoplasm affecting the temporo-mandibular joint and is in the category of an atyp-ical (neoplastic) localized arthropathy (Fig. 14).Diagnostic images that show unusual findings,such as multiple loose dense bodies, calcifica-tions, or very large synovial effusions are sugges-tive of atypical localized arthropathies such assynovial chondromatosis, crystal deposition jointdisease, and a synovial cyst (Fig. 15). Some pa-tients present with routine signs and symptoms

Fig. 13. A 61-year-old man with painful swelling of the rito the diagnosis of chondrocalcinosis (pseudogout). Thework-up and management. (A) MRI images showing denserow) (below) in joint space. (B). Arthroscopic surgery idenbiopsy of the tissue established the diagnosis of chondroc

and the diagnosis is confirmed with arthroscopicexamination and biopsy of pathologic tissue(Fig. 16). The algorithm for the diagnosis andmanagement of patients with atypical localizedarthropathies can be seen in Fig. 17. The impor-tance of establishing the correct diagnosiscannot be overemphasized.

False Arthropathy

Some patients present with the signs and symp-toms of temporomandibular joint internal derange-ment but the cause is not an intra-articulardisorder. The most common example of this isthe patients who develop trismus following an infe-rior alveolar nerve local anesthetic block. The

ght temporomandibular joint. Arthroscopic biopsy ledpatient was referred to a rheumatologist for furtherbody (Yellow arrow) (above) and effusion (Yellow ar-tified the calcifications in the synovial membrane andalcinosis.

Fig. 14. A 45-year-old man with osteochondroma of the left mandibular condyle. (A). Cone beam scan three-dimensional reconstruction showing osteochondroma of the left condyle. (B) Surgical specimen followingcondylectomy.

Fig. 15. Examples of atypical localized arthropathies affecting the temporomandibular joint. (A) Synovial chon-dromatosis. (B) Crystal deposition disease. (C) Synovial cyst.

Fig. 16. Arthroscopic biopsy of synovial disorder isextremely valuable in establishing the correct diag-nosis. Histopathology in this case was consistentwith synovial chondromatosis.

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trauma to the muscle and associated hematomaformation is the cause of the limitation of mandib-ular opening. Infection of the deep spaces of thehead and neck, as well as radiation fibrosis, arealso examples of a false arthropathy which arecommon and easy to diagnose based on the his-tory and clinical presentation.

False Arthropathy Caused by Neoplasia

There are some patients who present with signsand symptoms of pain and limitation of mandibularrange of motion, with a history of being treatedas a routine temporomandibular joint internalderangement, who ultimately are diagnosed witha neoplastic process. It is essential for oral andmaxillofacial surgeons to establish the diagnosisof false arthropathy caused by a neoplastic pro-cess as early as possible. Clinician should be sus-picious of a neoplastic process in patients who

SYSTEMIC ARTHROPATHY

ESTABLISH DIAGNOSIS

REFERRAL TREAT SYMPTOMS

REVERSIBLE TREATMENT

REGIMEN

INFLAMMATORY/DEGENERATIVE ARTHROPATHY

REVERSIBLE TREATMENT REGIMEN*PATIENT EDUCATION*REDUCE LOAD*MAXIMIZE MOBILITY*DECREASE INFLAMMATION*DECREASE PAIN*TINCTURE OF TIME

RESOLUTION PERSISTENT SEVERE SYMPTOMS

ARTHROSCOPYa

REHABILITATION

ARTHROCENTESIS

LOCALIZED ATYPICAL ARTHROPATHY

ESTABLISH DIAGNOSIS

TREAT SYMPTOMS

REVERSIBLE TREATMENT

REGIMEN

FALSE ARTHROPATHY

ESTABLISH DIAGNOSIS

EXPEDITED REFERRAL

TIMELY TREATMENT OF

PATHOLOGY

ARTHROSCOPY IF SYMPTOMS PERSIST

ARTHROSCOPY or ARTHROTOMY DEPENDING ON +/-JOINT SPACE, SYMPTOMS, &

HISTOPATHOLOGY

TREAT AASSSYYYMMMPPPTTTOMSOMSOMS

TREAT SYMPTOMS

Fig. 17. Management of disorders of temporomandibular joint causing internal derangement. a Arthroscopy isminimally invasive treatment of choice.


present with temporomandibular joint symptomswith the following:

1. Recent rapid weight loss2. Cranial nerve deficit3. Prolonged nonsurgical therapy without a

typical response to treatment in patients whohave not had diagnostic imaging

4. Orofacial pain that is atypical and not well local-ized to the temporomandibular joint

Although each case presents differently, theessential component in making the diagnosisis for clinicians to be diligent in continuallyreevaluating the diagnosis and response totreatment. Diagnostic imaging of the head andneck (computed tomography [CT] and MRI) iscritical in making the diagnosis (Fig. 18) and it isthe responsibility of the treating clinician to reviewthe images and not depend solely on the report

Fig. 18. A 79-year-old man referred to oral and maxillofasevere right TMJ pain, limitation of opening, and mandibulesion of the right condyle. Simultaneously, the patient wathe condyle was caused by metastasis. This false arthropa

by the radiologist. The algorithm for managementof patients who are suspected of having a falsearthropathy of the temporomandibular joint isshown in Fig. 17.

How Common Is Each Etiologic Category inthe Classification of Arthropathies of theTemporomandibular Joint?

Because an etiologic classification of temporoman-dibular joint disorder has not been routinely used,there is a paucity of information on the prevalenceof each category of arthropathy. Preliminaryresearch on this classification based on cause hasyielded surprising results. An unpublished reviewof 104 consecutive patients with signs and symp-toms of internal derangement and failure ofresponse to nonsurgical treatment, who underwentarthroscopic biopsies, has been conducted. Theetiologic classification was based on the history,

cial surgery by ear, nose, and throat for treatment oflar dysfunction. Cone beam and CT scans showed lytics diagnosed with pancreatic cancer. The lytic lesion ofthy simulated routine TMJ symptoms.

INFLAMMATORY/DEGENERATIVE ARTHROPATHY

SYSTEMIC ARTHROPATHY LOCALIZED ATYPICAL ARTHROPATHY FALSE ARTHROPATHY

CHRONIC JOINTOVERLOAD

SYNOVITISOSTEOARTHRITIS ADHESIONS

77%

RHEUMATOID ARTHRITISPSORIATIC ARTHRITISLYMECHONDROCALCINOSISEHLERS-DANLOS

SYNOVIAL CHONDROMATOSISCRYSTALLINE ARTHROPATHY

13%9%

1%

EXTRA-ARTICULAR DISORDER SIMULATING TMJ DISEASE

77%83% SHOWED ANTERIOR DISC POSITION ON MRI

Fig. 19. Diagnostic classification based on cause in 104 consecutive patients undergoing arthroscopic diagnosisand biopsy.

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diagnostic imaging, arthroscopic morphology, andhistopathologic findings. The results revealed thefollowing (Fig. 19):

Inflammatory/degenerativearthropathy caused by jointoverload

77%

Systemic arthropathy 13%

Localized atypical arthropathy 9%

False arthropathy 1%

Further investigation using an etiologic classifica-tion system is required, but even in this smallsample the results are surprising. Systemic arthrop-athies and localized atypical arthropathies affectingthe temporomandibular joint were common. A totalof 23% of the cases did not have the morecommon inflammatory/degenerative arthropathy,and thus treatment of these patient groups may bedifferent from treatment of those with themore common inflammatory/degenerative arthrop-athy (Israel H. Etiologic classification of temporo-mandibular joint disease in 104 consecutivepatients undergoing arthroscopic surgery. Manu-script in preparation, 2015).

SUMMARY: ETIOLOGIC CLASSIFICATION OFTEMPOROMANDIBULAR JOINT DISORDERS

A review of the current state of knowledge of in-ternal derangement of the temporomandibularjoint and synovial joint pathophysiology leads tothe conclusion that internal derangement is not

a disease. The signs and symptoms associatedwith internal derangement are caused by lossof the structure and function of the intra-articular tissues, ultimately leading to a failurein the biomechanics of the temporomandibularjoint. The cause of this tissue failure is mostoften joint overload, leading to tissue failureand an inflammatory/degenerative arthropathyof the temporomandibular joint. However, theintra-articular changes associated with internalderangement of the temporomandibular jointcan also be caused by a systemic arthropathyor a localized atypical arthropathy involving thetemporomandibular joint. In addition, there isa group of disorders that simulates the signsand symptoms of internal derangement, but arecaused by extra-articular disease, and thus areclassified as a false arthropathy of the temporo-mandibular joint. Clinicians must be diligent inestablishing the correct diagnosis and cause ofthe internal derangement, which ultimately leadsto the appropriate management of patients withthese disorders.

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