tmd clinical diagnostic classification (temporo mandibular ... · tmd clinical diagnostic...

Address for correspondence:

O. LAPLANCHEUFR D’Odontologie de Nice,24 avenue des Diables-Bleus,06300 [email protected]

DOI: 10.1051/odfen/2012102 J Dentofacial Anom Orthod 2012;15:202� RODF / EDP Sciences

1

TMD clinical diagnosticclassification(Temporo MandibularDisorders)

Olivier LAPLANCHE, Elodie EHRMANN,

Pierre PEDEUTOUR, Gerard DUMINIL

ABSTRACT

Practitioners should aim to diagnose as early as possible the development ofmalfunction of the masticatory system, or temporomandibular disorder (TMD),that causes pain, discomfort and a decrease in functional efficiency, especially inthose patients whose occlusion is being rehabilitated in the course oforthodontic treatment. This is particularly true for the segment of the patientpopulation who are characterized by certain risk factors.

Armed with a good understanding of the diagnostic classification of TMD,orthodontists will be better prepared to pinpoint and diagnose TMD and, ifnecessary, adopt the most appropriate mode of therapy for treating it.

Thanks to a good understanding of TMD nosology, orthodontists will be ableto distinguish between muscular and joint disorders and then manage patientsin accordance with specific diagnostic criteria.

KEY WORDS

Masticatory system,

Occlusion,

Malfunctioning of the masticatory system,

Muscles of mastication,

Temporomandibular joint – TMJ.

Conflicts of interest declared by author: NONEArticle received: 11-2011.

Accepted for publication: 12-2011.

Article available at http://www.jdao-journal.org or http://dx.doi.org/10.1051/odfen/2012102

http://www.jdao-journal.org

http://dx.doi.org/10.1051/odfen/2012102

1 – INTRODUCTION

The objective of orthodontic treat-ment is to obtain optimal occlusionwith good centric relation and with themandible well guided and in a solidposition at rest. The result should bethe achievement of good masticatoryfunction and excellent esthetic ap-pearance of the face and the dentition,all of which contribute to the longevityof the masticatory system.

In this context, orthodontists areoften called upon to swiftly recognizeand manage any possible dysfunctionof the masticatory system (known astemporomandibular disorder, or TMD).This recognition and managementshould begin at the initial consultation,where the clinician should be alert forany indications of potential TMD thatmay already be symptomatic or stillunrecognizable clinically. Further op-portunities are presented during thecourse of treatment and in post-treat-ment, where TMD could diminish thequality of results or be provoked by aninappropriate intervention by theorthodontist. Finally, a TMD problemmay itself be the reason for theconsultation because the patient orreferring physician justly consideredan orthodontist to be the appropriatespecialist in treating problems ofocclusion and malfunction of themasticatory system.

To discern and, if necessary, prop-erly manage cases of dysfunctions ofthe masticatory system, orthodontistsmust have a good understanding ofhow they are defined, their etiology,the principal clinical signs that char-acterize them, the way they evolve,and the complications and risks thataccompany them.

The essential definition of mastica-tory dysfunctions describes them aspathoses of the oral musculature andarticulation that, according to the typeof malfunction, can generate:– pain,– functional problems that range from

mild discomfort to real functionalhandicaps,

– and/or structural changes, includingalterations of the articular surfacesand muscular configurations.Orthodontists called upon to deal

with certain symptoms of clinicaldysfunction will be faced with avariety of problems: How should aspecific pathosis presented by thepatient be addressed therapeutically?How should this treatment programbe adjusted to react to new symptoms(e.g. by modifying, accelerating orinterrupting therapy)? And what arethe possible structural consequencesof the malfunction within the anato-mo-functional framework of the ther-apy. In reality, all occlusal rehabilitationmust be accomplished in harmonywith a physiological mandibular refer-ence position, which in orthodontics isa stabilized articular relationship35.This, according to Philippe38, shouldgenerate a harmonious state of mu-tual tolerance between the differentsystems of the masticatory system.

The objective of this article is to helporthodontists deal with the malfunc-tion problems they encounter in theirdaily practices by recalling some ofthe basic features of TMD and itsetiology, before presenting a clinicaldiagnostic classification that will helpthem detect and diagnose indicationsof TMD.

OLIVIER LAPLANCHE, ELODIE EHRMANN, PIERRE PEDEUTOUR, GERARD DUMINIL

2 Laplanche O, Ehrmann E, Pedeutour P, Duminil G.

TMD clinical diagnostic classification (Temporo Mandibular Disorders)

2 – DEFINITION AND FUNDAMENTAL ASPECTS OF TMD

TMD is defined as a muscular andarticular disorder21. This term includesanatomical, histological, and functionalanomalies in the functioning of themuscular and/or articular componentsof the system that are accompaniedby highly varied clinical signs andsymptoms. The general clinical con-sequences of discomfort, pain, anddisturbances of mastication are similarin most patients, and can thus besubsumed in the non-specific term,‘TMD’.

Accordingly, TMD is characterizedby clinical signs of pain or malfunctionoccurring jointly or separately11,34:– pain in the temporomandibular joint

(TMJ),– articular sounds,– pain in the muscles of mastication,– anomalies in mandibular move-

ments,– signs and symptoms that may be

associated with orofacial pain and/or cervicoscapular problems.A malfunction is an expression of

disturbance of functional activities thatcan provoke patients to make adaptivechanges. TMD corresponds, then, topain and dysfunction in the mastica-tory system related to musculoskele-tal anomalies and can refer to either orboth of the affected systems (muscu-lar and articular).

TMD problems are widespread,affecting 90% of the general popula-tion at one life stage or another42,especially 20-40 year-old women.However, only 10% of affected indivi-duals seek treatment for pain, and,less frequently, for articular noises5.

2 – 1 – Etiopathology of TMD

Many authors15-37 have proposedan etiopathological, multi-dimensionalmodel for TMD that integrates (Fig. 1):– a biological dimension: the general,

or systemic, influence the muscularand articular aspects of TMD;

– a psychosocial dimension: the psy-chological conformation of subjectsin the context of their environmen-tal and cultural milieu influencingmasticatory behavior and their per-ception of malfunction and pain13;

– and a structural dimension: the localsomatic component of the muscu-loskeletal organization associatedwith the TMJ and occlusion.Currently, a consensus exists on the

multi-factorial etiology of TMD thatcomprises structural, neuroendocrine,emotional, functional, and behavioralelements that can be classified clini-cally as ‘pre-disposing’, ‘triggering’and ‘maintenance’ aspects of TMD(Fig. 2).

In this model, the role played byocclusion is controversial7-9,12,19,20,39,43.De Boever9 sums up the current statusof occlusion, saying, ‘‘It is not primordial,but it is not a nullity.’’

It is widely acknowledged that ortho-dontic treatment can neither create aTMD problem nor cure one10,26,27.

Thus, dentists should not undertakemajor occlusal rehabilitation programsas a means of treating TMD but theyshould, nevertheless, accept theimportance of optimizing occlusalfunction.

TMD CLINICAL DIAGNOSTIC CLASSIFICATION (TEMPORO MANDIBULAR DISORDERS)

J Dentofacial Anom Orthod 2012;15:202 3

Orthodontists can refer to ‘‘theadvice of experts’’ and a biomechani-cal logic2,34,35 to systematically reducethe constraints operating on differentcomponents of the masticatory com-plex (articular, muscular, and dental),and to optimize occlusal functionbased on theoretical models28.

In addition to anomalies of form,tooth position, and arch arrangement,examiners must evaluate functionalanomalies of occlusion and their po-tential effect on other systems23.

As a schematic conception, we canassume that, in general, TMD devel-ops when there is some defect inmandibular posture, excessive con-straint in both time and force, and anon-adaptive or disproportionate re-sponse from the masticatory struc-tures and/or the central nervous

system, resulting most often fromstrain exceeding the patient’s adaptivecapacity.

2 – 2 – Global diagnosticapproach

Dentists should adopt a diagnosticapproach for TMD based on thenormalized and standardized clinicalmethods now available complemen-ted by photographic and radiographicimages4.

An essential first step is making anexclusion analysis, ruling out non-TMDpathoses whose prognoses could befar more serious, 32,33.

A second imperative in TMD diag-nosis is to adopt a global, bio-psycho-social viewpoint that, as suggested in

Figure 1Etiopathological model of TMD in three dimensions.




the previous pages, goes well beyonda mechanistic dental assessment.

Because electronic devices haveno proven reliability, orthodontistsshould use them guardedly in makingtherapeutic decisions. Careful andcomplete anamnesis, medical com-munication, and clinical examinationare of primary importance in detect-ing and diagnosing TMD4. John etal.18 have shown the reliability of wellconducted clinical examination.

2 – 3 – Therapeutic approach

None of the different therapeuticmodalities for TMD has proven to be

superior to all others, so dentistsmanaging the problem must directtheir efforts to relieving symptomswith conservative, reversible techni-ques that are as non-invasive aspossible.

Some authors1,35 also insist that inthe absence of scientific proofs, den-tists must be guided by clinical andbiological logic, i.e. they should reducenoxious constraints affecting variouselements of the masticatory complex,the teeth, the TMJ, and the muscu-lature, as the immutable objective ofany major occlusal rehabilitation.

3 – DETECTING THE PRESENCE OF TMD

We have listed the principal pastand current signs of TMD encoun-

tered by orthodontists either clinicallyor in the intake interview in Table I:

Predisposing factors :

natural or acquired they

create site of the malady :

Triggering factors :

They abruptly disturb the homeostasis of the masticatory

apparatus. A situation lacking equilibrium with its

progressive installation having permitted a structural

and functional modification, that can be decompensated

and provoke the appearance of clinical signs and

symptoms :

Maintaining factors :

They maintain the pathosis of the

structural, functional, or secondarily

neuropsychiatric :

– Anomalies of occlusal

functions ;

– Tension or emotional shock favoring

parafunctions ;

– Secondary tooth migrations ;

– Ligamentous looseness ; – Abrupt occlusal iatrogenic change from

orthodontic or prosthetic intervention ;

– Alveolar remodeling ;

– Parafunctions ; – Behavioral changes in chewing gum,

clenching, bruxism, nail biting ;

– Occlusoconscience ;

– Psychologically,

anxiety, depression.

– Traumatism: forced mouth opening in

dental or surgical treatment under general

anesthesia, or accidental trauma resulting

from, perhaps, an unexpected blow.

– Acquired proprio-deficiency ;

– Primary or secondary

hypersensitivity to pain ;

– Psychological fragility.

Figure 2Etiological or risk factors for TMD: summary table.



3 – 1 – Anomalies of mandibularmovement

Table II shows measurements forvarious anomalies in mandibularmovement, which include:– limitation of movement of the

mandible, which is frequently re-lated to a TMJ problem, such as adisc displacement or muscular mal-function;

– lack of control of mandibular trans-lation and rotary movement be-cause of acquired or systemicligamentous laxity14.In some cases, these problems can

be qualitative (Tab. III, Fig. 3) withalterations in mandibular trajectory onopening (e.g. deviations or deflec-tions).

3 – 2 – Articular sounds22

3 – 2 – 1 – Clicking

These sounds occur most fre-quently when the condyle moves overthe posterior glenoid of the disc duringthe translational actions of opening,propulsion, and contralateral excur-sion: there is then a lack of condyledisc contact during maximum inter-

cuspation and coaptation of the con-dyle and disc during condylartranslation.

This clicking can also occur becauseof friction between ligaments or asthe condyle passes in front of thearticular eminence of the temporalbone in a kind of subluxation fromhyper-translation.

3 – 2 – 2 – Crepitation

Crepitation resembles the sound ofwet sand moving over a surface. Indentistry, it is usually evoked by somechange in the articular surfaces thatdisrupt their ‘gliding’ contact.

3 – 3 – Pain

Pain can be highly variable, occur-ring spontaneously or being triggeredby mastication or palpation. Further-more, it can be localized (e.g. tomuscles or the TMJ) or referred to adistant region.

Clinical signs and symptoms of TMD

Anomalies of mandibular movement

Articular noises

Pain

Accessory symptoms potentially associated with TMD

Table I

Measurement of anomalies

of mandibular movement

Mouth opening in

mm

Normal mouth opening 35 to 45

Limitation of normal mouth opening < at 35

Exaggeration of mouth opening > 50

Table II

Qualitative alterations in

mandibular movement

Trajectory

Mandibular deviation Bayonet opening

Mandibular deflection Deviated rectangular opening

Table III




It is thus important for examiners tocharacterize precisely the nature ofTMD pain according to its type, site,radiation, development, duration, con-text, any associated signs, and itsimpact on the patient’s daily life.

In making a schematic representa-tion of TMD pain, its extremes to beconsidered are:– acute, experienced as penetration

of a needle, preceding articularmovement, exacerbated by masti-cation thus suggesting an articularmalfunction, particularly if painincreases during passive testing

such as mobilization of the mand-ible placed under articular tension;

– dull pain evoking a feeling of heavi-ness during clenching, for example,that is more diffuse in the massetermuscle, near the ear and in thetemporal bone, suggesting an originin muscular malfunction.Referred TMD pain is more complex

and more difficult to analyze anddiagnose precisely because of thedistance between its probable site oforigin and the location where it man-ifests. Orthodontists and general prac-titioners rarely see this type of slowlydeveloping chronic somatic pain.

Figures 3a to 3cDistinction between anomalies of mandibular movement.a: Limitation of opening (<30 mm);b: Deviation in opening;c: Deflection in opening.



3 – 4 – Symptoms potentiallyassociated with TMD

A certain number of highly incon-sistent, non-specific symptoms thatcannot be considered as reliable ele-ments for establishing a positivediagnosis of TMD include:– otic complaints such as tinnitus,

sensation of blockage, and sensa-tions of exaggerated or diminishedhearing;

– ocular disturbance such as peri orretro-orbital discomfort, and pro-blems of accommodation;

– cephalic discomfort derived fromtension of the frontal, temporal,and sub-occipital musculature;

– neurovegetative manifestations ofedema, rhinorrhea, and excessivelacrimation.

4 – IMPORTANCE OF DIFFERENTIAL DIAGNOSIS

Taking into account the seriousprognosis of other disorders, whosesymptomology is similar to that ofTMD, practitioners confronted withmaladies of the masticatory systemmust focus on excluding other possi-bilities in making a differential diag-nosis of TMD4,11,33,34,40.

Such a diagnosis will be based bothon pain and functional handicaps.Examiners must therefore have a clearunderstanding of the gamut of cranio-facial pain and discomfort11,36,37

(Tab. IV) and articular disorders6

(Tab. V).

5 – DIAGNOSTIC CLASSIFICATION

The large number of diagnosticelements that examiners must takeinto consideration makes it essentialfor them to use a precise system ofclassification for malfunctions of themasticatory system that, for eachtype, associates an ensemble of clin-ical and paraclinical signs and symp-toms together with therapeuticsuggestions.

The development of a clearer nosol-ogy of malfunctions will, accordingly,contribute to a standardization ofdiagnosis of the two types of TMD(muscular and articular (Tables VI and

VII)) and their optimal therapy in thefield.

5 – 1 Muscular malfunctions

Muscular malfunctions are the mostfrequent cause of anomalies of man-dibular movement such as limitationof amplitude and dyskinesia.• Muscular type of pain (Fig. 4)

The precise characterization of thepain experienced is an importantcomponent of an effective diagnosisof TMD.




Myalgia, or muscle pain, may comefrom muscle bundles, tendons, orfascia. According to Bell3, muscle painis the most frequent factor in head andneck discomfort. It is diffuse, de-scribed by patient as continual, deep,

dull, and felt, especially, when teethare clenched or under pressure. Itsvarying intensity, which is difficult forpatients to localize and often appearsbeneath the malar and temporal mus-cles and more rarely mesial to the

Classification of craniofacial pain

Intracranial pain Extracranial pain

Structural (e.g. tumor, aneurism, abscess,

Hematoma, edema)

Neuropathic, neurogenic

Paroxysmal : trigeminal, glossopharyngeal, upper laryngeal,

and occipital neuralgic

Continual : acute herpes, post-herpetic chronic neuralgic.

Primary cephalic, neurovascular pain:

migraine, vascular, chronic hemi-cranial

paroxysmal chronic tension headache

Eye, nose, throat (otitis, sinusitis)

Secondary headache (rebound, traumatic,

Hyperthermal, infectious, drug related)

Intraoral pain (dental, mucogingival, salivary gland, tongue)

Musculoskeletal pain

Cervical anomalies

Masticatory malfunction

Table IV

Differential diagnosis of non-TMD articular maladies

Infectious septic arthritis Acute, sub-acute, or chronic

Rheumatoid arthritis

Chronic juvenile arthritis

Ankylosing spondylitis

Psoriatic arthritis

Reactive arthritis

Degenerative lesions (Arthrosis)

Synovial chondromatosis

Villonodular synovitis

Condylar osteonecrosis

Metabolic arthropathy

Malformations

Condylar tumors and hyperplasia

Structural or mechanical arthrosis

Table V

Inflammatory rheumatism



TMJ, sometimes causes errors indifferential diagnosis between articu-lar and muscular TMD.

The pain, associated with function,is exacerbated by palpation of mus-cles, and, in relation to its duration,can be considered acute or chronic.

Muscular pain is a deep somaticpain that can be accompanied bycentral secondary effects includingautonomic and motor sensitivity, fre-quently resulting in restriction of man-dibular movements related tomuscular spasm.

Diagnostic classification of malfunction in the masticatory muscles

Acute attacks Splinting reflex

Muscular curvature

Spasm

Chronic attacks Myofacial pain (trigger points)

Myositis

Contraction (myostatic or fibrous)

Table VI

Figure 4Schematic representation of thesites most frequently experiencingmuscular (in blue) and articular(in red) pain.




In this article, we propose a classi-fication of muscular malfunctionsbased on that formulated by theAmerican Academy of Orofacial Pain(Tab. VI).

5 – 1 – 1 – Splint reflex

Splinting is a protection reflex in-itiated by the central nervous system(CNS) provoking muscular contractionand pain intended to protect an injuredregion from further trauma. The CNSincreases the activity of an antagonistmuscle when its agonist contracts, asoccurs when the masseters contractduring jaw opening.

In itself, splinting is a physiological,not a pathological response of theneuromuscular system.• Etiology

The splinting reflex is activatedimmediately after the occurrence ofone of a number of etiological events,including :– an alteration in proprioception or

sensitivity after the sudden appear-ance of an occlusal high pointperhaps caused iatrogenically byan orthodontic adjustment or place-ment of a prosthesis; a long periodof mouth closure, caused, perhaps,by an extended dental procedure;clenching or bruxism, traumaticapplication of local anesthesia, orTMJ malfunction;

– continual deep pain within a muscleor associated structure, such astendons, ligaments, or articulationsof teeth;

– stress, which influences the actionof the muscles of masticationthrough the intermediary of thegamma-efferent loop in muscle

bundles and can, accordingly, pro-voke clenching and bruxism13,41.

• Clinical signs

– Muscular malfunction: pain limitsthe patient’s ability to move theirmandible; however, examiners canencourage patients to recover theirnormal amplitude of mandibularactivity.

– Absence of pain when mandible isat rest.

– Aggravation of pain in function.– Sensation of muscular weakness.• Treatment

Because splinting, or immobiliza-tion, is a normal response of thecentral nervous system, the dentalexaminer should focus on determiningthe etiology of the TMD before elim-inating that source of disturbance,after which the muscular retractionreflex should rapidly dissipate. If, infollow-up visits, the patient appears tohave a major occlusal discrepancyrelated to recent tooth movements,dentists should deal either with thatanomaly or by stabilizing the occlu-sion, encouraging remission with sim-ple palliative remedies related to theetiology :– giving advice on oral behavior with

suggestions on how to rest theTMJ and the muscles;

– applying moist heat to painfulmuscles;

– using mild, short-term, peripheralanalgesics;

– fabricating an acrylic occlusal splintdesigned for neuromuscular recon-ditioning and protection againstnocturnal bruxism.Typically, splinting reflexes can arise

during any stage of orthodontic treat-ment in which tooth movement pro-vokes a major occlusal anomaly such



as as a transitory prematurity or aninadvertent, temporary occlusion of atooth cusp with an attachment.

However, these reflexes may betotally independent of any orthodonticor other dental treatment. They maydevelop from, for example, a changein sleeping posture or from prolongedpressure on the right side of the chinprovoking distal repositioning of themandible and exertion of pressure onthe left condyle triggering a splintingof the left lateral pterygoid muscle(Fig. 5).

5 – 1 – 2 – Delayed Onset MuscleSoreness

Delayed onset muscle sorenessresults from fatigue in the musclefibers and is a primary, non-inflamma-tory reaction of muscular tissue toprolonged tension or to the splintingreflex. It is, accordingly, a change inthe local muscular environment inwhich the central nervous systemplays no part.• Etiology

– Prolonged splinting reflex: a viciouscircle can be created if the curved

musculature can itself provoke asplinting reflex.

– Trauma: abusive use of musclegroups in gum chewing or, iatro-genically, from injection of a localanesthetic.

– Prolonged crispation of clenchedteeth, a noxious occlusal habit.

• Clinical signs

– Muscular malfunction: a slight de-crease in the amplitude of activemandibular movement. However,the examiner can gently guide thepatient’s jaw into movements ofmaximum amplitude.

– Slight pain when the jaw is at rest.– Pain exacerbated by function.– Muscular weakness.– Affected muscle is painful on palpa-

tion.Frequently examiners will note that

muscular volume is greater with in-creased use of that particular musclegroup.• Treatment

– Eliminate the initial cause of themuscle splinting reflex responsiblefor the onset of this vicious circle.

– Reduce muscle tension by limitingthe use of affected muscles in habitactivity.

– Give patients behavioral counselingwith regard to diet, the importanceof resting muscles, education inmuscle relaxation techniques, andincreasing awareness of dailyclenching episodes. The patientcan, and should, continue to useaffected muscles but not forcethem beyond the pain threshold.

– Advocacy of psychological relaxa-tion techniques if necessary.

– Use of an acry l i c occ lusa lsplint designed for neuromuscular

Figure 5Intraoral view: a reflex splinting of the lateral pterygoidtriggers a contralateral positioning of the mandible.




reconditioning and protectionagainst nocturnal bruxism.

– Using mild, short-term, peripheralanalgesics and muscle relaxants.Clenching of teeth remains one of

the principle causes of TMD, primarilyaffecting the masseter muscleswhere the site of pain may be sodeep that examiners confuse it withpain originating in the TMJ.

In orthodontics, paradoxically, thistype of muscle curvature frequentlyoccurs after termination of treatmentwhen the newly acquired correctintercuspation allows patients toclench their teeth in a way that wasnot possible when the malocclusionexisted.

5 – 1 – 3 – Muscular spasm

A muscle spasm is a violent, acute,sudden and involuntary contraction ofmuscle tissue provoked by the centralnervous system in which the fibersshorten and become painful. Thecontraction is continual and can beverified by surface electromyography(EMG) that shows considerablemuscular activity at rest, in contrastto other types of muscle problems.A muscle spasm, with its very painfulcramps, can last for a few minutes upto a few days. However, they rarelyoccur in the orofacial area.• Etiology

The etiology of muscle spasms isnot yet perfectly understood but sev-eral factors seem to be involved:– local conditions such as muscular

fatigue and electrolytic imbalance.Contraction seems to respond toexaggerated excitation of alphamotoneurons creating a pain-spasmcycle. The ischemia that follows

these events solidifies the contrac-tion leading to muscle fatigue withformation of lactic acid and theliberation of the peptide signalingmediator, bradykinin;

– variation among individuals’ sus-ceptibility to muscle spasms mayderive from systemic factors thathave not yet been elucidated.

• Clinical signs

– A marked limitation of mandibularmovement caused by musclespasms. Mouth opening, for exam-ple, will be limited when the mass-eters are affected.

– Acute occlusal malfunction, e.g.when the lower head of the inferiorpterygoid is in spasm, contralateralanterior contacts and an ipsilateraldis-occlusion will occur during max-imal inter-cuspation.

– Severe pain at rest and duringfunction that may be acute andlancinating, radiating toward theears, temples, and cheeks.

– Upon palpation, the muscle will befirm and the patient will likelyexperience pain.

• Treatment

It is important for the practitioner toinitiate treatment of the musclespasm promptly to prevent the devel-opment of myostatic or fibrous con-traction (cf. infra).– Kinesitherapy or physical therapy:

the application of heat and mas-sage is often effective at thebeginning of treatment; later, aftera few days, patients can beginstretching exercises to restoreproper function.

– Short-term use of medication, in-cluding peripheral analgesics andmuscle relaxants.

– If the contracting muscle resistsattempts towards relaxation,



practitioners may use local anesthe-sia to relieve the tension within it.

– Practitioners may begin to eliminateetiological factors, including occlu-sal prematurites and, possibly,overall stress.

– An acrylic splint may be indicated topromote neuromuscular recondi-tioning and control nocturnal brux-ism and clenching that may beetiologic factors.These muscular malfunctions of the

masticatory system are among themost frequently encountered pro-blems that orthodontists confront intheir daily practices.

This disturbance is ubiquitous, andcurvature accompanied by pain is alsoa revealing sign of some unwelcomeocclusal parafunctions such as clench-ing. Therapeutic tooth movementmust inevitably create transient ‘‘mal-occlusions’’ that trigger clenchingreflexes, so orthodontists seethis phenomenon more frequentlythan do their general practitionercolleagues.

Nevertheless, both groups of practi-tioners must know how to discern thisdiscrepancy and how to institutea prompt therapeutic program toeliminate it.

There are, however, other clinicalmuscular malfunctions that representchronic regional problems; here theperipheral symptoms, strongly influ-enced by the central nervous systemand their chronic character of contin-uous pain present for more than 6months, make local treatment highlyuncertain. Management of these pa-tients is best accomplished by multi-disciplinary teams. However, eventhough such problems are beyond

their level of specialization, orthodon-tists must understand them to makea satisfactory differential diagnosis(Tab. VI).

5 – 2 – TMJ malfunctions

Current understanding of the anato-mical and physiological features of theTMJ strongly suggests that it func-tions best in a state of coaptationwhere the condyles and discs aresupported by harmonious musclefunction that persists in static posi-tions of inter-cuspation as well asduring dynamic action when mandib-ular movement dictates condylar dis-placements. In sagittal section, normalarticulation is thought to involve theheads of the condyles contacting theintermediate zone of the temporoman-dibular discs and the two disc bands,with the whole ensemble resting onthe posterior wall of the temporaleminence. This disc band is theterminal tendon of the lateral ptery-goid muscle, which forms, along withthe temporal, masseter, and medialpterygoid muscles, the tensor com-plex that covers the head of thecondyle (Fig. 6a).

Examiners can verify the normalityof the TMJ clinically or by means of acondylograph if they find the heads ofthe condyles are capable of ample,regular, and symmetrical translations,without any deviations, that are super-posable during different types ofmandibular movement. Working sym-metrically, the two heads of thecondyle allow the mandible to dropsufficiently in opening, between 40and 50 mm in adults, without deviat-ing to the right or left (Fig. 6b and 6c).




5 – 2 – 1 – Anomalies of thedisc-condyle complex

These disorders are disturbances ofthe relative position of the two com-ponents of the TMJ.

Functional, anatomic, or traumaticfactors can cause varying degrees ofdisc displacement.

Situations differing from the normalanatomic relationships shown abovehave been described as disc displace-ment when, in most cases of separa-tion it is, in fact, the head of thecondyle that has moved distally, awayfrom a disc that has remained, more orless, in place.

This displacement can be :– partial or total in maximal inter-

cuspation with a reduction in con-dylar translation (reducible disc dis-placement) or;

– total with no reduction during dif-ferent movements of the mandible(permanent disc displacement).

> Reducible disc displacement

(Fig. 7).Anatomically, in these cases the

head of the condyle is no longerlocated in the intermediate zone ofthe disc, but rests on the posteriorosseous ring, or glenoid. The dis-placed disc is usually in an anterome-dial position, but sometimes lies ina directly anterior or anterolateralposition34.• Etiology

– Condyles moving distally becauseof excessive looseness or overworkof some TMJ components causedby noxious habits or occlusalinterferences.

– Hyperactivity of the tensor musclesof the disc, deep masseter, super-ior head of the lateral pterygoid, andposterior temporalis.

• Clinical signs

The pain suffered at the beginningof a TMD episode diminishes as thedisorder becomes chronic and tissues

Figures 6a to 6cModels of the normal arrangement of TMJ components.

a: Schematic representation;b: MRI view of normal TMJ, mouth closed: condyle, disc, temporal bone in coaptation;c: MRI of normal TMJ, mouth open: condyle in translation.



adapt to it. The inflammation of thebilaminar disc zone that accompaniesthe disc displacement, or distalizationof the condyle decreases but clickingsounds become more noticeable andsharper as the condyles confront theosseous ring, or posterior glenoid ofthe disc.

In the excursive movements ofopening, forward thrusting, or of con-tralateral movement right or left, click-ing sounds of varying intensitycorrespond to condylar projection orre-coaptation of the condyle and disc,accompanied by an abrupt change ofdirection of the mandible in motion.

Examiners can palpate this lateralprojection of the condyle.

They can also perceive a ‘‘recipro-cal’’ clicking during excursive move-ments when the mandible is near, butnot yet in, a position of maximuminter-cuspation.

Deviation in opening, in a bayonet-like projection is an important sign ofdisc displacement, but if the extent ofopening is not restricted, the disorderis not permanent (Fig. 8).• Therapy

Dentists treating TMD should notaim at re-capturing the displaced disc,

Figures 7a and 7bMRI of TMJ with non-per-manent disc displacement.a: Mouth closed, condyleseparated from disc;b: Mouth closed: condyleand disc have re-connected.

Figures 8a to 8cIntraoral views of a patient with bayonet mandibular deviation with no reduction in opening amplitude, characteristic

of non-permanent disc displacement.




which is a transient disorder, but atalleviating painful symptoms and opti-mizing condylar positions by encoura-ging the formation of fibrous tissuefrom the healing process between thecondyle and the mandibular fossa, inthe neo-disc area.

It is essential that treatment shouldbe conservative, consisting of:– advice on proper oral behavior;– use of medication, peripheral an-

algesics or anti-inflammatory drugs;

– use of an occlusal neuromuscularreconditioning or decompressionsplint;

– kinesitherapy or physical therapy toreverse over-relaxation of TMJtissues;

– optimization of occlusal functioning.> Permanent disc displacement

Permanent disc displacement canbe acute or chronic. In both cases, inmaximum intercuspation, the head ofthe condyle lies behind the glenoid, or

Figures 9a and 9bMRI of a TMJ with acutepermanent disc displace-ment.a: Mouth closed: disc dis-placed;b: Mouth open: persis-tence of displacementand limited condylar trans-lation.

Figure 10Deviation and decrease in opening amplitude are characteristic of permanent discdisplacement.



osseous ring and remains in thisposition during translation movementswithout ever returning to condyle-disccoaptation.

Two versions of this situation canbe described depending on whetherthe disc displacement is recent (in an

Figures 11a and 11bMRI of a TMJ withchronic permanent discdisplacement.a: Mouth closed, discdisplacement;b: Mouth open: persis-tence of disc displace-m e n t , b u t n o r m a lcondyle translation.

Diagnostic classification of articular malfunction in the masticatory system

Anomalies of condyle-disc

complex

Non-permanent reducible

disc displacement

Permanent disc displacement

Partial reducible disc

displacement

Condyle-disc reducible

luxation

Acute (lockjaw)

Chronic (longer than 4 months

Incompatibility of articular

surfaces

Anomalies of form

Adherence and adhesions

Subluxation (hyper-translation)

emporomandibular luxation

lockjaw

Inflammation Capsulitis/Synovitis

Retro-discitis

Arthritis (inflammatory component

of degenerative disease)

Degenerative disease

Primary

Secondary

Primary

Secondary

Table VII




acute phase) or is of at least 3–4months duration (i.e. is chronic).> Acute permanent disc displace-

ment (Fig. 9)• Etiology

Acute permanent disc displacementfrequently develops from an exacer-bation of an earlier episode of reduci-ble disc displacement that was firstrevealed in the intake interview whenthe patient reported a history ofpainless joint noises. However, theycan abruptly turn into permanent dis-placement after trauma, dental treat-ment under general anesthesia, awhiplash injury, or sudden TMJ strain.• Clinical signs

– Moderate-to-intense pain localizedin the TMJ area that worsens onmouth opening.

– Considerable limitation of mouthopening, with deviation toward theaffected side that sometimes pro-vokes locked jaw syndrome andblocks excursion to the contralat-eral side (Fig. 10).

– Absence of joint noise.• Treatment

– Medication with level II peripheralor central analgesics and anti-in-flammatory drugs.

– If the permanent disc displacementis relatively recent, of a few hoursor days duration, dentists mayattempt to recapture the disc byusing the Farrar maneuver and,with success, treat the problem likeany other reducible displacement.

– If the permanent displacement islonger in duration, the therapeuticobjective is conservative and con-sists of orthopedic managementwith a decompression splint of ahealing space in the TMJ. The goalis amelioration of the tropic poten-

tial of the space around the disc andthe relaxation of attached ligamentsto improve condyle translation.The modalities of treatment are

identical to those used for chronicpermanent d isc d isp lacement(cf. infra).> Chronic permanent disc displace-

ment (Fig. 11)• Etiology

These always follow an episode ofacute displacement that may havebeen asymptomatic. The etiology ofchronic disc displacement is identicalto that of acute displacement.• Clinical signs

– Slight pain that diminishes at thisevolving stage as the retro-disctissues adapt to the TMD.

– Mandibular movements return tonormal patterns as a result ofcompensatory hyper-rotation ofthe lower level of the TMJ orstretching of ligaments.There is, accordingly, a considerable

reduction of symptoms to a pointwhere they are not clinically detect-able. Twenty per cent of asympto-matic subjects are in this category29.• Therapy

The conservative therapeutic objec-tive is to encourage healing of thearticular space orthopedically and toimprove the relationship between thejoint components, i.e to bring the disccloser to the condyle using:– oral behavior counseling;– decompression splint;– periodic follow-up re-evaluations;– and exercising extreme prudence

when extensive orthodontic orprosthetic dental occlusal proce-dures are contemplated, becausethe disc displacement makes joint



relationships unfavorable as thepatient’s adaptive capacity isdecreased.At this point, the articular relation-

ships are pathological but can bestabilized with treatment.

In Table VII, we have noted anothergroup of disorders concomitant tothis list of condyle-disc complexanomalies.

By carrying out a complete andaccurate anamnesis and carefully ana-lyzing clinical signs, examiners canusually construct a precise diagnosis.

5 – 2 – 2 – Incompatibility ofarticular surfaces

There are four ways in whicharticular surfaces may be incompati-ble: different shapes; adherences andadhesions; subluxation; and true tem-poromandibular luxation.

> Anomalies of the shape of articu-

lar surfaces

Included in this category are pro-blems caused by morphologicalchanges of the articular surfaces ofthe TMJ or of its disc.

For the articular surfaces, mini-traumas (derived from habits orTMJ overloading) and major traumaare the etiological causes. These areresponsible for articular sounds dur-ing mandibular excursive move-ments that may or may not bepainful or deviated.

For the discs, the anomalies consistprimarily of a thickening of the poster-ior osseous ring, a mucoid degenera-t ion in adolescents, and disccalcification (chondrocalcinosis).

Clinical signs are quite different :– occasional audible clicking sounds

related to obstacles in the path ofcondylar translation ;

Figures 12a and 12bDifferential diagnosis of reducible disc displacement and substantial subluxation. The ‘clicking’ of subluxation occursat the point of maximal opening, which can be greater than 40 mm, and is followed by hyper-rotation of the mandible.




– aberrant or variable condylar move-ments.

> Adherence and adhesion

In adherence, articular surfaces aretemporarily attached by synovialmembranes, usually because of in-creased articular pressure caused bythe microtrauma of clenching andbruxism. The principal clinical sign isdifficulty in opening the mouth in themorning, which is usually accompa-nied by a clicking sound (as thesynovium detaches) and then a returnto normal mandibular movements.

Therapy consists of suppression ofthe etiological factors and the use ofan occlusal splint as a protectivedevice during sleeping hours.

Adhesions are the formation ofirreversible intra-articular fibrous con-nections between condyles and discsor between the temporal bone anddiscs. These often evolve from adher-ences or follow an intra-articular he-morrhage caused by trauma or asurgical procedure.

Patients with these problems haveabbreviated amplitude of one or moretypes of mandibular movement, de-pending on the site of the adhesion,accompanied by articular noises.

Patients are advised to avoid puttingstress on the TMJ, and given gentlekinesitherapy or physical therapy toassist the condyles in making transla-tional movements, arthroscopic la-vage and debridement of the TMJusing the most advanced techniques.> Subluxation (hyper-translation)

(Fig. 12)In cases of substantial acquired or

systemic ligamentous laxity17 or ofspecial morphological discrepancies ofthe temporal eminence, such as a

short and inclined posterior surface ora long anterior surface, the translationof the condyles is no longer containedand the condyle head may passentirely over the articular tubercle ofthe temporal bone, resulting in atemporomandibular luxation. Thismay be unilateral or bilateral.

When patients can reduce the con-dition themselves, it is described as asubluxation.

When patients with TMJs that aresusceptible to subluxation open theirjaws to the widest extent, a deep dullnoise is heard, which can be confusedwith a sign of disc displacement. Anidentical sound accompanies mouthclosure. The amplitude of mouthopening is exaggerated with a jumpat the maximum point and with a non-rectangular closure.

Therapy is palliative, based on oralbehavioral counseling on the dangersof yawning or eating large morsels offood, and on reinforcement exercisesfor the elevator muscles, the objectiveof which is to limit condylar translation.> True temporomandibular luxa-

tion (mouth-open lockjaw)

When a locked open jaw does notreduce itself spontaneously thismeans the condyle has slipped be-yond the articular eminence of thetemporal bone and the lateral ptery-goid and the masseter muscles havegone into spasm, preventing thepatient from closing their mouth. Thislocked open mouth with moderate tovery intense pain is a clear diagnosticsign. Usually a practitioner using theNelaton maneuver can assist thecondyle in re-integrating itself in themandibular fossa24.



5 – 2 – 3 – Inflammation

Inflammation of the TMJ itself canresult from :– anomalies of the condyle-disc

complex ;– micro- or macro-trauma ;– and, rarely, from an infection.

The inflammation may affect thecapsule (capsulitis), the synovial mem-brane (synovitis), the bi-laminar zoneresponsible for the vascularization andthe innervation of the TMJ (retro-discitis), or osseous tissues (arthritis).> Capsulitis and synovitis

Inflammation of the capsule or thesynovial membrane (it is impossible todistinguish clinically between the two)derives from a series of microtrau-matic incidents, or to a single majortraumatic episode, and suppressesthe functioning of the joint.• Clinical signs

– Pain in extreme mandibular move-ments, opening and maximum con-tralateral excursion.

– Absence of pain in maximal inter-cuspation or in mastication.

– Pain on lateral palpation.• Treatment

– Oral behavior counseling, and ad-vocacy of periods of TMJ rest.

– Prescription of short-term non-ster-oidal or corticosteroid medication.

> Retro-discitis

This inflammation of the retro-disctissue is related to suppression ofTMJ activity and the functional ortraumatic distal position of the headof the condyle.• Clinical signs

– Pain during maximal inter-cuspationocclusion or in mastication.

– Pain on palpation of retro-condylarregion, through external auditorycanal.

• Treatment

– Oral behavior counseling.– Prescription of short-term non-ster-

oidal or corticosteroid medication.– Use of a splint for several to place

the mandible in a slightly moreanterior position.

> Arthritis

This is an inflammatory componentof a degenerative disease affectingthe TMJ (cf. infra).• Clinical signs

– Pain localized in the TMJ duringmandibular movements.

• Treatment

– Oral behavior counseling.– Prescription of short-term non-ster-

oidal or corticosteroid medication.– Use of a decompression orthesis.

5 – 2 – 4 – Degenerative TMD(arthrosis) (Fig. 13)

In this destructive process, thearticular surface of the condyle and/or the articular tubercle of the tempor-al bone are altered due to over-loadingor macro-/micro-trauma to both rightand left TMJ.

Figure 13MRI of a TMJ with condylar arthrosis, showing ananterior osteophytic beak.




The equilibrium between the synth-esis and degradation of extracellularmatrix components controlled bychondrocytes is disturbed, provokinga cartilaginous deterioration that isexpressed biologically by:– swelling and softening of cartilage

(chondromalacia);– the localized deterioration of col-

lagenous fibrils at the interior of thematrix (fibrillation) and an asso-ciated inflammatory responsethrough the liberation of proteolyticenzymes;

– the loss of cartilaginous integritywith puffiness, horizontal fissures,shrinking, and adherences;

– the complete destruction of somecartilage exposing sub-chondralosseous tissue;

– the formation, by remodeling, ofsclerotic osseous tissue.TMJ degenerative disease, accord-

ingly, represents a disturbance of thebalance between degenerative andregenerative processes of cartilage,bone, and synovial fluid, all accompa-nied by secondary inflammatoryphenomena (cf. supra).

6 – DEALING WITH TMD IN THE CLINICAL SETTING

Before beginning any treatment,orthodont ists should establ ishwhether a prospective patient hadpreviously suffered from TMD orpresents any risk factors for its futuredevelopment.

For obvious medicolegal reasons, itis essential that they make a perma-nent record of any articular sounds,anomalies of mandibular movement oraccompanying pain. It is also impera-tive that formal informed consent forthe treatment of any specific clinicalsituation is obtained before strartingtherapy, and, according to Michelotti32,updated every six months during thecourse of treatment.

If signs or symptoms of TMD arepresent, especially painful ones, theclinician must establish a differentialdiagnosis by first excluding any patho-logical entities that are not TMD innature.

The differential diagnosis havingbeen completed, the orthodontistmust now establish a positive, rea-

soned diagnosis, based on the classi-fication system we have discussed indetail.

Management of TMD problemsshould emphasize conservative, rever-sible techniques including modestmedication, counseling, exercises,physical therapy, kinesitherapy31 andocclusal splints25. Michelotti32 sug-gests that orthodontists adopt theinvariable principle of not undertakingorthodontic treatment for patients thatare already in pain. For patients with ahistory of TMD, with or without pain,the disturbances that exist in theirmusculoskeletal system make it highlysusceptible to complications duringany type of occlusal rehabilitation9-36.

After patients have entered a periodof remission from painful symptoms,orthodontists can consider undertak-ing orthodontic treatment, but mustalways be mindful of their specialneeds and risks that include TMJinstability, history of TMD, and apropensity for tooth clenching.



If, during the course of orthodontictreatment, patients develop signs ofTMD, practitioners should treat theseas they would a patient not under-going orthodontic treatment by :– providing all useful information

about the nature of TMD, includingthe fluctuation of its symptoms andthe bewildering variety of forms itmay take. Relying on the advice ofan occlusion specialist, practi-tioners can usually reduce the en-ormity of the episode and reinforcethe explanations provided pre-viously to reassure the patient. Itshould also be possible to acquirethe data needed to make a precisediagnosis and formulate a treat-ment plan that will probably includethe postponement of active ortho-dontic treatment to avoid introdu-

cing possible exacerbating factors.A multi-faceted management plan(cf. supra) may then be instigated.At the conclusion of orthodontic

treatment, the orthodontist shouldpresent TMD patients with an unam-biguous analysis of the specific riskfactors that apply to them, togetherwith behavioral advice and manage-ment techniques specific to thatpatient with the aim of optimizingfunction and minimizing any TMDrelapse.

After therapy, orthodontists shouldintervene promptly to manage anyrecurrence of TMD signs or symp-toms, again establishing a precisediagnosis and managing the TMDproblem no differently than for a‘‘non-orthodontic’’ patient.

7 – CONCLUSION

Orthodontists may be confronted bya TMD problem at any time and mustbe prepared at least to describe itcompletely if not to make a fulldiagnosis.

This responsibility becomes abso-lute when orthodontists undertakeglobal rehabilitation projects that re-quire a valid mandibular referenceposition, centric relation, which isdependent upon the state of themusculoarticular relationship.

By accurately uncovering the originsof an existing malfunction and asses-

sing the risk factors at play, orthodon-tists can adopt an appropriatemanagement stance and modulatethe orthodontic treatment plan toserve the patient’s best interests.Orthodontists must remain vigilant,fully aware of the occlusal situationand ready to adjust occlusion when-ever needed without forgetting theneed to establish a differential diag-nosis that rules out ‘‘non-TMD’’ dis-orders that have the potential to be farmore deleterious.




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