Temporomandibular Disorders: Osteoarthritis

George A. Zarb, B Ch D, DDS, MS,MS, FRCDtC). Dr Odont he, LLD,MD

Professor and Associate DeanClinical Sciences

Professor and HeadProsthodontics

Faculty of DentistryUniversity of TorontoToronto. Ontario. Canada

Gunnar E. Carlsson, LDS. Odont Dr,Dr Odont he

Professor EmeritusFaculty of OdontologyGöteborg UniversityGöteborg, Sweden

Correspondenee to:Dr George A. ZarbFaculty of DentistryUniversity of Toronto124 Edward StreetToronto. OntarioM5G 1G6 CanadaFax: 416-979-9794E-rnsii: g.zarb@ütoronto.ca

The musculoskeletal sysrem may be affected by more than100 different diseases. Several also involve the temporo-mandibular joint (TMJ) and masticatory muscles and are

associared with symptoms of remporomandibular disorders(TMD). Dentists' knowledge in this area has been limited andregrettably beset with problems of definition and reliability of mea-sures. This has compromised the merits of many past reports, sincethe use of diagnostic labels has often verged on overdiagnosls.

In recent years, an emerging body of clinical and basic scienceinformation, conpled with strong academic resolve, has yieldedintellectual rigor in the undersranding and management of TMD.It has also permitted the introduction of a hmited diagnostic clas-sification, which recognizes 3 major groups of TMD diagnosis.^These are: I. muscle diagnoses, II. disc displacements, andIII. arthritis. The Dworkin and LeResche classification is a non-hierarchical one, and it conveniently recognizes the most fre-quently encountered TMD in clinical practice. It was originallyproposed for clinical and epidemiologic research purposes, but ithas proven to be a very useful clinical teaching and patient man-agement tool. This paper reviews salient aspects of Group III, orTMD that are arrhriris-relared.

Osteo- or degenerative arthritis (OA) is a non-inflammatory dis-ease of moveable joints. It is generally regarded as the result of atime-dependent pattern of joint reactions ro injury, rather rhan asa single entity. It is mainly a disease of articular cartilage that pro-duces symptoms in single body joints. It also can affect the TMJs,whose articular surfaces are covered with fibrocartilage rarherthan hyaline carrilage. "While the disease can be crippling, leadingto a vast range of morphologic and functional deformities, ir veryrarely affects the TMJs to such a dramatic extent.

The disease process is characrerized by deterioration and abra-sion of articular cartilage and soft tissue surfaces, the occurrenceof rhickening and remodeling of the underlying bone, and forma-tion of marginal spurs and subarticular "cysts." Such changes arevery common in many joints in older peopie but are often asymp-tomatic. These changes are, however, frequently accompanied bythe superimposition of secondary inflammatory changes, whichcan cause symptoms. It should be emphasized that the generalphysical health of the individual is seldom affected by the disease,in spite of its widespread nature and rhe risk of multiple joititinvolvement. Nevertheless, ir has been stated that OA may

Key words: osteoarthritis, osteoarthrosis, temporomandibulardisorders, clinical management, arthralgia,temporomandibular joint, crepitation

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account for more disability among the elderly thanany other disease, not because individuals with OAare severely disabled, but because the disease isdisabling in so many. Tbis statement sounds par-ticularly ominous when it is considered that OAaffects 1 in 10 Canadians or Americans and that,by age 70, 85% of tbe population is likely to beaffected.

Osteoarthritis has been generally regarded asinevitably progressive once it has become clinicallysymptomatic. More recent findings, however, sup-port the concept of reversibility of OA, and thesooner treatment is started, the more effective itwill be,̂ The progression of severity of TMJ arthri-tis is not known, but it is not regarded as beinglikely to lead to serious disability.

Prevalence

Osteoarthritis is a very common joint disorderthat occurs in all populations and is strongly cor-related with age. Its prevalence varies in differentjoints, wirb autopsy studies revealing that mostindividuals demonstrate macroscopic changes mtheir hip and knee joints. On the other hand, fre-quency of macroscopic OA lesions in TMJautopsy material has varied from 22 to 38%,•"Osteoarthritis occurs more often and is more gen-eralized in women than in men, but this differencedoes not become evident until after age 50,Whereas radiographie and histologie studiesreport a very high prevalence of osteoarthriticchanges, clinical investigations usually find muchlower frequencies of signs and symptoms. Thislack of correlation between structural OA changesand pain and other clinical symptoms has beenemphasized for several joints.

The lack of concordance between structuralchanges and pain also applies to OA of the TMJ.Therefore, reports on the prevalence of O A in theTMJ tend to be confusing, since patients with OAdo not differ from patients with other TMD withrespect to subjective symptoms. This is compli-cated further by a growing recognition of a con-ceptual framework that regards OA as a latesymptomatic stage in a continuum of adaptivejoint changes or a process of joint degeneration.Such symptoms tend to subside on a variable time-dependent basis. "While epidemiologic data onsigns and symptoms of TMD occurrence are read-ily available, a specific focus on OA is lacking.One study reported a 24% prevalence of OA in apopulation of shipyard workers in southernSweden.'' This study did rely, however, on the

assertion that the occurrence of TMJ crepitarionwas a reproducible clinical sign of OA,

Most reported studies on the prevalence of OAbave relied on interpretations of radiograpbicsigns. This method can be inconclusive, sinceincipient or early OA is unlikely to sbow up onconventional TMJ radiographs.^ It appears that asubstantial change in mineralized tissues isrequired for such changes to be recognized radio-graphically. Nevertheless, Boering^ observed radio-graphic cbanges in 86% of individuals under 20years of age, but many of these findings disap-peared with time and were prohably often a resultof remodeling associated with growth and recov-ery or repair. This should have resulted in adapta-tion and normalized function.' Furthermore, theline of demarcation between adaptive jointchanges and degenerative ones is not a very clearone, and in the absence of frank clinical symp-toms, a diagnosis of OA may not be the correctone.*̂ '̂

There is a controversy in the literature withrespect to the prevalence of osseous changes inasymptomatic TMJs, Almost half of a sample of80 symptom-free individuals demonstrated radio-graphic changes, including OA ones in the TMJs.'"Such observations are commonly encountered (onestudy even reported osseous changes in 90% ofTMJs^), and clinical experience also suggests tbefrequent lack of a significant correlation berweenthe presence of symptoms and the degree of radio-graphic changes. In a recent study^ that usedcephalometrically corrected tomograms, minimalflattening of the condyie or eminence was seen in35% of TMJs in asymptomatic persons who hadno arthrographic or magnetic resonance imaging(MRI) evidence of internal derangement. Moreadvanced osseous changes were not seen, and theauthors concluded that minimal flattening is prob-ably of no clinical significance. It appears that OAprevalence is age- and gender-related and notunlike arthritis in other body joints.

Etiology

The etiology of OA is unclear but appears toinclude both systemic and local factors. Someautbors suggest that OA may be a final commonpathway for several joint conditions, includinginflammatory, endocrine, metabolic, developmen-tal, and biomecbanical disorders. Age is clearly apredisposing factor, since both frequency andseverity of the disease appear to increase with age.However, the evidence in favor of functionally

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important, age-dependent alterations in joint tis-sues is not clear-cut. This tends not to support thenotion that aging per se plays a primary etiologicrole. On the other hand, the aging masticatory sys-tem is frequently associated with a high prevalenceof complete and partial edentulism. it is thereforetempting to suggest that it is in this context ofdepleted dentitions and consequent adverse biome-chanical loading that aging's role becomes signifi-cant. This correlation has, however, not been con-vincingly validated.

it has been proposed that OA is analogous tothe process of heart failure, since it reconciles con-cepts of absolute and relative overloading. In theformer, repetitive or abnormal demands (loading)may exceed functional capacity. In the latter, thefunctional capacity is intrinsically reduced,although the loads may be within a normal range.in the cardiac situation, heart failure secondary tohypertension results from an increase in the func-tional demands on essentially healthy tissues.Alternatively, heart failure after myocardial infarc-tion leads to a decrease in the functional capacityof the tissues themselves. Both situations have theircounterparts in the masticatory system; in the for-mer, overload of parafunction can elicit gradualadaptive changes in the TMJs, which can spill overor "cross the threshold""-'^ into OA. in the latteranalogy, a macrotraumatic episode of the TMJ orthe gross insult of sudden loss of molar supportcan render it vulnerable to future demands, withOA developing eventually. The overlap of bothanalogies would, of course, be likely to accelerateor magnify the process, with the earher develop-ment of perhaps more severe signs and symptomsof OA. While this proposed paradigm may appearsomewhat simplistic, it continues to offer a usefulexplanation for the condition as well as a rationalbasis for its clinical management.

Both physicians and dentists have been inclinedto believe that the single most popular etiologicfactor IS increased mechanical loading, althoughOA is known to develop in non-heavy load-bear-ing joints, eg, the sternoclavicular joints. Thereexists good evidence in favor of the TMJs beingexposed to increased load during function. Thisincreased loading may lead to the conversion ofshearing stresses into compressive stresses. Thisoccurs in particular during parafunction, when agreat deal of force acts across a joint—a force res-olution that could very well be influenced by themorphologic state of the dentition. Autopsy evi-dence suggests a strong correlation berween loss ofmolar support and the occurrence of OA, espe-cially in those individuals over 40 years of age.

These studies suffer from the limitations implicit inall correlative studies. However, when the findingsare reconciled with the frequent clinical associa-tion of compromised dentitions and clinical signsand symptoms of OA, the concept of OA as a pro-cess, rather than a disease entity per se, becomesan attractive hypothesis.

While the TMJ appears to demonstrate animpressive adaptive response to morphofunctionalneeds, it is clearly a vulnerable component of themasticatory system. It is vulnerably located; most,if not all, of mandibular movements terminatewith contact between rigid, unyielding enamel sur-faces; and the variable areas of contact surfaces onocclusal tooth morphology offer considerablescope for stress concentration and deflection in theTMJ. Clearly both the macro- and micro-trau-matic episodes that induce |omt tissue changes,which occur at different tissue levels, may becumulative in nature. They become part of thecontinuum of an adaptive response, which mayeventually be exceeded. Clearly the adaptivecapacity of the TMJ is not infinite.'^ Conse-quently, strong convictions still prevail amongdentists, who identif}' various dentally related fac-tors as acting singly or in combination to predis-pose the TMJ ro OA. Differences in jaw morphol-ogy, malocclusion, occlusal discrepancies, chewinghabits, partial edentulism, and parafunction arefrequently indicted. However, it must be empha-sized that strong scientific support for an etiologicrole for any dentally related factors is lacking, eventhough some evidence has been presented."''"

In the absence of conclusive evidence to confirmthis, it cannot be stated that biomechanical factorsalone are causative. The "wear and tear" explana-tion associated with such a notion and especiallywith aging is attractive and popular, and it is sup-ported by several studies, whicb suggest that thereis a link between repeated occupational activitiesand OA in overused joints. Other studies, how-ever, have not been able to verif;' this hypothesis.In this context it can also be mentioned that sev-eral studies on former long-distance runners toevaluate whether they are at an increased risk ofknee OA have given conflicting results. Further-more, individuals believed to be occupationallyprone to OA, eg, pneumatic drillers, parachutists,divers, etc, have not been found to have a higherincidence than the rest of the general population.However, previous major joint injury appears tobe a common cause of OA; and in people withrepeated joint use, for example, as in joggers andrunners, a history of major joint injury seems toincrease the risk of OA.

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For the masticatory system, biomechanical fac-tors such as long-term bruxism and extensiveocclusal wear have been correlated to an increasedrate of TMJ changes. It is not clear, however, ifthese changes were only adaptive, indicatingremodeling, or were really OA ones. Some authorsmaintain that there is no scientific evidence thatthe increased mechanical loading during bruxismshould lead to OA of the TMJ, and clinical experi-ence shows that many bruxists have no signs ofjoint degeneration. Tbe important consideration inthe development of OA may very well be the con-dition of the joint tissues, rather than the impact ofloading. It is therefore presumed that in the patho-logic state, the balance between catabolic andanabolic responses of affected articular tissue isupset, and adaptation yields to disease.'-•'•''

Pathogenesis

Animal experimentation, computer-simulatedmodels, and structural changes resulting from discperforations, displacements, and discectomy'*underscore the very likely fact that the TMJs areload-bearing joints. Furthermore, the articulardiscs appear to afford protection against excessiveloading.-'̂

The work of Radin et al'^ suggests that repeti-tive impulse loading elicits subtle and clinicallyundetectable bone cbanges. Tbese changes consistof an increase in rigidity of subchondral cancellousbone caused by callus formation, secondary to iso-lated trabecular fatigue fractures. The net effect isan impairment in the joint's capacity to dampenpeak dynamic stresses so that damage occurs tothe cartilage. "While Radin et al emphasize theoccurrence of microfractures, which lead to thehardening of subchondral bone and the precipita-tion of lesions in the articular surfaces, otherauthors opt for the conviction that OA starts inthe articular surfaces per sc. Still others claim thatsimultaneous changes occur both on the surfaceand subchondrally."^' Several researchers reportthat the first affected tissue is hyaline cartilage,with the synovial surface of the cartilage undergo-ing fragmentation of the collagen network, achange known as fibrillation. Fibrillation is associ-ated with depletion or degradation of the othermajor cartilage component, the proteoglycanswhich are largely water-binding molecules. It isnot clear whether this change is a cause or a conse-quence of the disease.

A reduction in resistance to shearing and com-pressive forces results, and the tissues become

softer and prone to deformation. If progressive,this process can lead to degradation of the articu-lar soft tissue surface. When degradation productsare produced in large quantities and cannot be effi-ciently resorbed from the joint cavity by tbe syno-vial membrane, an inflammatory response may beelicited and synovitis may develop.^" Sucb aninflammation is a potential cause of pain.However, there are many unanswered questionsrelated to pain in OA. Recent medical literatureproposes mechanical (eg, increased pressure ordestruction) and chemical (eg, inflammatory medi-ators, such as prostaglandins, kinins, and his-tamine) stimuli to various components of the joint(bone, periosteum, synovium, and capsule) andperiarticular structures as possible causes of painin and around osteoartbritic joints.^^ Degenerativecbanges in articular cartilage and synovia might bereflected at the clinical level as impairment of thenormal, freely sliding, low-friction qualities of themajor joint components. It is believed that jointpain and stiffness, as well as reduced mobility, arefrequently a result of secondary inflammation ofthe capsular tissue. Pyrophosphate is also formedin high concentrations in synovia! fluid in jointswith OA. The pyrophosphate combines with cal-cium to form crystals, wbich may elicit an acuteinflammatory response.

A change in function and an increased loadingof the articular tissues of the TMJ, which isassumed to follow loss of molar support, or othermajor changes in the occlusion may stimulateremodeling of tissues. This process involves anincreased synthesis of proteoglycans and a thicken-ing of the soft tissue layer due mainly to cartilageformation, which makes the tissue more resistantto compression forces. Remodeling is frequent inthe posterior-lateral part of the temporal eminenceand in the anterior-lateral part of the condyle,which is supposed to carry the greatest load.- '̂̂ ^

Undifferentiated mesenchymal cells in the proiif-crative layer of the temporal and condylar jointcomponents are thought to play an important partin the remodeling process. The temporomandibu-lar disc, however, lacks this reserve remodelingcapacity and is frequently involved first in OA.̂ ^Long-standing increased compressive forces herelead to thinning, cell necrosis, intercellular matrixdegradation, and eventually perforation. Anincreased vascularization in damaged discs hasbeen observed and interpreted as a sign of anattempt at repair. The thinning of the discincreases the strain on the other opposing compo-nents, and if their adaptability is exceeded, OAdevelops here, too.

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Table 1 Diagnostic Criteria for TMJ Arthralgia, Arthritis, and Arthrosis (Group III TMD)*

Group Symptoms

A. Artbralgia Pain and tenderness in (he ¡oint capsule and/or synovial lining of tbe TWJ, includirig (1) Pgin in one or both jointsites (lateral pole and/or poslenor attachment) during palpation; plus 12) One or more of the following self-reports of pain: pain m the region of tbe joint, pain in tbe joint during máximum unassisted opening, pain in thejoinl dunng assisled opening, pain in the joint during lateral excursion- and (3) For a diagnosis of simple artbral-gia, coarse crepitus must be absent,

B. OsteosMbritis Inflammatory condition within the joint tbat results from a degenerative condition of the joint stnjctures.of tbe TMJ (1) Artbralgia (see A.), plus (2) Either or hoth of: coarse crepitus in the joint, ortomograms that show 1 or

more ol the following: erosion of normal cortical delineation, sclerosis of part or all of the condyie and articulareminence, flattening of joint surfaces, or osteophyte formation,

C. OsteoarthrosLS Degenerative disorder of the |oint in which joint form and structure are abnormal. Includes: (1) Absence of allof tbe TMJ signs of arthralgia, ie, absence of pain in Ihe region of the joint, and absence of pain in the joint on palpation

during maximum unassisted opening and on lateral excursions (see A.), plus (2) Either or both of. coarse crepitusin the [oint. or tomograms showing 1 or more of the following: erosion of normal cortical delineation, sclerosisof part or all of the condyie and articular eminence, flattening of joint surfaces, or osteophyte formation.

•From tJworlun and LeResche': repnnied wilh permission.In making diagnoses of disorders in this group, polyarthrilides, acute traumaiic injuries, and irifeclions in the foini should first be njled out

Different authors have given conflicting answersto the question of where OA changes can first heseen and in which joint component. One study-''indicated that early degenerative changes canoccur with similar frequency, hut not necessarily atthe same time. Thus, sevete changes were observedin the condyie, together with an unaffected tempo-ral component, and vice versa. It was also foundthat there was no complete correlation betweenmicroscopic, macroscopic, and radiologie exami-nation of the same joint components. These find-mgs further illustrate the unclear demarcationbetween remodeling and degeneration processes.^^

The remodeling process can produce macro-scopic changes in the form of the joint withoutsubsequent development of OA; this should bekept m mind in the interpretation of radiographiefindings. In severe cases the combined effect of OAand remodeling will result in a severely deformedjoint with macroscopic hone exposure. However,the hone tissue in such lesions is covered by a thinconnective tissue layer.^'''•^^ This finding mayexplain the fact that bony ankylosis is extremelyrare, even in severe OA,

A synthesis of recent basic research suggests thatthe molecular events that may underlie TMJremodeling and degenerative disease are compiexand poorly understood. Structural changes may bethe result of a series of cascading molecular eventsthat include neuropeptide synthesis and release,generation of free radicals, cytokine synthesis,increased arachidonic acid metabolism, activationof matrix-degrading enzymes, inhibition and/orreduced synthesis of protease inhibitors, andaltered cell-extracellular matrix interactions.''

Diagnosis of Osteoarthritis

The Dworkin and LeResche diagnostic criteria forOA, which includes arthralgia, arthritis, andarthrosis, arc summarized in Table 1.

Clinical Findings

General symptoms of OA include pain or stiffnessin the face and jaws, pain on wide opening, painon chewing, inability to open wide, locking orcatching of the mandihle, and joint noise. Clinicalsigns include tenderness to palpation of the TMJand/or the muscles of mastication, limited or devi-ated mandibular movements, pain with movement,locking or subluxation, and joint sounds. It is clearthat recorded signs and symptoms are very similarto those of other TMD, with some subtle yet sig-nificant exceptions:

1. They almost invariably occur unilaterally.2. Tbe symptoms appear to worsen as tbe day goes

on.3. Pain IS over the joint per se, especially the distal

aspect when the mouth is open.4. Crepitation (crepitus), as distinct from clicking

sounds, is often present, although clicking mayalso be present.

5. Radiographie changes are frequent.

It should be pointed out that other aspects ofTMD can be superimposed upon OA, and that thepain and stiffness are probably due to secondaryinflammation of capsular tissue or the other causesdiscussed previously. The clinical sign of crepitusdeserves some emphasis. It is a grating, grinding,

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Table 2 Development of Signs and Symptoms ofOsteoarthritis in Phases and Stages"'

Pha5c

1. Clicking2. Periodic looking3. TMJ pam at rest4. TMJ pain on function5. Residual symptoms

oiher tinan pain6. Absence of symptoms

Stage

InitialInitialIntermediateintermediateLate

Late

iHecl aftei Rasmussen "[liar some pahents do not ex

eed direcfly to pliflse 3 Furthee or report phjradiographie t

ed charges.hang

or 2 ands do nol

or crunching sound, which may be audible duringopening, but especially during lateral mandibularmovements. It is better palpated than heard, andwhile some aurhors feel that little or no additionalinformation is gained with the use of a stetho-scope, other authors consider it a necessity.

Diagnosis of OA is based on patient history andimaging information. It also has been demon-strated to benefit from the apphcation of specificorthopedic tests, which include active jaw move-ment, passive ]aw opening, and palpation.^' Theactive movement test includes opening, closing,lateral, and prorrLisive movements of the mandiblecarried out by the patient. Passive opening involvesapplication of gentle stretch by the clinician on theincisai edges of rhe maxiiiary and mandibularincisors to increase mandibular opening followingan acrive opening movement. Palpation entailshilateral palpation of masseter and remporalismuscles, rhe insertion of the medial pterygoid mus-cle, and the lateral and dorsal part of the condyle.These tests yield information that can be synthe-sized to identif}' the likely diagnostic subgroup thepatient will fall inro.

Kopp-^ concluded that the presence of crepita-tion differentiated patients with TMJ OA frompatients with masticatory muscle disorders. Healso observed that patients with TMJ OA differedfrom other patients with TMD with respect totheir greater age but not with respect to sex, localsymptoms (except joint sounds), duration of symp-toms, headache, or symptoms in other joints. Thesymptoms of pain and dysfunction could of coursebe an lnrerim phase in a continuum of the trauma/adaptation balance, which seems to underscore thedevelopment of the condition.-**

Rasmussen^^ described the development of thesymptomatology of OA (or temporomandibular

arthropathy, as referred to by the author) in 3stages and 6 phases (Table 2). In the first stage, thediagnosis of OA is difficult to separate from othertypes of TMD, including internal derangement ofthe TMJ, by means of both clinical and radio-graphic examination. In the second or intermediatestage, the TMJ hecomes painful. The last stage isaccompanied by a reduction of symptoms and nor-malization of function, while radiography revealsincreasing deformation and a high frequency ofdisc perforation.^"

Similar interpretations of the mainly favorableprognosis of the long-term development of OA havebeen reported by several authors. A patient illus-trating the varying clinical and radiographie devel-opment of OA is shown in Figs 1 and 2. In spite ofsevere osseous changes, certainly including disc per-foration, a painless function was maintained in thispatient, as it is in most subjects with OA.

The relationship between disc displacement andOA IS controversial, with a frequently reportedopinion that disc displacement causes OA. It hasbeen proposed that internal derangement is a signof OA rather than its cause, and it has been con-cluded that OA is the basic condition that causesTMD. In fact, Stegenga et al proposed a unifyingconcept for TMD in 1989.^' They argued that theTMJ was very similar to other joints in the body,in spite of its unique features; rhat the genesis ofOA in non-calcified tissue (hence not readilyradiographicaliy detectable) is unlikely to be theresulr of an occlusal etiology; that the complex 2-way relationships between OA and disc displace-ments are an acceptable response to the proposalthat rhe latter always leads to the former; and thatextracapsular or myofascial problems are onlysecondary responses to a primary OA process.While such a concept is attractive, it fails toaccount for the entire spectrum of TMD and theiracknowledged multifactorial etiology. None-theless, the Dutch work underscores the very closerelationship between 2 of the 3 utilities describedhy Dworkin and LeResche' and deserves seriousconsideration. A report by Lobbezoo-Scholte etaP^ confirmed that in routine clinical practice,history-taking and conventional radiographyshould be accompanied by a functional examina-tion so as to reduce confusion about an arthroge-nous, myogenous, or combined origin of the dis-order.

The proposed examination would comprise pal-pation, active mandibular movements, and passivejaw opening. This research indicates that the activemovement test was the most powerful for distin-guishing between pairs of diagnostic subgroups.

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Fig 1 A 56-year-old woman with movement pain, palpation tenderness, and crepitation inthe left TMJ and an eventual diagnosis of OA, Slie had experienced long-standing mild tomoderate pain after extensive mouth opening ;ind intensive chewing. Increased problemsafter a locking of the TMJ led to the referral to the T.MD clinic. Reprinted from Zarb andCarisson'" with the permission of Munksgaard,

Fig la [Left] Frontal view of patient indicating location of pain.

Fig lb {Above) Orthopanromogram showing bilateral 30-year-old lossof molars and suggested structural changes of the left TMJ and normaloutline of the right TMJ.

Figs l c and Id Lateral tomo-gratns of the left IMJ, showingextensive deformation, indicatingOA (compare the mainly normalappearance of the right joint in Figlh). {Left] Lateral section. {Right)Central aspect of the joint. Proposedtreatment consisted of a shorrperiod of splint therapy (which thepatient did not like), counseling onthe benign character of OA, and therecommendation to avoid extensivejaw movement. After about 4months the patient had improvedsubstantially and requested no moretreatmem, A follow-up appointmentafter 2 years showed that the patienthad no problems bur still avoidedextensive chewing.

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Figs 2a and 2b Lateral toniograms of the right TMJ of the patient in Fig 1,indicating increased sclerosis and some condylar surface irregularity [left: lat-etai aspect; right: central aspect: of the joint). The patient returned after 8 yearswith movement pain in the nght TMJ after a locking episode of that joint. Theleft joint had crepitation but painless function, and no obvious changes in theradiographie appearance of the left joint occurred during the previous 8 years(see Figs Xc and Id). The treatment consisted of noiisteroidal anti-inflammatorydrugs and information about the condition (the patient did not wish to have asplint). Reprinted from Zarb and Carlsson'" with the permission ofMunksgaard.

Furthermore, palpation and passive opening werealso useful for distinguishing between patients andcontrol subjects, and between arthrogenous andmyogenous patients.

Laboratory Findings

At this particular stage of reporting, laboratoryfindings in TMJ synovial fluid appear to be oflimited value.̂ ^ This is because collection of suchfluid is not routinely practical given the smallquantities available, or the total lack of fluid.Ongoing research has shown that release ofinflammatory mediators is associated with diseaseactivity,^'' and the enzymatic events involved inthe process of OA are being characterized.̂ *^ Theseproducts may be useful markers for the evaluationof cartilage matrix degradation in patients withsuspected OA. On the other hand, these productsmay also be associated with adaptive remodehngchanges and may not be disease process-specific.The interpretation of such evolving monitoringmethods in different genders, age groups, andstages of the disease offers much research scopebut is currently not applicable to OA diagnosis.

Radiologie Findings

There are diverse methods for imaging the TMJs(see Pharoah''), with tomograms being a particu-larly popular technique. In both osteoarthritis andosteoarthrosis of the TMJ, tomographic imagingwill show 1 or more of the following: erosion o£normal cortical delineation, sclerosis of part of orall of the condyle and articular eminence, flatten-ing of joint surfaces, and osteophyte formation(Figs 1 and 2). It must be re-emphasized that 1 ormore of the above changes are frequently found inboth symptomatic and asymptomatic joints (Table1), This fact underscores the significance of theclinician's inability to differentiate between thepresumed stages/changes in the remodeling pro-cess. These changes may be indefinitely asymp-tomatic, or they may culminate in a symptomaticand thus clinical diagnosis of OA (Table 2). TheOA process, confirmed by symptoms and imagingevidence, may then ctoss an asymptomatic thresh-old and linger as a memory of an arthritic orsymptomatic exacerbation.

It is interesting to note that a recent study of thespines of people without back pain found thatnearly two thirds had spinal abnormalities, includ-ing herniated or degenerated discs. In a paper

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published in The New England Journal ofMedicine,'"^ California researcbers concluded tbatin many cases it may be sbeer coincidence, notcause and effect, wben a person witb back pain isfound to have an abnormal disc. The dental litera-ture indicates that a similar conclusion may be rel-evant for OA of the TMJ.

Management of Osteoarthritis

The apparent multifactorial etiology of TMDdemands an eclectic approacb to tbeir manage-ment. Wbile the general features of this proposedstrategy can, with selected modifications, beapplied to all 3 major encountered disorders (seeStohler and Zarb^ ), we have fine-tuned tbeapproach here to address the specific managementof OA. A proposed therapeutic approach includes(1) symptomatic treatment, (2} control or reduc-tion of contributory or predisposing factors, and(3) treatment of pathologic sequelae. An importantoverall consideration is the generally favorableprognosis of OA.

Symptomatic Treatment

Tbis comprises a formula of 3 general items:patient reassurance, medication, and physical ther-apy. Reassurance demands a sympatheric dentist, asimple explanation of the problem and its possiblemultifactorial etiology, and a carefully explainedand justified course of treatment. If OA is diag-nosed, then it should be explained tbat symptomsmay worsen before they improve, although in mostcases the joint will eventually "'heai" or recover. Auseful way of illustrating this is to draw a well-shaped graph or curve, which will assist in e.xplain-ing tbe prognosis of the condition^^ (Fig 3). It isconceded to the patient that ar the time of consul-tation it may be difficult to assess tbe patient's pre-cise position on tbe curve. Therefore, if the OA sta-tus is at point A, a period of deterioration willprecede improvement; if on the other hand it is atpoint B, the condition is well on its way to gettingbetter. It must be stressed, however, tbat withproper management, progress is frequently in thesame direction, from left to right. Fortunately, OApatients with TMJ involvement do not appear tosuffer from significant functional jaw problems,and it is only acute TMJ pain episodes that tend tonecessitate active intervention.

Medication- Pain relief forms a major part oftreatment, and all patients with joint pain shouldbe provided with a regular background of

Fig 3 A sitniLit graph may be used to explain the patern of OA behavior (after Ogus atid Toller̂ )̂.

analgesics. It should be pointed out, however, thatthere is no evidence to suggest that the natural his-tory of OA is significantly affected by these drugs,nor, incidentally, tbat those who feel little painbecause of a high pain tbreshold fare any worsethan others. The ratio of hazard to therapeuticeffectiveness of many of the available drugs ishigher than in most other diseases, so that goodjudgment in the choice of treatment is required.Occasionally, specific anti-arthritic preparationsare used. In patients with severe pain, intra-articu-lar injections of anti-inflammatory agents may beused.

Physical Therapy. Rest, acbieved via voluntaryor imposed immobilization; heat; and remedialmuscle exercises are likely modalities included in aphysical therapy regimen. Tissue rest is a func-tional tenet of arthritic therapy, and with the TMJIt can be achieved by varying degrees of controlledjoint immobilization, ranging from a soft diet andvoluntary avoidance of excessive mandibularmovement, to infrequent use of interarcb elasticsfor very short periods of time (3 to 5 weeks). Suchrelative jaw immobilization fulfills the objective ofprotection from "weight bearing" during mastica-tion, although it is probably not useful in theavoidance of other and probably more importanttraumatic activity, eg, bruxism. Pain seldom arisesspontaneously from the rested symptomatic joint;it is usually due to some form of overload ortrauma (typically minor) to which the joint is par-ticulariy vulnerable. This may be a stretching or"strain" of some soft tissue joint component, a

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subchondral bone trabecular fracture, or a mppmgof structures between the articular-hearing surface,or else capsule tension when the range of move-ment exceeds certain limits. The summation of allthese minor episodes may suggest a continuousprocess, but careful history-taking will usuallyreveal the episodic nature of the symptoms. Heator short-wave diathermy or ultrasonic treatmentmay he useful adjuncts in the relief of pain andmuscle sriffness. Seif-massage of adjacent muscula-ture and joints per se, when tolerated, is alsoreported to be helpful, particularly since it is soeasily carried out. The value of the more sophisti-cated techniques may be partly psychologic, in thatthe patient is made to feel that a great deal is beingdone to ease the discornfort.

The rationale for remedial e.verciscs is to pro-mote normal mandibular function. Several jawexercises have been proposed, and they all seem toaim at achieving (1) the strengthening of the mus-cle groups controlling affected joints, (21 the pre-vention of future overloading or abuse to thejoints, and (3) re-education in the use of damagedjoints.

Control or Reduction of Contributory orPredisposing Factors

Strong anecdotal evidence suggests that overloadfrom parafunction and/or biomechanical factorsare contributory to OA, Consequently, limiteddental initiatives, such as consideration of restora-tion of missing molar support, may he of primaryconcern to the denrist. Clinical impressions suggestthe miportance of restoration and maintenance ofa functional occlusion, which includes bilateraland an adequate number of centric stops. Thisobjective may require the fabrication of a stabiliza-tion appliance or a removable provisional prosthe-sis to restore unsupported or inadequate posteriordentitions. There is, however, a lack of evidence tosupport che claim that occlusal therapy per se is ofvalue in the treatment of OA, since a subtle butprofound difference exists hetween the prescrip-tion of a stabilization appliance, which presumablyalleviates intracapsular effusion in an arthriticjoint, and occlusal therapy. The presumed objec-tive of a stabilization appliance is to reheve jointpressure in OA, aithough there is no evidence tofully support this. The accompanying ensuinguneven interocclusal relationship (which is change-able in the context of reduction in the interarticu-lar inflammation) can then be easily modified onthe acrylic resin splint surface in response to effu-sion changes. This is not unlike the effect of differ-

ent bandaging techniques as an adjunct to ortho-pedic management.

It should also be emphasized rhat the notion ofshortened dental arches (eg, bilateral stable quad-rant reiationsbips with exclusive bicuspid support)does not appear to automatically imply anincreased vulnerability to OA,'* On the otherhand, Pullingcr and Seligman""' referred ro a possi-ble correlation between age, number of opposingposterior occlusal units, and occurrence of OAsymptoms.

The hite plane or interocclusal stabilizationappliance is therefore particularly useful in amechanical orthopedic sense, as well as in itsestablished role in the reduction of nocrurnal andpossibly diurnal bruxism. Its versatility is such thatit can be designed both to replace missing poste-rior teeth and to provide an optimal verticaldimension of occlusion. This becomes particularlyapt if parafunction is identified as being a con-tributing etiologic factor. When dental methodsappear to he inadequate, help from alhcd profes-sionals should be prescribed for these patients.

Treatment of Pathologic Sequelae

Most TMD resolve spontaneously or are directedto an earlier resolution via the previouslydescribed interventions. The nature of OA sug-gests a variable symptomatic progression that usu-ally "burns out" in 12 to 24 months. This hasalso been interpreted as more or less completerepair or resolution of symptoms within 1 to 2years.*" Osteoarthritie lesions appear ro increaseslowly and are frequently asymptomatic.Symptomatic exacerbations appear to be self-lim-itmg, and the previously outlined treatment strate-gies are supportive in nature and usuaiiy provideadequate relief. Above all, these methods aim atminimizing functional disturbances by controllingthe risk of overloading or traumatizing the joint.On the other hand, some patients do end up withprolonged discomfort and intracrable pain, proba-bly as a result of provoked tissue changes that arehy that point clearly pathologic. Such irreversiblesequelae are sometimes considered treatable onlyby TMJ surgery. While few authors have givenspecific criteria for patient selection for surgicaltreatment, it seems reasonable to concede that asmall percentage of patients will benefit from sur-gical intervention if the cause is overt TMJ dis-ease. The surgical procedures that have been mostfrequently employed are condylectomy, condylo-tomy, discectomy and, more recently, disc repairrather than disc removal (for review see

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Outcome studies of discectomy performed onstrict indications have shown excellent long-termresults."'"' The prognosis after disc repair has notbeen so favorable, ar least when contributory orpredisposing factors have been inadequarely con-trolled."'"'

Current—albeit incomplete—understanding ofthe pathogenesis of OA and in particular the gene-sis of disc displacements provides rhe clinicianwith more of a rarionale for avoiding surgery ar allcosts. This should be tempered with the recogni-tion that improved diagnosis and underst.mding ofTMJ disease necessitates recognition of the infre-quent yet indispensable role to be played bysurgery.

Some authors"*-̂ counsel the use of intra-arricularinjections of anti-inflammatory medications intothe TMJs of patients who do not respond to con-servative treatment. Both short- and long-termresults of single injections of corticosteroids havebeen reported to be successful in efficient painreduction, normalized joint function, and noradiographie signs of advanced joint destruction infollow-ups of more than 8 years."'̂ An alrernariveagenr, wirh probably fewer side effects, is sodiumhyaluronate. This drug bas also been shown togive a significant short- and long-term reduction ofsubjective symptoms and clinical signs in patientswith persistent TMJ problems that had notresponded to conservative treatment.''^

Conclusions

The presumed time-dependent implications offunctional or parafunctional loading may elicitadaptive and ultimately even degenerative changesin the TMJs. Under certain conditions—geneticpredispositions, trauma, dental morphologicdefects, etc—the adaptive or degenerative changesmay cross the threshold from an asymptomaticstate into a symptomatic one. In a clinical contextit is prudent to regard such joint pain as the lastlink in a long chain of events and to try to deter-mine where stress or stresses on an affected jointcan be reduced or eliminated. Non-drug treatmentseeks to reduce joint overload so rhat healing canoccur; consequently, rest and exercise are regardedas an important part of a self-care strategy. It isalso believed that provisional and reversible dentalinterventions (such as appliance therapy orrestoration of posterior occlusal support) may pro-duce long-range benefits. This sort of prostbodon-tic intervention is particularly popular as definitivetreatment, but has not yet been conclusively shown

to be effective in well-controlled clinical trials. It iswell documented, however, that OA may not bean irreversible disorder, and while its signs andsymptoms fluctuate, they tend to decrease withtime and will gradually and frequently disappear.The long-rerm clinical prognosis of OA is usuallyfavorable, in spite of regularly observed severeradiographie changes.

In rhe absence of an experimental animal modelro test hypotheses of disease etiology, we continueto rely on inferences and observations. The latterhave stood us in good rherapeutic stead, particu-larly when clinical discretion and prudence lead tothe avoidance of irreversible dental reconsrructiveprocedures.

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