Degenerative Disease of the Temporomandibular Joint

Lome S. Kamelchuk, DDS, MScClinical Instructor, Research FellowDepartment of Stomatology

Paul W, Major, DDS, MSc, MRCDtC)Associate ProfessorDepartment of Stomatology

university of AlbertsEdmonton, AlbertaCanada

Correspondence to:Dr Lorne S, KamelchukUniversity of Alberta4068 Dentistry Pharmacy CentreEdmonton, Alberia T6G 2N8Canada

Progression of degenerative joint disease is dependent on theunderlying patbotogic and/or reactive processes involved that, ingeneral, compromise tissue adaptability. A review of clinical andexperimental literature relating to degenerative joint disease is pre-sented. Epidemiology, pathogenesis, diagnosis, treatment, andprognosis are described witb particular emphasis given to the tem-poromandibular joint. Tbis article describes factors affecting tbetemporomandibular joint remodeling/degeneration parity and pre-sents rationale for approacbes to diagnosis and treatment.J OROFACIAL PAIN 1995;9:I68-13O,

key words: temporomandibular joint, degenerative joint disease,osteoarthriris

Breakdown of temporomandibular joint (TMj) tissues, andarticular surfaces in general, may occur due to an increasedmechanical stress and/or a reduced ability for the tissues to

adapt to applied stress. Local and systemic factors have beenidentified in the etiology, progression, and ultimate quiescence ofdegenerative joint disease (DJD), The purpose of this article is todescribe factors affecting the TMJ remodeling/degeneration par-ity and, in doing so, present rationale for diagnosis and treat-ment.

Temporomandibular disorders (TMD) generally represent asmall group of separate musculoskeletai disorders' that are distinctbut related.-"* Six types of TMD specific to the TMJ proper havebeen recognized.'' The TMJ disorders may be divided inro specificarticular disorders related to (1) deviation m form; (2) disc dis-placement with or without reduction; (3) dislocation; (4) inflamma-tory conditions including synovitis and capsulitis; (5) arthritidesincluding osteoarthrosis, osteoarthritis, and polyarthritis; and (6)ankylosis,'' Specific TMJ disorders can contribute, in varyingdegrees, to an overall TMD,"

Degenerative joint disease is a descriptive term, often used as adiagnosis, that fails to identify a specific etiology. Various muscu-loskeletai disease and reactive processes""" have been commonlyimplicated in the progression of DJD, Diagnoses of DJD reflect dis-ease processes of tissue deterioration in which soft tissue, cartilage,and bone are converted into or replaced hy tissue of inferior qual-ity,'" Generally, DJD appears to be the manifestation of an imbal-ance between an adaptive response (remodeling) and a nonadaptiveresponse (degeneration).

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Epidemiology

Literature relating to epidemiology of degenerativedisease of the TMJ is descriptive and retrospective,Schiffman et al''' conclude that approximately 7%of the general population may benefit from treat-ment for TMJ problems and that tnost symp-tomatic subjects can function adequately withouttreatment. Of patients treated at cemporomandihu-lat dysfunction clinics, 8% to 12% receive diag-noses of DJD.""'" Autopsy results confirm TMJdegenerative disease prevalence that varies from22% to greater than 40% of the population,'"''with osteoarthritis of the TMJ commonly appear-ing asymptomacically.-- Data support the conceptthat aging women seem co be more prone to DJDthan are men."''°'"-^

Pathogen es is

Role of Aging

There is a general association between the incidenceof DJD and increasing age. Studies indicate that thefrequency of DJD increases in older persons,""-'-'""suggesting that age is a predisposmg factor. Themcidence of tooth loss and osteoarthritis is associ-ated with increasing age,"'-*"" hut vi'hen age is con-trolled, the associarion is coincidental.•'•̂ " Attritionhas also, independently of age," heen associatedwith TMJ osteoarthritis despite irs questionable eti-ologic role.'"' Although age may be correlated withobservations of temporomandibular DJD, the pos-sible correlation does not elucidate etiology.

Age-related changes in articular tissues have beendocumented. The fibrous component of the matrixof aged articular tissue of the TMJ consists of awell-organized collagen network occasionally dis-persed with elastic fibers." The overall amount ofcollagen does not .significantly decrease with aging;however, infrastructural alterations occur. Proteo-glycan content decreases and binding quality isaltered. In mice, TMJ cellularity generally decreaseswith aging, resulting in loss of proliferative zonepotential." Such age-related changes in the articulartissues affect their mechanical properties and, inturn, may facilitate rhe pathogenesis of DJD,

Joint Loading and Stress Distribution

Strong evidence exists to suggest the TMJ is loadedduring function.^'"'* Intensity and direction ofStresses generated hy various occlusal forces havebeen analyzed utilizing three-dimensional math-

ematical""'" and finite element-analysis mod-els.""'" Each TMJ is a pressure-bearing, compound,double-synovial joint.'"

Repetitive cyclic microtrauma has heen impli-cated in the etiology of DJD. Repeated impactloading of cartilage-lined articular surfaces resultsin an increased rate of osteogenesis in subchondraihone evidenced radiographicaily as subchondraisclerosis.'" Affected hone, of increased stiffness,may increase the susceptibility of articular carti-lage to trauma caused hy impact," with loss ordegeneration of cartilage normally resistant tocompressive stress. In the TMJ, reducing disc dis-placements may potentiate repetitive impact load-ing*' and consequently lead to a subchondrai scle-rosing known to occur prior to the onset of DJD."Whether or not DJD can be attributed to thecumulative effect of repetitive minor trauma tonormal TMJ articular tissue remains debatable.

Major trauma to synovial joints may progress toDJD,'"' Excessive |oint loading may disrupt the nor-mal adaptive capacity of articular tissue, resultingin eventual cartilage breakdown and elevated pro-teoglycan levels in the synovial fluid.''" Kopp etal*" conclude, however, that degenerative changesdescribed in their autopsy material are probablymostly due to local factors. While synovial fluidaspirates of joints that show arthroscopic evidenceof DJD contain elevated levels of keratin sulfate,'"histochemical studies of articular surfaces thatmacroscopically demonstrate DJD have shown areduction in sulfated glycosammoglycan."

Arthritic lesions of the TMJ are most oftenlocalized in the lateral aspect of the temporalfossa, compared to the medial aspect.'"-''" Lesionsare markedly fewer in the condyle than in the tem-poral component. In a study of location of osteo-archritic lesions in patellofemoral compartments of39 cadaveric knee joints," it was hypothesized thatarticular cartilage adapts mechanically to transmit,without sustaining damage, the stress to which it ismost regularly subjected, and that damage occursonly if cartilage is subjected to less frequent butmuch higher stress.'" Articular tissue thickness anddistribution probably reflect areas of stress concen-tration in the condylar and temporal compo-nents,*̂ ' with the lateral part of the joint exposed tothe largest functional and parafunctional loads."Incongruities between loaded TMJ articular sur-faces predispose to stress concentrations that areobserved more frequently in the temporal compo-nent where degenerative lesions more commonlyoccur,"

Adequate lubrication of the TMJ components isrequired to facilitate the mechanics of joint mo-

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tion. The tipper joint compartment is subject totransktory movenietit while the lower undergoesrotational movement."' Differences in the fre-qtiency of degenerative lesions hetween the condy-lar anid temporal components may he dtic togreater frictiona! loading between the disc andtemporal components than hetween the condyleand disc. Nitzan and Dolwick'̂ suggest that a lackof gliding in the joint can be attributed to discadherence to the fossa by a reversible effect stich asvacuum and/or decreased volume of high-viscositysynovial fluid. Decreased synthesis of the glycopro-tein luhricin, normally associated with the lubrica-tion fraction of synovial fluid, may be involved inthe etiology of DJD.'' Lack of joint lubrication mayexacerbate articular tissue failure by increasing fric-tional resistance during loaded joint movements.

Internal Derangement

Internal derangement of the TMJ, particularlywith disc deformation, may progress to DJD.Position and configuration of the articular disc hasbeen related to DJD.'"-"" Westesson" conducted aradiographie study including arthrograms on 12Spatients with internal derangements. Osseouschanges were seen in 50% of the patients withanterior disc displacement without reduction butseldom in patients with disc displacement withreduction. Degenerative changes were consistentlyfound in joints with disc perforation. Andersonand Katzberg"' obtained comparable findings witha tomographic and arthrographic study of 141patients with temporomandibular dysfunction.Only 9% of the patients with a reducing displace-ment showed signs of degeneration, but 39% ofthe patients with nonreducing disc displacementand 60% of the patients with perforation haddegenerative changes. These authors*"'"' concludethat, in many cases, internal derangement of theTMJ precedes degenerative disease.

There is a relationsbip between disc perforationand degenerative disease of the TMJ."*""- Surgicalcreation of hilateral disc perforation in Macacafascicularis monkeys produces pathologic alter-ations consistent with DJD in the majority ofexperimental joints."'"' In humans, observed perfo-rations localized ro the posterior attachment of thedisc" suggest the attachment does not have thesame resistance to compressive loading as does thedisc Itself."" Despite the relationship between discdisplacement and disc perforation,̂ '"*•'" rhe conceptthat DJD IS the result of displacement and perfora-tion of the disc is disputed.'"" In a blind study ofjoints with normally positioned discs, displaced

but reducing discs, and displaced nonredticingdiscs, perforations were found only in cases withDjD."' However, 73% of the cases with DJD didnot have perforations. These observations suggestit is more likely that DJD is the cause and perfora-tion is rhe effect.

Schellhas"' regards internal derangement of theTMJ as an irreversible and generally progressivedisorder that may he staged clinically. Stegengaet al*' hypothesized that TM joints are subject toa continual process of articular surface break-down and repair. If the degradarive responseexceeds the reparative response, then a DJD pro-cess is initiated. The gliding capacity of the artic-ular disc may become impaired, thus predispos-ing to internal derangement. Stegenga et ai"-suggested that internal derangement is an accom-panying sign of DJD and is capable of causing arapid progression of the disorder. Stegenga et al*̂concluded that in many cases of temporoman-dibular dysfunction, DJD is the primary disor-der, and that the accompanying muscle pain andinternal derangement is secondary.'^

Inflammatory/Histochemical Considerations

Histologie studies of synovium of degenerativejoints show a significant amount of inflamma-tion""*" and proteoglycan turnover.*""'" In appen-dicular joints with cartilage articular surfaces,early stages of DJD show fibrillation and fissuresat the articular surface level that will eventuallyprogress to a complete erosion of rhe cartilage."Pathologic changes appear ro be related to in-creased levels of metalloproteinases that produceboth a breakdown of the collagen network""'" anda size reduction of the proteoglycan monomer."'"''The TMJ articular surfaces are covered with fi-brous connective tissue, as opposed to hyaline car-tilage, but research suggests*'**'" that inflammatorychanges in articular matrix components are (1)responsible for impairment of the physicochemicalproperties of the articular surfaces and (2) likely tocontribute to the development of DJD.

In addition to mediators of inflammation," otherbiochemical mediators have been identified withDJD and osteoarthrosis. The cytokmes interleukin-1 (IL-1) and interleukin-6 (IL-6) mediate chondro-cyte protease production causing cartilage destruc-tion in DJD.'™-'"̂ Proteases such as collagenaselike(CL) peptidase"""'™ and prolyl endopeptidase(PEP)'"""''- increase in serum concentration in miceinbred for osteoarrhrosis of the TMJ.'" Articularcartilage is also an estrogen-sensitive tissue."•' It hasbeen demonstrated that tamoxifen, an estrogen

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antaguriLSt, reduces the developmenr of experimen-tally induced DJD in rabbits, in conrrasr, estradiolfacilitares the process. Both estradiol and tamoxifenaffect proteoglycan, prostaglandin, and proteogly-caiiase production hy cartilage cells."^

Limitations of Remodeling

Change in condylar morphology, as a result otremodeling, is a normal biologic adaptation to con-tinual functional demands made on the TMJ. In astudy of 96 joint specimens from young adults,localized surface changes were common."" Localmodifications of both the condylar surface and theoverall condylar shape appear to be interrelatedadaptive responses to functional stimuli. Re-modeling changes, however, present with high vari-ability. Different presentations of remodeling maybe observed between the lateral and medial aspectsof the joint components within the same joint.Although DJD usually occurs in an articular areaformerly subjected to remodeling," the variablepresence of adaptive remodeling alone cannot pre-dict a progression to active degenerative disease.

Different functional demands made on the man-dibular complex contribute to the variable natureof remodeling changes. Animal studies indicate thatchanges in mandibular position obtained by intra-oral or extraoral devices induce characteristicremodeling changes in the articular surfaces."'""Anterior condyle placement caused by the applica-tion of Class II orthodontic forces is accompaniedby osteogenesis on the posterior aspect of thecondyle and increased periostea! deposition on thepost glenoid tubercle. Distal placement of thecondyle wirh Class III orthodontic forces producesregressive remodeling of the posterior condyiar sur-face and anterior surface of the post gienoid tuber-cle."' Internal derangement viiith anterior disc dis-placement may lead to flattening of the anteriorcondyiar surface, whereas posterior disc displace-ment IS accompanied by flattening of or concavitiesin the posterior aspect of the condyle.'-"

Contribution of Occlusion

Functional demands may be imposed on the TMJ,in part, by altered occlusal relationships. Charac-teristics of the occlusal scheme may depict pattern-ing and intensity of forces transferred to the articu-lar surfaces of the joints.'^' Biomechanical analysesof the mandibular complex predict that joint load-ing is increased as the point of application of biteforce is moved anteriorly.'"Unilateral loss of toothsupport will increase loading in the contralateral

joint/' as does unilateral chewing."''•'" Althoughthe etiologic contribution of excessive joint loadingto onset of osteoarthtosis is plausible, the directetioiogic effect oí occlusion is debatable. Theremodeling capacity of the TMJ demonstrates thatthe joint can accommodate and adapt to variousocclusal conditions.'-"

Pullinger et al"^ analyzed occlusal variation in anosteoarthrotic sample of patients and reported thatocclusion was neither a unique nor a dominant fac-tor in defining the sample. They concluded that fea-tures such as anterior open bite in patients withosteoarthrosis are the consequence of, rathet thanan etiology for, DJD. Seligman and Pullinger'"stated that epidemioiogic studies may demonstrateassociations between occlusa! factors and DJD butfail to prove the etiologic contributions of occlusion.It is currently open to speculation whether specificocclusal factors predispose to DJD"'-'--" or ratherresult from intracapsular or capsular changes.'" Thespecific etiologic role of occlusion, with tespect toTMD in general, remains to be proven.'-''•'"

DiagnosJs

Clinical Considerations

Clinical findings vary with the course of degenera-tive disease of the TMJ. There is a potentiallyasymptomatic DJD population segment who, undercertain circumstances, may suddenly become symp-tomatic."" Trauma, in general, is a common precip-itating factor. Principal clinical findings in osteo-arthrosis of the TMJ include pain on movement orbiting, reduced range of motion, joint tenderness topalpation, and crepitus.'^'" Rasmussen'""-'" re-ported that during the early painful phases,restricted joint mobility and limited excursivemovements ate accompanied by tenderness of thejoint capsule and pain in the masticatory muscles.As the pain ceases, mobility improves and crepita-tion, if not already present, may appear.

Except for crepitation, the clinical signs andsymptoms of patients with TMJ degenerative dis-ease do not differ from those of other patients withmandibular dysfunction.'" Crepitus is an accuratepredictive sign of DJD'''''"" but has low sensitivityas a diagnostic sign. Rohlin et al'" found that 10 of12 joints with crepitation had degenerative changeswhile the remaining two had extensive remodeling.In one study,"' only one half of joints with con-firmed DJD exhibited ctepims. If crepitation is usedas the only diagnostic criteria, joints with DJD willnot be properly diagnosed.

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Imaging Considerations

Radiograpliic observattons characteristic of DJDinclude reduced joint space, osseous flattening,subchondral sclerosis, erosions or loss of corticallintng, and presence of osteophytes,'"*'•'•' Reducedjoint space, particularly in association with crepi-tation, tnay represent articular soft ttssue destruc-tion. However, Kopp and Rockier"" concludedthat redticed ¡oint space is probably not an indica-tor of DJD if molar support is present and theradiographs are exposed with the mandible in theintercnspal position. In advanced cases, osteo-pbytes and lipping may be found in the anteriorpart of the condyle. Apparettt osteophytes can becaused by either apposition of bone or simulatedapposition due to destruction of adjacent areas. Ifcondylar surface erosions or irregularities areobserved, tbey are predotninantly located in thelateral pole."'

It is often difficult, if not impossible, to radio-graphically differentiate between degenerativechanges and adaptive remodeling.'"""' Osseouschanges must be pronounced to be detected radio-graphically;''" tbus, early degenerative changes inrhe articular soft tissue may occur long beforeradiographie signs are visible." •'•" Condylar andeminential flattening are frequently associated witbbony condensation or subchondral sclerosis, inde-pendent of arthrosis,'* and may be adaptive re-sponses to increased functional loading."' Espe-cially in the absence of degenerative signs such assurface erosions or irregularities, condylar flatten-ing and subchondral sclerosis are usually represen-tative of remodeling. However, the absence ofradiographie changes cannot exclude the presenceof degenerative lesions,

Osteoarthritic hard and soft tissue ahnormahtteshave been identified using magnetic resonanceimaging (MRI).'•"""' Cartilage erosions, visiblewitb MRI, are potentially quantifiable,'" In rhesusmacaques knees, MR relaxation times and protondensity values have been sbown to vary with tbeseverity of osteoarthrttts.'"' In other antmal mod-els, MRI is positive for accutnulation of synovialfluid and cartilage degradation."'' Researchers havealso shown correlarional trends between areas ofdecreased signal mtensity and histologie degenera-tive changes in cartilage of goat knees.'" In tbehuman hip, MRI may be sensitive for specific earlydegenerative change'"''' but may underestimatecartilage and osseous abnormalities,""'''' AlthoughMRI of tbe TMJ may confirm disc displace-ment,""""- it has been shown to underdiagnoseosseous changes, adhesions, and perforations.'"'"

Histochemical Considerations

Histochemical markers of cartilage metabolismhave been identified, and they correlate with earlysoft tissue changes associated with onset of osteo-arrhritis.'"'•""• Results of synovial fluid assays suggestthat the enzyme activities of N-acetyl-beta-glu-cosaminidase and N-acetyl-beta-galacrosaminidasereflect rhe degree of TMJ dysfunction,'" Fibronectinfragments are detectable in synovial fluid aspirates ofparients with osteoarthritis and are known to poten-tiate release of meta II o protein ases resulting in pro-teoglycan depletion,'" '"' In mice inbred forosteoarthrosis, observed increases in serum collage-naselike (CL) peptidase and prolyl endopeptidase(PEP) occurred at an earlier stage tban histologiechanges,"- Histochemically detectable entities maybe useful as early biochemical markers of tbe onsetof osteoarthrosis.

Treatment

Palliative Treatment

Palliative care should begin with an explanation ofthe nature and prognosis of TMJ degenerative dis-ease,'" Management is primarily symptom directed,based on the understanding that DJD appears torun a clinical course of 1 to 3 years generally fol-lowed by a natural regression of symptoms.''•"•""•'''Modification of parafunctional habits sucb asclenching, bruxing, and gum chewing should beundertaken. Patients should be advised tbat thejoints may be easily irritated,'"'' and unnecessarymechanical stresses on the joint may be avoided bychanging the diet to softer, smaller food,'"' Physio-therapy, utilizing various modalities to controlinflammation, reduce secondary muscle spasm, andimprove joint mobility, sbould be undertaken andfollowed by home exercises,''"'"''' If pain relief isinadequate, short-term analgesic and anti-inflam-matory medication may be helpful."*

Splint Therapy

Existing concepts of DJD etiology suggest treat-ment should attempt to reduce loading in the TMJ.Distraction of the TMJ may be an effective meansof eliminating ¡oint loading and has beenattempted with spring mechanics,'"' splints withincreased vertical dimension,'~' and pivotingsplints.'""'"" However, the effect of sphnt therapyon condylar distraction has been shown to bequestionable,''- Rasmussen'" reported that treat-

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ment of DJD with pivotal splints resulted in relieffrom pain but increased the extent of the radio-graphically observed degenerative disease,

Occlusal splint therapy remains a common treat-menr modality, Ito et al"- investigated joint loadingassociated with several different splint designs.Splints without posterior tooth support result inincreased joint loading during clenching. Likewise,splmts with unilateral posterior contact createincreased loading in rhe contralateral joint, withdistraction of the ipsilateral joint. Bilateral centricstops on posterior teeth appear important for pro-tecting the joints from excessive loading, particu-larly during parafunctional activities, Occlusaisplint therapy can reduce joint loading indirectlyby reducing muscle hyperactivity,'''"'" and it mayprovide symptom relief by decreasing coexistentneuromuscular symptoms.'"''""*

Injection Modalities

Intra-articular injections bave been proposed as apossible treatment modality for some types ofTMD.'" Human osteoarthritic synovial membranesexperimentally treated with hydrocortisone demon-strate decreased production of alpha and betaIL-l'"" known to be involved in the osteoarthritispathophysiologic process. Corticosteroid injectionshave also been shown to suppress enzyme synrhesisin experimental osteoarthritis.'"" Clinically, intra-anicular corticosteroid injection is known to giveshort-term symptom relief'*" but is also controver-sial.'™ Intra-articular corticosteroid injecrions havebeen associated wirh both beneficial and adverseeffects.'"-'"

Intracapsular injections of hyaluronic acid havebeen shown ro provide relief from TMJ pain,"''The sodium salt of hyaluronic acid, sodiumhyaluronate, is a high-molecular weight polysac-charide'" that functions as a lubricant in normalsynoviai fluid,'" Short-term results of intra-articu-iar injections inro painful shoulders have producedrapid symptom relief from pain,'"" However,Bertolami er al"* reported that patients with tem-poromandibukr DJD who received intracapsularsodium hyaluronate, compared to placebo injec-tions, sbow no significant difference in treatmentoutcome.

Surgical Treatmenf

Temporomandibular joint surgery is restricted topatients with long-sranding, severe pain andrestricted range of mandibular movement whoshow no favorable response to conservative treat-

ment,"" Arthroscopy has been introduced intostandard therapy for TMJ internal derangementand osteoarthritis, and it compares favorably witbopen surgical techniques,'™ Arthroscopy also hasdiagnostic merit with the potential to providehighly tissue-specific pathologic information.'"'Short-term outcome of patients treated witharthroscopic surgery, compared with nonsurgerypatients, includes subjective reports of increasedmobility and pain relief.-"' In experimental models,however, arthroscopic intervention may cause irre-versible changes in TMJ articular tissues.^"' Dif-ferent approaches, using animal and human mod-els, provide continued rationale for open andarthroscopic surgical techniques,̂ " -̂'"

Prognosis

Degenerative joint disease appears to have an itii-tial destructive phase, and a subsequent reparativephase, that terminates in healing. Rasmussen"'esti-mated that the destructive and reparative phaseslast 1 to 1,5 years each. In 75% of subjects exam-ined, the entire course is estimated to be less than18 months, and subjects generally complete thehealing phase by 3 years. Despite improvement insubjective symptonis, however, radiographie evi-dence of healing is minimal,-"'-̂ "' Generally, subjec-tive symptoms subside,'"'"' and the joints appearclinically stable. Residual symptoms such as mildrestriction of movement and crepitus remain inmany patients long after rhe subjective symptomssubside.'"'™ Long-term studies confirm that themajority of DJD parients with crepirus show noclinical change in crepitation,-'"

Rasmussen"- compared effects of various treat-ment modalities on subjective symptoms ofpatients wirh DJD, Treatment included flat planesplints, pivotal splints, steroid injection, and notreatment. No statistically significant differencewas found in rhe duration of presence of symp-toms with the different treatment modalities in thestudy population. Pullinger and Seligman'""-"' sug-gested that there are two distinct populations ofpatients with DJD, One group is mainly composedof patients under 35 years of age where internalderangement precedes onset of DJD, A secondgroup is composed of an older population whereinternal derangement is secondary to the DJD pro-cess. The concept that although the end result issimilar, there is more than one pathogenesis helpsto explain many of the apparent conflicts regard-ing etiology, diagnosis, and management ofpatients presenting with DJD.

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Conclusion

Temporomandibular DJD is a pathologic responseto mechanical stress placed upon the articular sur-faces of the joint. There is a delicate balancebetween adaptive response (remodeling) and non-adaptive response (degeneration) to functionaldemands. Articular surface breakdown can occurbecause of increased mechanical stress or reducedability of the tissue to withstand and adapt to theapplied stress. The aim of treatment of DJD is toshorten its natural course or at least to make itmore tolerable. It is hoped that treatment duringthe active phases of the disease will reheve pain,preserve function, and prevent or minimize defor-mity. Once the disease process has stabilized, treat-ment is aimed at minimizing TMJ loading. Theseobjectives are, most likely, best achieved with amultiprofessionai approach.

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Journal of Orofscial Pain 179

Kamele hu k/M ai or

Resumen

Enfermedad Degenerativa deTemporomsndibular

Zusammenf assu ng

la Articulación Degenerative Eriírankungen des Kiefergelenkes

La progresión de la enfermedad degenerativa de la artioulacióndepende de los procesos patológicos subyacentes y/o reac-tivos envueltos, y que en general, com pro nieten la adaptabilidadtisutar. Se presenta una revisión de literatura clínica y eïpen-mental relacionada a la enfermedad degenerativa de la articu-lación. Se describe la epidemiología, patogénesis, diagnóstico,tratamiento, y pronóstico con jn énfasis particular en la articu-lación temporomandibular (ATM) Este articulo describe los fac-tores que afectan ia paridad en la re m o dei ación/degene ración ypresenta i a rajón funda m en ta i de ios enfoques de diagnóstico ytratamiento.

Das Fortschreiten einer degenerativen Gelenkerkrankung hangtvom ihr zugrundeliegenden palhoiogischen und/oder reaktivenProzess ab. der. im allgemeinen, die Adaptationsfáhigkeit desGewebes einschränkt. Es wird eine Übersicht über klinische undexperimentelle Literatur zu degenerativen Geienkerkrankungenvorgestellt. Epidemiologie. Pathogenese, Diagnose. Therapie,und Prcgncse werden beschrieben, mit speziellem Schwerge-wicht auf dem Kiefergelenk Der Artikel behandelt Faktoren, diedas Gleichgewicht zwischen Remodeling und Degeneration imKiefergelenk beeinflussen kónnen und stellt Grundprinzipien zurDiagnose und Therapie vor.

ABOP Certification

The American Board of Orofacial Pain (ABOP}was founded in 1994 in response to the need for avalid certification process for dentists practicingorofacial pain management. The ABOP will offerannual certification examinations to dentistslicensed in the United States. The application forthe 1996 examination will be available on June 1,1995. For more information, please write to: TheAmerican Board of Orofacial Pain, 10 JoplitiCourt, Lafayette, California 94549.

•sao Volume 9. Number 2, 1995