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Home , Osteoarthritis

Temporomandibular Disorders: Osteoarthritis

George A. Zarb, B Ch D, DDS, MS, MS, FRCDtC). Dr Odont he, LLD, he musculoskeletal sysrem may be affected by more than MD 100 different . Several also involve the temporo- Professor and Associate Dean Tmandibular (TMJ) and masticatory muscles and are Clinical Sciences associared with symptoms of remporomandibular disorders (TMD). Dentists' knowledge in this area has been limited and Professor and Head regrettably beset with problems of definition and reliability of mea- Prosthodontics sures. This has compromised the merits of many past reports, since the use of diagnostic labels has often verged on overdiagnosls. Faculty of Dentistry In recent years, an emerging body of clinical and basic science University of Toronto information, conpled with strong academic resolve, has yielded Toronto. Ontario. Canada intellectual rigor in the undersranding and management of TMD. It has also permitted the introduction of a hmited diagnostic clas- Gunnar E. Carlsson, LDS. Odont Dr, sification, which recognizes 3 major groups of TMD diagnosis.^ Dr Odont he Professor Emeritus These are: I. muscle diagnoses, II. disc displacements, and Faculty of Odontology III. . The Dworkin and LeResche classification is a non- Göteborg University hierarchical one, and it conveniently recognizes the most fre- Göteborg, Sweden quently encountered TMD in clinical practice. It was originally proposed for clinical and epidemiologic research purposes, but it Correspondenee to: has proven to be a very useful clinical teaching and patient man- Dr George A. Zarb agement tool. This paper reviews salient aspects of Group III, or Faculty of Dentistry TMD that are arrhriris-relared. University of Toronto Osteo- or degenerative arthritis (OA) is a non-inflammatory dis- 124 Edward Street ease of moveable . It is generally regarded as the result of a Toronto. Ontario time-dependent pattern of joint reactions ro , rather rhan as M5G 1G6 Canada a single entity. It is mainly a of articular that pro- Fax: 416-979-9794 E-rnsii: g.zarb@ütoronto.ca duces symptoms in single body joints. It also can affect the TMJs, whose articular surfaces are covered with fibrocartilage rarher than hyaline carrilage. "While the disease can be crippling, leading to a vast range of morphologic and functional deformities, ir very rarely 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 occurrence of rhickening and remodeling of the underlying , and forma- tion of marginal spurs and subarticular "cysts." Such changes are very common in many joints in older peopie but are often asymp- tomatic. These changes are, however, frequently accompanied by the superimposition of secondary inflammatory changes, which can cause symptoms. It should be emphasized that the general physical health of the individual is seldom affected by the disease, in spite of its widespread nature and rhe risk of multiple joitit involvement. Nevertheless, ir has been stated that OA may

Key words: osteoarthritis, osteoarthrosis, temporomandibular disorders, clinical management, , , crepitation

J OROFAC 1999;13:295-3OÈ.

Journal of Orofacial Pain 295 Zarb/Carisson

account for more among the elderly than assertion that the occurrence of TMJ crepitarion any other disease, not because individuals with OA was a reproducible clinical sign of OA, are severely disabled, but because the disease is Most reported studies on the prevalence of OA disabling in so many. Tbis statement sounds par- bave relied on interpretations of radiograpbic ticularly ominous when it is considered that OA signs. This method can be inconclusive, since affects 1 in 10 Canadians or Americans and that, incipient or early OA is unlikely to sbow up on by age 70, 85% of tbe population is likely to be conventional TMJ radiographs.^ It appears that a affected. substantial change in mineralized tissues is Osteoarthritis has been generally regarded as required for such changes to be recognized radio- inevitably progressive once it has become clinically graphically. Nevertheless, Boering^ observed radio- symptomatic. More recent findings, however, sup- graphic cbanges in 86% of individuals under 20 port the concept of reversibility of OA, and the years of age, but many of these findings disap- sooner treatment is started, the more effective it peared with time and were prohably often a result will be,^ The progression of severity of TMJ arthri- of remodeling associated with growth and recov- tis is not known, but it is not regarded as being ery or repair. This should have resulted in adapta- likely to lead to serious disability. tion and normalized function.' Furthermore, the line of demarcation between adaptive joint changes and degenerative ones is not a very clear Prevalence one, and in the absence of frank clinical symp- toms, a diagnosis of OA may not be the correct Osteoarthritis is a very common joint disorder one.*^'^ that occurs in all populations and is strongly cor- There is a controversy in the literature with related with age. Its prevalence varies in different respect to the prevalence of osseous changes in joints, wirb autopsy studies revealing that most asymptomatic TMJs, Almost half of a sample of individuals demonstrate macroscopic changes m 80 symptom-free individuals demonstrated radio- their and joints. On the other hand, fre- graphic changes, including OA ones in the TMJs.'" quency of macroscopic OA lesions in TMJ Such observations are commonly encountered (one autopsy material has varied from 22 to 38%,•" study even reported osseous changes in 90% of Osteoarthritis occurs more often and is more gen- TMJs^), and clinical experience also suggests tbe eralized in women than in men, but this difference frequent lack of a significant correlation berween does not become evident until after age 50, the presence of symptoms and the degree of radio- Whereas radiographie and histologie studies graphic changes. In a recent study^ that used report a very high prevalence of osteoarthritic cephalometrically corrected tomograms, minimal changes, clinical investigations usually find much flattening of the condyie or eminence was seen in lower frequencies of . This lack of correlation between structural OA changes 35% of TMJs in asymptomatic persons who had and pain and other clinical symptoms has been no arthrographic or magnetic resonance imaging emphasized for several joints. (MRI) evidence of internal derangement. More advanced osseous changes were not seen, and the The lack of concordance between structural authors concluded that minimal flattening is prob- changes and pain also applies to OA of the TMJ. ably of no clinical significance. It appears that OA Therefore, reports on the prevalence of O A in the prevalence is age- and gender-related and not TMJ tend to be confusing, since patients with OA unlike arthritis in other body joints. do not differ from patients with other TMD with respect to subjective symptoms. This is compli- cated further by a growing recognition of a con- Etiology ceptual framework that regards OA as a late symptomatic stage in a continuum of adaptive joint changes or a process of joint degeneration. The etiology of OA is unclear but appears to Such symptoms tend to subside on a variable time- include both systemic and local factors. Some dependent basis. "While epidemiologic data on autbors suggest that OA may be a final common signs and symptoms of TMD occurrence are read- pathway for several joint conditions, including ily available, a specific focus on OA is lacking. inflammatory, endocrine, metabolic, developmen- One study reported a 24% prevalence of OA in a tal, and biomecbanical disorders. Age is clearly a population of shipyard workers in southern predisposing factor, since both frequency and Sweden.'' This study did rely, however, on the severity of the disease appear to increase with age. However, the evidence in favor of functionally

296 Volume 13, Number 4, 1999 Zarb/Csrisson important, age-dependent alterations in joint tis- These studies suffer from the limitations implicit in sues is not clear-cut. This tends not to support the all correlative studies. However, when the findings notion that aging per se plays a primary etiologic are reconciled with the frequent clinical associa- role. On the other hand, the aging masticatory sys- tion of compromised dentitions and clinical signs tem is frequently associated with a high prevalence and symptoms of OA, the concept of OA as a pro- of complete and partial edentulism. it is therefore cess, rather than a disease entity per se, becomes tempting to suggest that it is in this context of an attractive hypothesis. depleted dentitions and consequent adverse biome- While the TMJ appears to demonstrate an chanical loading that aging's role becomes signifi- impressive adaptive response to morphofunctional cant. This correlation has, however, not been con- needs, it is clearly a vulnerable component of the vincingly validated. masticatory system. It is vulnerably located; most, it has been proposed that OA is analogous to if not all, of mandibular movements terminate the process of heart failure, since it reconciles con- with contact between rigid, unyielding enamel sur- cepts of absolute and relative overloading. In the faces; and the variable areas of contact surfaces on former, repetitive or abnormal demands (loading) occlusal tooth morphology offer considerable may exceed functional capacity. In the latter, the scope for stress concentration and deflection in the functional capacity is intrinsically reduced, TMJ. Clearly both the macro- and micro-trau- although the loads may be within a normal range. matic episodes that induce |omt tissue changes, in the cardiac situation, heart failure secondary to which occur at different tissue levels, may be hypertension results from an increase in the func- cumulative in nature. They become part of the tional demands on essentially healthy tissues. continuum of an adaptive response, which may Alternatively, heart failure after myocardial infarc- eventually be exceeded. Clearly the adaptive tion leads to a decrease in the functional capacity capacity of the TMJ is not infinite.'^ Conse- of the tissues themselves. Both situations have their quently, strong convictions still prevail among counterparts in the masticatory system; in the for- dentists, who identif}' various dentally related fac- mer, overload of parafunction can elicit gradual tors as acting singly or in combination to predis- adaptive changes in the TMJs, which can spill over pose the TMJ ro OA. Differences in jaw morphol- or "cross the threshold""-'^ into OA. in the latter ogy, malocclusion, occlusal discrepancies, chewing analogy, a macrotraumatic episode of the TMJ or habits, partial edentulism, and parafunction are the gross insult of sudden loss of molar support frequently indicted. However, it must be empha- can render it vulnerable to future demands, with sized that strong scientific support for an etiologic OA developing eventually. The overlap of both role for any dentally related factors is lacking, even analogies would, of course, be likely to accelerate though some evidence has been presented."''" or magnify the process, with the earher develop- In the absence of conclusive evidence to confirm ment of perhaps more severe signs and symptoms this, it cannot be stated that biomechanical factors of OA. While this proposed paradigm may appear alone are causative. The "wear and tear" explana- somewhat simplistic, it continues to offer a useful tion associated with such a notion and especially explanation for the condition as well as a rational with aging is attractive and popular, and it is sup- basis for its clinical management. ported by several studies, whicb suggest that there Both physicians and dentists have been inclined is a link between repeated occupational activities to believe that the single most popular etiologic and OA in overused joints. Other studies, how- factor IS increased mechanical loading, although ever, have not been able to verif;' this hypothesis. OA is known to develop in non-heavy load-bear- In this context it can also be mentioned that sev- ing joints, eg, the sternoclavicular joints. There eral studies on former long-distance runners to exists good evidence in favor of the TMJs being evaluate whether they are at an increased risk of exposed to increased load during function. This knee OA have given conflicting results. Further- increased loading may lead to the conversion of more, individuals believed to be occupationally shearing stresses into compressive stresses. This prone to OA, eg, pneumatic drillers, parachutists, occurs in particular during parafunction, when a divers, etc, have not been found to have a higher great deal of force acts across a joint—a force res- incidence than the rest of the general population. olution that could very well be influenced by the However, previous major joint injury appears to morphologic state of the dentition. Autopsy evi- be a common cause of OA; and in people with dence suggests a strong correlation berween loss of repeated joint use, for example, as in joggers and molar support and the occurrence of OA, espe- runners, a history of major joint injury seems to cially in those individuals over 40 years of age. increase the risk of OA.

Joumal of Orofacial Pain 297 Zarb/Carlsson

For the masticatory system, biomechanical fac- softer and prone to deformation. If progressive, tors such as long-term bruxism and extensive this process can lead to degradation of the articu- occlusal wear have been correlated to an increased lar soft tissue surface. When degradation products rate of TMJ changes. It is not clear, however, if are produced in large quantities and cannot be effi- these changes were only adaptive, indicating ciently resorbed from the joint cavity by tbe syno- remodeling, or were really OA ones. Some authors vial membrane, an inflammatory response may be maintain that there is no scientific evidence that elicited and may develop.^" Sucb an the increased mechanical loading during bruxism is a potential cause of pain. should lead to OA of the TMJ, and clinical experi- However, there are many unanswered questions ence shows that many bruxists have no signs of related to pain in OA. Recent medical literature joint degeneration. Tbe important consideration in proposes mechanical (eg, increased pressure or the development of OA may very well be the con- destruction) and chemical (eg, inflammatory medi- dition of the joint tissues, rather than the impact of ators, such as prostaglandins, kinins, and his- loading. It is therefore presumed that in the patho- tamine) stimuli to various components of the joint logic state, the balance between catabolic and (bone, periosteum, synovium, and capsule) and anabolic responses of affected articular tissue is periarticular structures as possible causes of pain upset, and adaptation yields to disease.'-•'•'' in and around osteoartbritic joints.^^ Degenerative cbanges in articular cartilage and synovia might be reflected at the clinical level as impairment of the Pathogenesis normal, freely sliding, low-friction qualities of the major joint components. It is believed that joint Animal experimentation, computer-simulated pain and stiffness, as well as reduced mobility, are models, and structural changes resulting from disc frequently a result of secondary inflammation of perforations, displacements, and discectomy'* the capsular tissue. Pyrophosphate is also formed underscore the very likely fact that the TMJs are in high concentrations in synovia! fluid in joints load-bearing joints. Furthermore, the articular with OA. The pyrophosphate combines with cal- discs appear to afford protection against excessive cium to form crystals, wbich may elicit an acute loading.-'^ inflammatory response. The work of Radin et al'^ suggests that repeti- A change in function and an increased loading tive impulse loading elicits subtle and clinically of the articular tissues of the TMJ, which is undetectable bone cbanges. Tbese changes consist assumed to follow loss of molar support, or other of an increase in rigidity of subchondral cancellous major changes in the occlusion may stimulate bone caused by callus formation, secondary to iso- remodeling of tissues. This process involves an lated trabecular fatigue fractures. The net effect is increased synthesis of and a thicken- an impairment in the joint's capacity to dampen ing of the soft tissue layer due mainly to cartilage peak dynamic stresses so that damage occurs to formation, which makes the tissue more resistant the cartilage. "While Radin et al emphasize the to compression forces. Remodeling is frequent in occurrence of microfractures, which lead to the the posterior-lateral part of the temporal eminence hardening of subchondral bone and the precipita- and in the anterior-lateral part of the condyle, tion of lesions in the articular surfaces, other which is supposed to carry the greatest load.-^'^^ authors opt for the conviction that OA starts in Undifferentiated mesenchymal cells in the proiif- the articular surfaces per sc. Still others claim that crative layer of the temporal and condylar joint simultaneous changes occur both on the surface components are thought to play an important part and subchondrally."^' Several researchers report in the remodeling process. The temporomandibu- that the first affected tissue is , lar disc, however, lacks this reserve remodeling with the synovial surface of the cartilage undergo- capacity and is frequently involved first in OA.^^ ing fragmentation of the network, a Long-standing increased compressive forces here change known as fibrillation. Fibrillation is associ- lead to thinning, cell necrosis, intercellular matrix ated with depletion or degradation of the other degradation, and eventually perforation. An major cartilage component, the proteoglycans increased vascularization in damaged discs has which are largely water-binding molecules. It is been observed and interpreted as a sign of an not clear whether this change is a cause or a conse- attempt at repair. The thinning of the disc quence of the disease. increases the strain on the other opposing compo- A reduction in resistance to shearing and com- nents, and if their adaptability is exceeded, OA pressive forces results, and the tissues become develops here, too.

293 Volume 13, Number 4. 1999 Zarb/Csrisson

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 joint sites (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 the joinl dunng assisled opening, pain in the joint during lateral excursion- and (3) For a diagnosis of simple artbral- gia, coarse 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 articular eminence, flattening of joint surfaces, or formation, C. OsteoarthrosLS Degenerative disorder of the |oint in which joint form and structure are abnormal. Includes: (1) Absence of all of 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 crepitus in the [oint. or tomograms showing 1 or more of the following: erosion of normal cortical delineation, sclerosis of 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 , and irifeclions in the foini should first be njled out

Different authors have given conflicting answers Diagnosis of Osteoarthritis to the question of where OA changes can first he seen and in which joint component. One study-'' The Dworkin and LeResche diagnostic criteria for indicated that early degenerative changes can OA, which includes arthralgia, arthritis, and occur with similar frequency, hut not necessarily at arthrosis, arc summarized in Table 1. the same time. Thus, sevete changes were observed in the condyie, together with an unaffected tempo- Clinical Findings ral component, and vice versa. It was also found that there was no complete correlation between General symptoms of OA include pain or stiffness microscopic, macroscopic, and radiologie exami- in the face and jaws, pain on wide opening, pain nation of the same joint components. These find- on chewing, inability to open wide, locking or mgs further illustrate the unclear demarcation catching of the mandihle, and joint noise. Clinical between remodeling and degeneration processes.^^ signs include tenderness to palpation of the TMJ The remodeling process can produce macro- and/or the muscles of mastication, limited or devi- scopic changes in the form of the joint without ated mandibular movements, pain with movement, subsequent development of OA; this should be locking or , and joint sounds. It is clear kept m mind in the interpretation of radiographie that recorded signs and symptoms are very similar findings. In severe cases the combined effect of OA to those of other TMD, with some subtle yet sig- and remodeling will result in a severely deformed nificant exceptions: joint with macroscopic hone exposure. However, 1. They almost invariably occur unilaterally. the hone tissue in such lesions is covered by a thin 2. Tbe symptoms appear to worsen as tbe day goes connective tissue layer.^'''•^^ This finding may on. explain the fact that bony is extremely 3. Pain IS over the joint per se, especially the distal rare, even in severe OA, aspect when the mouth is open. A synthesis of recent basic research suggests that 4. Crepitation (crepitus), as distinct from clicking the molecular events that may underlie TMJ sounds, is often present, although clicking may remodeling and are compiex also be present. and poorly understood. Structural changes may be 5. Radiographie changes are frequent. the result of a series of cascading molecular events that include neuropeptide synthesis and release, It should be pointed out that other aspects of generation of free radicals, cytokine synthesis, TMD can be superimposed upon OA, and that the increased arachidonic acid metabolism, activation pain and stiffness are probably due to secondary of matrix-degrading enzymes, inhibition and/or inflammation of capsular tissue or the other causes reduced synthesis of protease inhibitors, and discussed previously. The clinical sign of crepitus altered cell-extracellular matrix interactions.'' deserves some emphasis. It is a grating, grinding,

Joumal of Orofacial Pain 299 Zarb/Carl s son

Table 2 Development of Signs and Symptoms of , as referred to by the author) in 3 Osteoarthritis in Phases and Stages"' stages and 6 phases (Table 2). In the first stage, the diagnosis of OA is difficult to separate from other Stage Pha5c types of TMD, including internal derangement of 1. Clicking Initial the TMJ, by means of both clinical and radio- 2. Periodic looking Initial graphic examination. In the second or intermediate 3. TMJ pam at rest Intermediate 4. TMJ pain on function intermediate stage, the TMJ hecomes painful. The last stage is 5. Residual symptoms Late accompanied by a reduction of symptoms and nor- oiher tinan pain malization of function, while reveals 6. Absence of symptoms Late increasing deformation and a high frequency of iHecl aftei Rasmussen " disc perforation.^" [liar some pahents do not ex e or report phj or 2 and eed direcfly to pliflse 3 Furthe radiographie t hang s do nol Similar interpretations of the mainly favorable ed charges. prognosis of the long-term development of OA have been 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 of severe osseous changes, certainly including disc per- or crunching sound, which may be audible during foration, a painless function was maintained in this opening, but especially during lateral mandibular patient, as it is in most subjects with OA. movements. It is better palpated than heard, and The relationship between disc displacement and while some aurhors feel that little or no additional OA IS controversial, with a frequently reported information is gained with the use of a stetho- opinion that disc displacement causes OA. It has scope, other authors consider it a necessity. been proposed that internal derangement is a sign Diagnosis of OA is based on patient history and of OA rather than its cause, and it has been con- imaging information. It also has been demon- cluded that OA is the basic condition that causes strated to benefit from the apphcation of specific TMD. In fact, Stegenga et al proposed a unifying orthopedic tests, which include active jaw move- concept for TMD in 1989.^' They argued that the ment, passive ]aw opening, and palpation.^' The TMJ was very similar to other joints in the body, active movement test includes opening, closing, in spite of its unique features; rhat the genesis of lateral, and prorrLisive movements of the mandible OA in non-calcified tissue (hence not readily carried out by the patient. Passive opening involves radiographicaliy detectable) is unlikely to be the application of gentle stretch by the clinician on the resulr of an occlusal etiology; that the complex 2- incisai edges of rhe maxiiiary and mandibular way relationships between OA and disc displace- incisors to increase mandibular opening following ments are an acceptable response to the proposal an acrive opening movement. Palpation entails that rhe latter always leads to the former; and that hilateral palpation of masseter and remporalis muscles, rhe insertion of the medial pterygoid mus- extracapsular or myofascial problems are only cle, and the lateral and dorsal part of the condyle. secondary responses to a primary OA process. These tests yield information that can be synthe- While such a concept is attractive, it fails to sized to identif}' the likely diagnostic subgroup the account for the entire spectrum of TMD and their patient will fall inro. acknowledged multifactorial etiology. None- theless, the Dutch work underscores the very close Kopp-^ concluded that the presence of crepita- relationship between 2 of the 3 utilities described tion differentiated patients with TMJ OA from hy Dworkin and LeResche' and deserves serious patients with masticatory muscle disorders. He consideration. A report by Lobbezoo-Scholte et also observed that patients with TMJ OA differed aP^ confirmed that in routine clinical practice, from other patients with TMD with respect to history-taking and conventional radiography their greater age but not with respect to sex, local should be accompanied by a functional examina- symptoms (except joint sounds), duration of symp- tion so as to reduce confusion about an arthroge- toms, headache, or symptoms in other joints. The nous, myogenous, or combined origin of the dis- symptoms of pain and dysfunction could of course order. be an lnrerim phase in a continuum of the trauma/ adaptation balance, which seems to underscore the The proposed examination would comprise pal- development of the condition.-** pation, active mandibular movements, and passive jaw opening. This research indicates that the active Rasmussen^^ described the development of the movement test was the most powerful for distin- symptomatology of OA (or temporomandibular guishing between pairs of diagnostic subgroups.

300 Volume 13, Number 4. 1999 Zarb/Carlsson

Fig 1 A 56-year-old woman with movement pain, palpation tenderness, and crepitation in the left TMJ and an eventual diagnosis of OA, Slie had experienced long-standing mild to moderate pain after extensive mouth opening ;ind intensive chewing. Increased problems after a locking of the TMJ led to the referral to the T.MD clinic. Reprinted from Zarb and Carisson'" 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 loss of molars and suggested structural changes of the left TMJ and normal outline of the right TMJ.

Figs lc and Id Lateral tomo- gratns of the left IMJ, showing extensive deformation, indicating OA (compare the mainly normal appearance of the right joint in Fig lh). {Left] Lateral section. {Right) Central aspect of the joint. Proposed treatment consisted of a shorr period of splint therapy (which the patient did not like), counseling on the benign character of OA, and the recommendation to avoid extensive jaw movement. After about 4 months the patient had improved substantially and requested no more treatmem, A follow-up appointment after 2 years showed that the patient had no problems bur still avoided extensive chewing.

Journal of Orofaciai Pain 301 Zarb/Carlsson

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 years with movement pain in the nght TMJ after a locking episode of that joint. The left joint had crepitation but painless function, and no obvious changes in the radiographie appearance of the left joint occurred during the previous 8 years (see Figs Xc and Id). The treatment consisted of noiisteroidal anti-inflammatory drugs and information about the condition (the patient did not wish to have a splint). Reprinted from Zarb and Carlsson'" with the permission of Munksgaard.

Furthermore, palpation and passive opening were Radiologie Findings also useful for distinguishing between patients and control subjects, and between arthrogenous and There are diverse methods for imaging the TMJs myogenous patients. (see Pharoah''), with tomograms being a particu- larly popular technique. In both osteoarthritis and Laboratory Findings osteoarthrosis of the TMJ, tomographic imaging will show 1 or more of the following: erosion o£ At this particular stage of reporting, laboratory normal cortical delineation, sclerosis of part of or findings in TMJ appear to be of all of the condyle and articular eminence, flatten- limited value.^^ This is because collection of such ing of joint surfaces, and osteophyte formation fluid is not routinely practical given the small (Figs 1 and 2). It must be re-emphasized that 1 or quantities available, or the total lack of fluid. more of the above changes are frequently found in Ongoing research has shown that release of both symptomatic and asymptomatic joints (Table inflammatory mediators is associated with disease 1), This fact underscores the significance of the activity,^'' and the enzymatic events involved in clinician's inability to differentiate between the the process of OA are being characterized.^*^ These presumed stages/changes in the remodeling pro- products may be useful markers for the evaluation cess. These changes may be indefinitely asymp- of cartilage matrix degradation in patients with tomatic, or they may culminate in a symptomatic suspected OA. On the other hand, these products and thus clinical diagnosis of OA (Table 2). The may also be associated with adaptive remodehng OA process, confirmed by symptoms and imaging changes and may not be disease process-specific. evidence, may then ctoss an asymptomatic thresh- The interpretation of such evolving monitoring old and linger as a memory of an arthritic or methods in different genders, age groups, and symptomatic exacerbation. stages of the disease offers much research scope It is interesting to note that a recent study of the but is currently not applicable to OA diagnosis. spines of people without back pain found that nearly two thirds had spinal abnormalities, includ- ing herniated or degenerated discs. In a paper

302 Volume 13, Number4, 1999 Zarb/Csrisson

published in The New England Journal of Medicine,'"^ California researcbers concluded tbat in many cases it may be sbeer coincidence, not cause and effect, wben a person witb back pain is found 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 TMD demands an eclectic approacb to tbeir manage- ment. Wbile the general features of this proposed strategy can, with selected modifications, be applied to all 3 major encountered disorders (see Stohler and Zarb^ ), we have fine-tuned tbe Fig 3 A sitniLit graph may be used to explain the pa approach here to address the specific management tern of OA behavior (after Ogus atid Toller^^). of 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 important overall consideration is the generally favorable . It should be pointed out, however, that prognosis of OA. there is no evidence to suggest that the natural his- tory of OA is significantly affected by these drugs, Symptomatic Treatment nor, incidentally, tbat those who feel little pain because of a high pain tbreshold fare any worse Tbis comprises a formula of 3 general items: than others. The ratio of hazard to therapeutic patient reassurance, medication, and physical ther- effectiveness of many of the available drugs is apy. Reassurance demands a sympatheric dentist, a higher than in most other diseases, so that good simple explanation of the problem and its possible judgment in the choice of treatment is required. multifactorial etiology, and a carefully explained Occasionally, specific anti-arthritic preparations and justified course of treatment. If OA is diag- are used. In patients with severe pain, intra-articu- nosed, then it should be explained tbat symptoms lar injections of anti-inflammatory agents may be may worsen before they improve, although in most used. cases the joint will eventually "'heai" or recover. A . Rest, acbieved via voluntary useful way of illustrating this is to draw a well- or imposed immobilization; heat; and remedial shaped graph or curve, which will assist in e.xplain- muscle are likely modalities included in a ing tbe prognosis of the condition^^ (Fig 3). It is physical therapy regimen. Tissue rest is a func- conceded to the patient that ar the time of consul- tional tenet of arthritic therapy, and with the TMJ tation it may be difficult to assess tbe patient's pre- It can be achieved by varying degrees of controlled cise position on tbe curve. Therefore, if the OA sta- joint immobilization, ranging from a soft diet and tus is at point A, a period of deterioration will voluntary avoidance of excessive mandibular precede improvement; if on the other hand it is at movement, to infrequent use of interarcb elastics point B, the condition is well on its way to getting for very short periods of time (3 to 5 weeks). Such better. It must be stressed, however, tbat with relative jaw immobilization fulfills the objective of proper management, progress is frequently in the protection from "weight bearing" during mastica- same direction, from left to right. Fortunately, OA tion, although it is probably not useful in the patients with TMJ involvement do not appear to avoidance of other and probably more important suffer from significant functional jaw problems, traumatic activity, eg, bruxism. Pain seldom arises and it is only acute TMJ pain episodes that tend to spontaneously from the rested symptomatic joint; necessitate active intervention. it is usually due to some form of overload or Medication- Pain relief forms a major part of trauma (typically minor) to which the joint is par- treatment, and all patients with joint pain should ticulariy vulnerable. This may be a stretching or be provided with a regular background of "strain" of some soft tissue joint component, a

Journal of Orofactal Pain 303 Zarb/Carl s son

subchondral bone trabecular fracture, or a mppmg ent bandaging techniques as an adjunct to ortho- of structures between the articular-hearing surface, pedic management. or else capsule tension when the range of move- It should also be emphasized rhat the notion of ment exceeds certain limits. The summation of all shortened dental arches (eg, bilateral stable quad- these minor episodes may suggest a continuous rant reiationsbips with exclusive bicuspid support) process, but careful history-taking will usually does not appear to automatically imply an reveal the episodic nature of the symptoms. Heat increased vulnerability to OA,'* On the other or short-wave diathermy or ultrasonic treatment hand, Pullingcr and Seligman""' referred ro a possi- may he useful adjuncts in the relief of pain and ble correlation between age, number of opposing muscle sriffness. Seif- of adjacent muscula- posterior occlusal units, and occurrence of OA ture and joints per se, when tolerated, is also reported to be helpful, particularly since it is so symptoms. easily carried out. The value of the more sophisti- The hite plane or interocclusal stabilization cated techniques may be partly psychologic, in that appliance is therefore particularly useful in a the patient is made to feel that a great deal is being mechanical orthopedic sense, as well as in its done to ease the discornfort. established role in the reduction of nocrurnal and possibly diurnal bruxism. Its versatility is such that The rationale for remedial e.verciscs is to pro- it can be designed both to replace missing poste- mote normal mandibular function. Several jaw rior teeth and to provide an optimal vertical exercises have been proposed, and they all seem to dimension of occlusion. This becomes particularly aim at achieving (1) the strengthening of the mus- apt if parafunction is identified as being a con- cle groups controlling affected joints, (21 the pre- tributing etiologic factor. When dental methods vention of future overloading or abuse to the appear to he inadequate, help from alhcd profes- joints, and (3) re-education in the use of damaged sionals should be prescribed for these patients. joints. Treatment of Pathologic Sequelae Control or Reduction of Contributory or Predisposing Factors Most TMD resolve spontaneously or are directed to an earlier resolution via the previously Strong anecdotal evidence suggests that overload described interventions. The nature of OA sug- from parafunction and/or biomechanical factors gests a variable symptomatic progression that usu- are contributory to OA, Consequently, limited ally "burns out" in 12 to 24 months. This has dental initiatives, such as consideration of restora- also been interpreted as more or less complete tion of missing molar support, may he of primary repair or resolution of symptoms within 1 to 2 concern to the denrist. Clinical impressions suggest years.*" Osteoarthritie lesions appear ro increase the miportance of restoration and maintenance of slowly and are frequently asymptomatic. a functional occlusion, which includes bilateral Symptomatic exacerbations appear to be self-lim- and an adequate number of centric stops. This itmg, and the previously outlined treatment strate- objective may require the fabrication of a stabiliza- gies are supportive in nature and usuaiiy provide tion appliance or a removable provisional prosthe- adequate relief. Above all, these methods aim at sis to restore unsupported or inadequate posterior minimizing functional disturbances by controlling dentitions. There is, however, a lack of evidence to the risk of overloading or traumatizing the joint. support che claim that occlusal therapy per se is of On the other hand, some patients do end up with value in the treatment of OA, since a subtle but prolonged discomfort and intracrable pain, proba- profound difference exists hetween the prescrip- bly as a result of provoked tissue changes that are tion of a stabilization appliance, which presumably hy that point clearly pathologic. Such irreversible alleviates intracapsular effusion in an arthritic sequelae are sometimes considered treatable only joint, and occlusal therapy. The presumed objec- by TMJ surgery. While few authors have given tive of a stabilization appliance is to reheve joint specific criteria for patient selection for surgical pressure in OA, aithough there is no evidence to treatment, it seems reasonable to concede that a fully support this. The accompanying ensuing small percentage of patients will benefit from sur- uneven interocclusal relationship (which is change- gical intervention if the cause is overt TMJ dis- able in the context of reduction in the interarticu- ease. The surgical procedures that have been most lar inflammation) can then be easily modified on frequently employed are condylectomy, condylo- the acrylic resin splint surface in response to effu- tomy, discectomy and, more recently, disc repair sion changes. This is not unlike the effect of differ- rather than disc removal (for review see

304 Volume 13, Number 4, 1999 Zarb/Carlsson

Outcome studies of discectomy performed on to be effective in well-controlled clinical trials. It is strict indications have shown excellent long-term well documented, however, that OA may not be results."'"' The prognosis after disc repair has not an irreversible disorder, and while its signs and been so favorable, ar least when contributory or symptoms fluctuate, they tend to decrease with predisposing factors have been inadequarely con- time and will gradually and frequently disappear. trolled."'"' The long-rerm clinical prognosis of OA is usually Current—albeit incomplete—understanding of favorable, in spite of regularly observed severe the pathogenesis of OA and in particular the gene- radiographie changes. sis of disc displacements provides rhe clinician In rhe absence of an experimental animal model with more of a rarionale for avoiding surgery ar all ro test hypotheses of disease etiology, we continue costs. This should be tempered with the recogni- to rely on inferences and observations. The latter tion that improved diagnosis and underst.mding of have stood us in good rherapeutic stead, particu- TMJ disease necessitates recognition of the infre- larly when clinical discretion and prudence lead to quent yet indispensable role to be played by the avoidance of irreversible dental reconsrructive surgery. procedures. Some authors"*-^ counsel the use of intra-arricular injections of anti-inflammatory medications into the TMJs of patients who do not respond to con- References servative treatment. Both short- and long-term results of single injections of corticosteroids have 1. Dworkin SF, LeResche L (eds). Research Diagnostic been reported to be successful in efficient pain CiiterLa for Temporomandibular Disorders. J Cranio- reduction, normalized joint function, and no mandil) Disord Facial Oral Pain 1992;Ê:301-355. 2. Bland JFI. The reversibility of osteoarthritis: A review. Am radiographie signs of advanced joint destruction in JMed l983;74:l6-26. follow-ups of more than 8 years."'^ An alrernarive 3. Ax:els5on S. Fiunian and expérimental ostcoarrhrosis of agenr, wirh probably fewer side effects, is sodium ihe lemporomandibular joint. Morphological and bio- hyaluronate. This drug bas also been shown to chemical studies. Swed Dent J 1993; suppl 92. give a significant short- and long-term reduction of 4. Hansson T, Nilner M. A study of the occurrence of symp- toms of diseases of tbe temporomandibular joint, mastica- subjective symptoms and clinical signs in patients tory musculature and related structures. J Oral Rehabil with persistent TMJ problems that had not l975;2:3l3-324. responded to conservative treatment.''^ 5. Brooks SL, Westesson P-L, Eriksson L. Hansson LG. Barsotti JB. Preval a nee of osseous changes in the temporo- mandibular joinr of asymptomatic persons without inter- nal derangemenr. Oral Surg Oral Med Oral Parhol Conclusions 1992;73; 122-126. 6. Boedng G. Arrhrosis defurmans van het KaakgewricKt The presumed time-dependent implications of Ithesis]. Groninyen: Drukkerji Van Denderen. 1,966. functional or parafunctional loading may elicit 7. Stegenga B. TemporumanJibular Joint Osteoartlirosis and Internal Derangement. Diagnostic and Therapeutic adaptive and ultimately even degenerative changes Outcome .•Assessment Irhesisl. Groningen: Rijksuniversiteit in the TMJs. Under certain conditions—genetic Groningen, 1991. predispositions, trauma, dental morphologic 8. Carlsson GE, Öberg T. Remodelling of the temporo- defects, etc—the adaptive or degenerative changes mandibular joints. Oral Sei Rev 1974;6:53-S.5. may cross the threshold from an asymptomatic 9. Wedel A, Carlsson GE, Sagne S. Temporomandibular joint morphology in a medieval skull material. Swed Dent state into a symptomatic one. In a clinical context J 1978;2:I77-187. it is prudent to regard such joint pain as the last 10. Ericson S, Lundberg M. Structural changes in the finger, link in a long chain of events and to try to deter- wrist and temporomandibular joints. A comparative mine where stress or stresses on an affected joint radiologie study. Acra Odontol Scand 1968;2é:l 11-126. can be reduced or eliminated. Non-drug treatment 11. Storey AT. Bio m echa nica! and anaromical aspects of the remporomandihukr joint. In: Sessle BJ, Bryant PS, Dionne seeks to reduce joint overload so rhat healing can RA |eds). Temporomandibular Disorders and Related occur; consequently, rest and are regarded Pain Conditions. Seattle: IASP Press, 1995: 257-272. as an important part of a self-care strategy. It is 12. Moffett BC. Classification and diagnosis of remporo- also believed that provisional and reversible dental mandibular joint disturbances. In: Solberg WK, Clark GT interventions (such as appliance therapy or (edsl. Temporomandibular Joint Problems. Chicago: restoration of posterior occlusal support) may pro- Quintessence, 19S0. 13. Milam SB. Anicular disk displacements and degenerative duce long-range benefits. This sort of prostbodon- temporomandihular ]oint disease. In; Sessle BJ, Bryant PS, tic intervention is particularly popular as definitive Dionne RA (eds). Temporomandibular Disorders and treatment, but has not yet been conclusively shown Related Pain Conditions. Seattle: IASP Press, 1995:89-112.

Journal of Orofacial Pain 305 Zarb/Carisson

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