Degenerative Disease of the Temporomandibular Joint Lome S. Kamelchuk, DDS, MSc Clinical Instructor Research Fellow Department of Stomatology Paul W, Major, DDS, MSc, MRCDtC Associate Professor Department of Stomatology university of Alberts Edmonton Alberta Canada Correspondence t o : Dr Lorne S Kamelchuk University of Alberta 4068 Dentistry Pharmacy Centre Edmonton Alberia T6G 2N8 Canada Progression of degenerative joint disease is dependent on the underlying patbotogic and/or reactive processes involved that, in general, compromise tissue adaptability. A review of clinical a n d experimental literature relating to degenerative joint disease is pre- sente Epidemiology, pathogenesis, diagnosis, treatment, and prognosis are described witb particular emphasis given to the tem- poromandibular joint. Tbis article describes factors affecting tbe temporomandibular joint remodeling degeneration parity and pre- sents rationale f or approacbes to diagnosis and treatment. J OROFACIAL PAIN 1995;9:I68-13O, key words: temporomandibular joint, degenerative joint disease, osteoarthriris B reakdown of temporomandibular joint (TMj) tissues, and articular surfaces in general, may occur due to an increased mechanical stress and/or a reduced ability for the tissues to adapt to applied stress. Local and systemic factors have been identified in the etiology, progression, and ultimate quiescence of degenerative joint disease (DJD), The purpose of this article is to describe factors affecting the TMJ remodeling/degeneration par- ity and, in doing so, present rationale for diagnosis and treat- ment. Temporomandibular disorders (TMD) generally represent a small group of separate musculoskeletai disorders' that are distinct but related.- * Six types of TMD specific to the TMJ proper have been recognized.'' The TMJ disorders may be divided inro specific articular 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 ) arthritides including osteoarthrosis, osteoarthritis, and polyarthritis; and 6 ) ankylosis,'' Specific TMJ disorders can contribute, in varying degrees, to an overall TMD, Degenerative joint disease is a descriptive term, often used as a diagnosis, that fails to identify a specific etiology. Various muscu- loskeletai disease and reactive processes have been comm only implicated 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- i t y,' Generally, DJD appears to be the manifestation of an im bal- ance between an adaptive response (remodeling) and a nonadaptive response (degeneration). 168 Volumes Number 2 1995
Degenerative Disease of the Temporomandibular Joint
Lome S. Kamelchuk, DD S, M Sc
Clinical Instructor Resea rch Fellow
Department of Stomatology
Paul W , Major, DDS, MSc, M RC DtC
Associate Professor
Department of Stomatology
university of Alberts
Edmonton Alberta
Canada
Correspondence to :
Dr Lorne S Kamelchuk
University of Alberta
4068 Dentistry Pharmacy Centre
Edmonton Alber ia T6G 2N8
Canada
Progression of degenerative joint disease is dependen t on theunderlying patbotogic and /or reactive processes involved that, in
general, compromise tissue adaptability. A review of clinical andexperimental literature relating to degenerative joint disease is pre-sente 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,
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 specific
articular 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 comm onlyimplicated 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).
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, independen tly of ag e, 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 of
collagen 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 S tress 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-
em ati ca l ' 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 results
in 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 impa ct, 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 the
cumulative effect of repetitive minor trauma tonormal TMJ articular tissue remains debatable.Major trauma to synovial joints may progress to
DJD,' ' 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 flu id .'' 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 of cadaveric knee joints , it was hypothesized tha tarticular 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-
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 and
temporal 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 the
TMJ precedes degenerative disease.There is a relationsbip between disc perforation
and 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 disc
displacement and disc perforation,^'"*•'" rhe conceptthat DJD S 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 d isorder. 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.'^
Inf lammatory/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 breakdow n 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
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 produc tion hy cartilage cells."^
imitations 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 depos ition 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 anterior
condyiar surface, whereas posterior disc displace-ment S 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 analyses
of 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 various
occlusal conditions.'-"Pullinger et al"^ analyzed occlusal variation in an
osteoarthrotic 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 w ho, 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 the
joint 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.
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. How ever, 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 are
observed, tbey are predotninantly located in thelateral pole. '
It is often difficult, if not impossible, to radio-graphically differentiate between degenerativechanges and adaptive rem odelin g.' ' Osseouschanges must be pronounced to be detected radio-graphica lly;'' tbu s, early degenerative changes inrhe articular soft tissue may occur long beforeradiographie signs are visible. •'• Condy lar 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).'• ' Cartilag e ero sio ns, visible
witb MRI, are potentially quan tifiable,' 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 k ne es .' In tbehuman hip, MRI may be sensitive for specific earlydegenerative change' ' ' ' but may underestimate
cartilage and osseous abno rmalities, '''' AlthoughMRI of tbe TMJ may confirm disc displace-ment, - it has been shown to und erdiag noseosseous changes, adhesions, and per fora tion s.' '
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 p ro-teoglycan d ep let io n, ' ' ' 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 onset
of osteoarthrosis.
Treatment
Palliative T reatment
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 to
run a clinical course of 1 to 3 years generally fol-lowed by a natural regression of symptoms.''• • •'''Mo dification of parafu nctio nal hab its 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 and
followed 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 e l iminating ¡oint loading and has beenattempted with spring mechanics,' ' splints with
increased vertical dimension, '~ ' and pivotingsplints.' ' Ho we ver, the effect of sph nt therapyon condylar distraction has been shown to bequestionable,''- Ras mu ssen ' reporte d that treat-
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 may
provide symptom relief by decreasing coexistent
neuromuscular sym ptom s.' ' ' *
njection Mod alities
Intra-articular injections bave been proposed as a
possible treatment modality for some types of
TM D .' Hum an 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 sym ptom relief from pain, ' Ho we ver,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 to
patients with long-sranding, severe pain and
restricted range of mandibular movement who
show 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 has
diagnostic 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 and
arthroscopic surgical techniques,^ ^-'
PrognosisDegenerative 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 the
healing phase by 3 years. Despite improvement in
subjective 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 in
many patients long after rhe subjective symptomssubside.' '™ Long-term studies confirm that the
majority of DJD parients with crepirus show no
clinical change in crepitation,-'Rasmussen - compared effects of various treat-
ment modali t ies on subjective symptoms of
patients wirh DJD, Treatm ent included flat planesplints, pivotal splints, steroid injection, and no
treatment. No stat istica lly significant differencewas found in rhe duration of presence of symp-toms with the different treatment modalities in the
study population. Pullinger and Seligman' - ' sug-
gested that there are two distinct populations of
patients 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 is
similar, there is more than one pathogenesis helpsto explain many of the apparent conflicts regard-ing et iology, diagnosis , and m a na ge m e n t of
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. These
objectives are, most likely, best achieved with amultiprofessionai approach.
References
1. Bell WE. Orofa dal Pains. Classification, Diagnosis, Man-agement, ed 4. Chicago: Year Book Medical, 1989il01-113.
2 . Bell WE. Tem porom andibu lat D isorders. Classification,Diagnos i s , Management , ed 3 . Chicagoi Yea t BookMedical, 1990:166-176.
3. Griffiths RH . Repo tI of the presid ent s conference on
examinat ion, diagnosis and management of tempoto-mandibular disorders, I Am Dent Assoc 1983 ;106:75-77 ,4. Am eticati Academy of Orofacial Pain. McNeill C (ed).
Temporomandibular Disorders. Guidelines for Classifi-cation, Assessment, and Management. Chicago: Quin-tessence. 1993:11-13, 29, 40 , 41, 4S-53 , 122.
5. Amer ican Academy of Cran iom and ibuia r D isorders .McNeill C (ed). Craniomandibulat Disorders. Guidelinesfor Evaluat ion, Diagnosis , and Management . Chicago:Quintessence, 1990.
6. Moh l ND , Dixon DC. Cutrent status of diagnostic proce-dures for temporomandibular disorders. J Am Dent Assoc1994;125:56-64.
7. Suso S, Peidro L, Ram on R. Avascu lar necrosis of the
humeral head after dislocation with fracture of the greatertuberosity. Acta Orrhop Beig \992-,Si-A l^59.
8. Hauf W, Mittlmeier T, Hagen a FW, Plitz W. Me thod for
patella. Biomed Tech (Berlin) 1992;37:263-272,9. Tho rkeldsen A, Cantlllon V, Idiop athic osreonecrosis of
the hip. J Manipulat ive Physiol Ther 19 93 ;I6 :37 ^2 .10 , Khan FM, Wil l iams PI. Do uble- bl ind co mp ariso n of
etodolac SR and diclofenac SR in the treatment of patientswith degeneraiive joint disease of the knee. Curr Med ResOpin 1992^13:1-12.
11 , Ellman H, Harris E, Kay SP, Early degenerative joint dis.ease s imulat ing impingement syndrome: Arthroscopic
findings. Arthroscopy 199 2;8 :48 2^8 7.12 , L a f eb e r FP , V a n d c r - K r a a n P M , H u b e r - B r u n i n g O ,
Vanden-Berg W B, Bijlsma JW . O ste o arthritic h um an carti-lage is more sensitive to transforming growth factor betathan is normal cani lage, Br Rheumatol l993;3 2:28 1-28 6.
13 . Ratcliffe A, Rosen wasser MP , M ahm ud F, Glazer PA,Saed.Neiad F, Lane N, Mow VC. The in yivo effects ofnaproxen on canine experimental osteoarthriric articularcartilage: Composition, metalloproleinase activities andmetabolism. Agents A<;tions SuppI I 99 3;39 :2O 7-2 I1.
14 . Schiffman EL, Fricton jR, Haley DP, Shap iro BL. Theprevalence and treatment needs of subjects wiih temporo-m a nd i bu l a r d i s o r de r s . J A m D e nf A s s oc 1 990 ; 1 20 :
29.5-303.15. Toller PA. Osteo arthro sis of tbe mand ibular cond yle. Br
D e n t J 1973; 134 :223-231 ,16 . Heloe B, Heloe LA. Characteristics of a grou p of patients
wi th t emporomandibula r jo in t d i sorders . Communi tyDent Oral Epidemiol l?7S ;3:72 -79.
17 . Mejers)o C, Hollend er L. Radiog raphy of the temporo-mandibular joint in female parients with TMJ pain or dys-function. Acta Radiol [Diagl 1984;25:169-176.
18 . Crook s MC , Ferguson JW, Edw ards JL. Clinical presenta-tion and final diagnosis of patients referred to a tempoto.mandibular joint c l inic, NZ Dent J 1 991 :87:1 13- l lS .
19. Oberg T, Carlsson GE, Fajers CM . The temporom andibu-
lar ioint: A morpbologic study on human autopsy mate-rial Acta Odontol Scand 1971;29i349-384.20. Rohlin M , Westesson P-L, Ericksson L. The correlation of
t empotomandibula r jo in t sounds wi th morphology infif ty-five auto psy spe cime ns. J Ora l Maxil lufa c Surg 9 85;43 i 194-200.
2 1 . Blackwood HJJ. Arthritis of the mand ibular joint. Br DentJ I 9 6 3 ; n 5 : 3 1 7 - 3 2 é .
22. Barrett AW, Griffiths MJ, Scully C. Osteo arth rosi s, thetemp orom andib ular joint , and Eagle s syndrome. OralSurg Oral Med Oral Pathol 199 3;75:273-2 75.
2 3 . Ishigaki S, Bessette RW , Ma ruy am a T. The distribution ofinternal derangement in patients witb temporomandibularjoint dysfunction—Prevalence, diagnosis, and tteatments,J Craniomand Pract 1992;10:289-296.
24. Axelsson S, Fitins D, Hellsing G, Ho lmlu nd A. Arthtoticchanges and deviation in form of the temporomandibularjoint—An autopsy s tudy. Swed Dent J 1987;11^155-200 .
2 5. Bayliss MT , Ali SY, Age-related changes in the composi-tion and structure of human articular-cartilage proteogly-cans. Biocbem J 19 78;176 :683-693 ,
2 6. Kopp S. Subjective symptoms in temp orom and ibular jointosteoarthtosis. Acta Odontol Scand 1977;35:207-215.
2 7. Weslesson P-L, Rohlin M . Internal detangem ent related toosteoartbrosis in temporomandibular joint autopsy speci-mens. Oral Surg Oral Med Oral Path 198 4; i7i17 -22 .
2 8. Kirveskari P, Alanen P. Association between tooth lossand TMJ dysfunction. J Oral Rebabil 1985;12:189-194.
29. Gra nad os JI. The influence of the loss of teeth and attri-tion on the articular eminence. J Prostbet Dent 1979;42:78-85 .
30 . Wh ittaker DK, Davies G, Brown M. loo th loss, attrition,and temporomandibular joint changes in Romano-Britishpopulat ion. J Oral Rehabi l 19 8i ; 12:407 -419,
31 . Wb ittaker DK. Surface and form change s in the temporo -mandibular joinrs of 18th century Londoners. ] PtosthetRes 1989;68(special issue): [abstract 1211].
32 . Wh i t t aker DK, Jones JW, Edw ards PW, Mol leson T .Studies on tbe temporomandibular joints of eighteenth-
century London population (Spitalfields). J Oral Rehabd199Üil7:89-97.
33. Hodges DC. Tem porom andibular joint (isreoarchritis in aB r i t i sh s ke l e t a l pop u l a t i on . Am J P hys A n t h r o po l1991;85:367-377.
7 3 . Helmy E, Bays R, Sharawy M . Osteoartb rosis of tbe tem-poromandibular joint following experimental disc perfora-t ion in Macaca fascicularis . J Oral Maxil lofac Surg1938;46:979-990.
74. Helmy E, Bays R, Sharawy M . Synovial chondro mato sisassociated with experimental osteoarthritis in adult mon-keys. J Oral Maxillofac Surg 1989i47:823-827.
7 5 . Scapino RP . The pos te r ior a t t achment : I t s s t ruc ture ,function, and appearance in TMJ imaging studies. Patt I.J C r a n i om a nd i b D i s o r d F a c i a l O r a l P a i n 1991 ; 5 :S 3 - 9 5 .
7 6. Van Hoe L, Gesteleyn L, Glaeys T, Bertrand P, VanWilderode W, Depuyt F. Arthrographic imaging of post-t r a um a t i c t e m por om a nd i bu l a r j o i n r d i s o r de r s . A c t aStomatol Beig 1992;89:169-179.
7 7 . Nant imark U, Sennerby L, Haraldson T. Macroscopic,microscopic and radiologie assessment of the condylarpatI of rbe TMJ in elderly subjects. An autopsy study.Swed DentJ . 1990;14:163-169.
7 8. Latheim TA, Bjornland T. Arthrog raphic findings in thetemporomandibular joint in patients witb rheumatic dis-ease. J Oral Maxillofac Surg 198?i47t780-784.
7 9. Sa lo L , Raus t i a A, Pernu H , Vi r t a nen K. In te rna lderangement of tbe temporomandibular joint: A histo-c he m i c a l s t udy . J O r a l M a x i l l o f a c S u r g 1991^ 49 :17 1 - 17 6 .
80 . Brand JW, Whinery JG, Anderson QM , Keenan KM. Theeffects of temporomandibular joint interval derangementand degenerative joint disease on tomogtaphic and arthro-romographic images. Oral Surg Oral Med Oral Pathol19S9;67:220-223.
81 . Schel lhas KP. Intern al deran gem ent of the tem po ro-mandibular joint: Radiologie staging with clinical, surgi-cal, and pathologic correlat ion. Magn Reson Imaging
82 . Stegenga B, deBont LG, Boenng G. Osteoarthritis as thecause of craniumandibular pain and dysfunction: A uni-f y i n g c o n c e p t . J O r a l M a x i l l o f a c S u r g 1 9 8 9 ; 4 7 :249 - 25 6 .deBont LG, Sregenga B. Pathology of temporomandibular¡oint internal derangement and osteoarthrosis. Int J OtalMaxillofac Surg 1993;22:71-74.Pelletier JP, Martel-Pelle tier J. Evidence for the invo lve-ment of Interleukin 1 in human osteoarthritic cartilagedegradation: Protective effect of NSAID. J RheumatclSuppl 1989i l8 : I9-27 .Hulmlund A, Hellsing G. Arthroscopy of the temporo-mandibular joint: Occurrence and location of osteoarthro-s is and syn ovi t i s in a pa t i en t ma te r i a l . In t J Or a lMaxillofac Surg 1988;17:36^O.Strom H, Alexandersen S, Poulsen OM, Hau J. Synovialfluid proteins in degenerative joint disease in dogs. VetItnmunol Immunopathol 1989;2Z;187-196.Holmlund AB, Gynther G, Reinhol t FP. Rheumatoidarthritis and disk derangement of the temporomandibularjoint. A comparative arthroscopic study. Oral Surg OralMed Oral Pathol 1992;73i273-277.Thonar EJ, Glart T. Serum keratan sulfate: A marker ofp r e d i s pos i t i on t o po l ya r t i c u l a r o s t e oa r t h r i t i s . C l i nBiochem 1992;25:175 -180.Malemud GJ. Ghanges in proteoglycans in osteoarthritis:
Biochemistry, ultcastructure and biosynthetic processing. JRheumatol Suppl 1991;27 :60-â2.Hardingham T, Bayliss M. Proteoglycans of articular car-t i lage: Ghanges in aging and in joint disease. SeminArthritis Rheum 1990;20(3 suppl l}:12-33.
Montella A, Manunta A, Espa E, Gasparini G, De SantisE , G u l i s a no M . H um a n a r t i c u l a r c a r t i l a ge i nosteoa rthrosis . 1. The m atrix. Transm iss ion electronmicroscope srudy. Arch I tat Anat Enibriol 1992;97:1-12.Richard M Broquet P. Vignon E, Pescbard MJ, GarretJP , Louisot P. Galmodulin-dependent collagenase and
proteoglycanase activities in cbondrocytes from humanosteoarthritic cartilage. Biochem Biophys Res Commun199T;174:1204-1207 .Gruz TF, Mills G, Pritzket KP, Kandel RA. Inverse cor-relation between tyrosine phosphorylation and collage-nase produc t ion in chondrocytes . B iochem J 1990;2 6 9 : 7 1 7 - 7 2 1 .Docherty AJ, Murphy G. The tissue metalloproteinasefamily and the inhibitor TIMP: A study using cDNAsa nd r e c om bi na n t p r o t e i n s . A nn R he um D i s 1990 ;49 : 469 - 7 9 .Martel-Pelletier J, Pelletier JD, Malemud GJ. Activationof neutral metalloprotease in human osteoarthritic kneecartilage: Evidence for degradation in the core protein of
sulpha ted proteoglycan . Ann Rheum Dis ]988;47 :801-808 .Gbenilï JE. Rheumatoid arthritis and its implications int e m por o m a nd i bu l a r d i s o r de r s . J G r a n i om a nd P t a c t1992;10:59-69 .Woessner JF Jr, Gunja-Smith Z. Role of metallopro-teinases in human osteoarthri t is . J Rbeumatol Suppl1991;27 :99-101 .Dean DD, Martel-Pelletier J, Pelletier JP, Howell DS,Woessner JF Jr. Evidence for metalloproteinase and met-al loproteinase inhibi tor imbalance in human osteo-artbritic cartilage. J Glin Invest 1989;84:é7B-685.Quinn JH, Bazan NG. Identification of prostaglandin E2
and leukotriene B4 in the synovial fluid of painful, dys-functional temporomandibular joints. J Oral MaxillofacS u r g 9 9 0 ; 4 8 : 9 6 8 - 9 7 1 .Huet G, Flipo RM, Golin G, Jatiin A, Hemon B, Collyn-d'Hooghe M, et al. Stimulation of the secretion of latentcysrein protein a se activity by tum or necro sis factor alphaand in ter I eu kin-L Arthritis Rheum 199 3i3 é:77 2-7 80.Venn G, Nietfeld JJ, Duits AJ, Brennan FM, Arner E,Covington M, et al . Elevated synovial fluid levels ofinterleukin-6 and tumor necrosis factor associated withe a r l y e xpe r i m e n t a l c a n i ne o s t e oa r t h r i t i s . A r t h r i t i sRheum 1993;36:819-826.Ishimi Y, Abe E, Jin CH, Miyaura C, Hong MH, OshidaM , et al. Leukemia inhibitory factor/diffetentiation-stlm-ulating factor (LIF/D-factor) Regulatioti of its prodifc-t ion and poss ible roles in bone metabol ism. J Cel lPhysiol 1992i l52:71-78.Pujol JP, Galera P, Redini F, Mauviel A, Loyau G. Roleof cytokines in osteoarthritis: Comparative effects ofinterleukin 1 and transformin g grow th factor-beta oncul tu ted rabbi t a r t i cu la r chondrocytes . J RheumatolSuppl 1991;27:76-79.Loyau G, Pujol JP. The role of cyrokines in the develop-ment of osteoarthritis . Scand J Rheumatol Suppi 1990;81:8-12 .Wood DD, Ihrie EJ , Hamerman D. Release of inter-leu kin-1 from bu ma n syn ovial tissue in v itro. A rthritis
Rheum 1935 ;28:8Í3-862.Iro A, Hagihara M, Nagatsu T, Iwata H, Miura T.Gollagenase-like (GLj peptidase activity in synovial fluidfrom patients with rheumatoid arthritis. Glin Gbim Acta1987;170:291-296.
107, Iw ase -O ka da K , Na ga t su T , Fu j i ta K , To r ika i K ,Hamamoto T, Shibata T, er al . Serum collagenase-likepepridase activity in rheumatoid arthriris and systemiclupus erythematosis. Cl in C him Acra 198 5a4 6;75 -79 ,
108, Koiima K, Kinoshita H, Karo T, Nagatsu T, Takad a K,Sakakibara S, A new and highly sensitive fluorescenceí issay for col lagenase-l ike pept idase af t ivi ry. Anal
Biochem 1979; 100:4 3-50,109, Kato T. Na ka no T, Ko)ima K, Nagatsu T, Sakakibara S,Changes in prolyl endopepridasc durmg maturation ofrjt brain and hydrolysis of subsrance P by the purifiedenzyme, J Neurochem 1980;35 :527-535 ,
110, Wa lter R. Partial purification and charac terization of post-proline cleaving enzyme: Enzymatic inactivation of neuro-hypophyseal hormones by kidney preparations of variousspecies, Biochim Biophys Acta 1976;422:13S-158,
111, Wa lter R, Shiank H, Glass JD , Schwartz IL, Kerenyi TD ,Leucyl glycinamide released from oxytocin by humanuterine enzyme. Science 1971;173:827-829,
112, Yoshim oto T, Ogita K, Walter R, Koida M, Tsuru D,Post-proline cleaving enzyme. Synthesis of a new fluoro.
genie substrate and distribution of the endopeptidase inrat rissaes and body fluids of man, Biochem BiophysActa 1979;569;184-192.
113, Fukuoka Y, Hag ihata M . Nagatsu T, Kaneda T. Therelationship between collagen metabolism and temporu.m a n d i b u l a r j o i n t o s t e o a r r h r o s i s i n m i c e . J O r a lMaxi llofac Surg 1993;51:2 88-29 1,
114, Rosner IA, Malem ud CJ, Hassid Al, Goldberg VM, BujaBA, Moskowirz RW, Estradiol and tamoxifen stimula-tion of lapine articular chondrocyte prostaglandin syn-thesis, Prostaglandins 19S3;26:123-138,
116, Solberg WK, Hatisson TL, Nordsrrom B, The remporo-mandibular joint In young adults at autopsy: A morpho-log ic c l a ss i f i ca t ion and eva lua t ion . J Ora l Rehabi l1985;12 :303-321 ,
117, Mc Nam ara JA Jr, Carlson DS, Qua ntitative analysis oftemporomandibular joinr adaprations to protrusive func-t ion. Am J Orthod 1979;76:593-611,
118, Mc Nam ara JA Jr, Functional adaprations of tbe tetnporo -mandibular joint. Dent Clin North Am 1975;19:457-471,
115, Hickory W, Na nda R, Adapt ive changes of temporo -mandibular joint ro maxillary protraction in monkeys, JDent Res 1981;60(specL3l issue A}:arricle 915,
120, Mo ngini F, Rem odeling of rhe ma ndib ular condyle in
rhe adult and its relationship to the condition of the den-tal arches. Acta Anai {Basel) 1972;82:437-453,121, Korioth TW, Han nam AG, Effect of bilateral asymmer-
ric toorh clenching on load distribution at the mandibu-lar condyles. J Prosthet Dent 1990;54:62-73.
122, dos Santos J Jr, de Rijk WG . Vectorial analysis of rheinsrantaneous equilibriutn of forces between incisai andcondylar guidances, J Craniomand Pract 1992;I0 :3O5-312.
123, McNeill DJ, How ell PG. Com puterized kinesiography inrhe srudy of masrication in dextrate subjects, J ProsthetDent 198Ê;55:62S-638,
124, Lipp MJ, Tem porotn andibu lar symptoms and occlusion:A teview of the literature and the concept, J Golo DentAssQc l991 ;69 :18-22 ,
125, Pullinger AG, Seligman DA, Gorn bein JA, A multiplelogistic regression analysis of the risk and relative oddsof temporomandibular disorders as a function of com-mon occlusal features, J Dent Res 1993;72:96a-979,
138,
139,
142,
143,
Sehgman DA, Pullinger AG, Association of occlusalvariables among refined TM patient diagnostic groups.J Craniomandih Disord Facial Otal Pain 1989^3:227-236 ,Bush FM, Malocciusion, masticatory muscle and tem-p o r u m a n d i b u l a r j o i n r t e n d e r n e s s , J D e n r R e s1985;64:129-133,
De Laat A, van Steenberghe D, Lesaffre E, Occlusal rela-t ionships and TMJ dyi lunct ion. Part I I , Corre la t ionbetween occlusal and articular parameters and symp-toms of TMJ dysfun ction by mean s of stepwise logisticregression, J Prosthet Dent 1986;55 :116-121 ,Droukas B, Lindee C, Garlsson CE, Occlusion andma ndib ular dys function: A clinical study of patientsreferred for functional disturbances of rhe masticatorysystem, J Prosthet Dent 1985;53:402^06,Dii inkerke AS, Lutei jn F , Bouman TK, dejong HP,Relat ions between TMJ pain dysfunct ion syndrome(PDS| and some psychologic and biologic variables.Community Denr Oral Fpidcmiol ]985;13il8.î-189,Hannam AG, De Cou RF, Scott JD, Wood WW, Therelationship between dental occlusion, muscle acriviryand associated jaw movement in man. Arch Oral Biol1977;22:25-32,Pulhnge r AG, Se l igman DA, So lbe rg WK,Temporomandibulat disorders. Part II: Occlusal factorsassociared with temporomandibular joinr tenderness anddysfunction, J Prosthet Dent 1988i59:3ft3-3é7,Pullinger AG, Seligman DA, Overbite and overjer chat-acreristics of refined diagnostic groups of remporo-mandibular patients. Am J Orthod Dentofacial Orthop1991;100:401-115,Seligman DA, Pullinger AG, The role of futictiotial inter-cuspal relationships in cemporomandibular disorders: A
review, J Craniomandib Disord Facial Oral Pain 1991;5:96-106,Watmian A, Agerberg G, Etiology of craniomandibulardisorders: Evaluation of some occlusal and psychosocialfactots in 19-year.olds, J Craniomandib Disord FacialO ta l Pain 1991 ;5 :35^4 ,e l - L a b b e n N G , H a r r i s M , H o p p e r C , B a r b e r P ,Degenerative chan¡;es in masseter and temporalis mus-cles in limited mouth opening and TMJ ankylosis. OralSurg Oral Med Oral Pathol 1990; 9:423-425,Kampe T, Hannerz H. Five-year longitudinal srudy ofadolescents with intact and restored dentitions: Signsand symptoms of temporomandibular dysfunction and
functional recordings, J Oral Rehabil l991 ;18:3 87-3 98,Berretr A, Radiography of the temporomandibular joint.Dent Clin Notcli Am 1983;27:527-540,Ogtis H. Degenerative disease of the tetnporomandibularjoint and pain dysfunction syndrome, J Royal Soc Med1978;71:748-754-R a s m u s s e n O C , T e m p o r o m a n d i b u l a r a r t h r o p a t h y :Cl in i ca l , r ad io log ie , and the rapeur i c a spec t s , w i thetnphasis on diagnosis, Int J Oral Surg 1983;12:365-397,Rasmussen OC, Chnjcal finditigs during rhe course ofcemporomandibu ia r a rchropa thy , Scand J Denr ResI981 ;89 :283-28g ,Kopp S, Glinical findings in temporomandibulat joint
osteoarrhrosis, Scand Dent Res 1977;85:434-443,Bean LR, Omnell KA, Oberg T, Comparison berweenr a d i o g r a p h i e o b s e r v a t i o n s a n d m a c r o s c o p i c t i s s u ecbanges in temporotnandibular joints, DentomaxillofacRadiol 1977:6:90-106,
Kopp S, Rockler B, Relationsliip between clinical andradiographie findings in patiems with mandibular painor dysfmicrion. Acta Radiol |Diag] 1979;20:465^77,Rasmiisîen C. Longitudinal study of cransphatyngealradiography in cemporomandibular arthrop athy, Scand JD e m R e s l 980 ; 88 ; 257 - 2é 8 ,Kopp S, Rockler B, Variation ¡n interpretation of radio-
graphs of temporomandibular and hand joints, Dento-maxillofac Radiol 1978;7;95-1O2,Lindvall AM, Helkimo E, Hollendtr L, Carlsson GE,Radiographie examinat ion of the temporomandihularjoints, A comparison between radiographie findings andg r o s s m i c r o s c o p i c m o r p h o l o g i c o b s e r v a t i o n s ,Dentomaxillofac Radiol 1976;5:24-32.Carlsson GE, Lundberg M, Oberg T, Welander U, Thetemporomandibular joint, A comparative anatomic andradiologie study, Odont Revy 1968;15a7l-185,Martel W, Adler RS, Chan K, Nika son L, HeWie MA ,j ons s on K , O ve r v i e w ; N e w m e t hods i n i m a g i ngosreoarthriris, J Rheumatol Suppl 1991;27;32-37,McAlindon TE, Wart I, McCrae F, Goddard P, Dieppe
PA, Magnetic resonance imaging in osteoarrhritis ot theknee: Correlation with radiographie and 5cintigraphicfindings, Ann Rheum Dis 1991;50;14-19,Munk PL, Vellet AD, Lesions of cartilage and bonearound che knee. Top Magn Reson Imaging 1993;5:249-262,Adams ME, Li DK, McConkey JP, Davidson RG, Day B,Duncan CP, Tron V, Evaluation of cartilage lesiotis bymagnetic resonance imaging at 0,15 T: Comparison witha n a t o m y a n d c o n c o r d a n c e w i t h a r t h r o s c o p y , JRheumatoi 1991;18,1S73-158O,Gahunia HK, Lsmaire C, Cross AR, Babyn P, KesslerMJ, Pntzker KP, Osteoarthrosis in rhesus macaques:
Assessment of cartilage matrix quality by quantitativemagnet ic resonance imaging. Agents Act ions Suppl1993 ; 39 : 2 i i - 259 ,O'Byrne EM, Paul PK, Roberts ED, Blancuzzi V, WilsonD , Goldberg RL, DiPasquale G, Comparison of mag-netic resonance imaging (MRI) and histopathology inrabbit models of osteoarrhriris and immune arthritis.Agents Actions 1993;39(special issue C¡il57-159,Ho C, Cervilk V, Kiellin 1, Hagh.gi P, Amiel D, TrudellD . Resnick D, Magnetic resonance imaging in assessingcartilage changes in experimenral osreoarthrosis of theknee. Invest Radiol 199 2;27:84 -90,Kalunian KC, Hahn BH, Eassett L, Magnetic resonanceimaging identifies early femoral head ischémie necrosis
in patients receiving systemic glucocorticoid therapy, JRheumatoi 1989;16:959-963,B ong a r t z G , B o t k E , H o r ba c h T , R e qua r d t H ,Degenerative cartilage lesions of rhe hip: Magnetic reso-n a n c e e v a l u a t i o n , M a g n R e s o n I m a g i n g I 9 8 9 ; 7 :179-186,Blaekburii WD Jr, Bernreuter WK, Rominger M, LooseLL, Arthroscqpic evaluation of knee articular cartilage:A comp arison with plain radiog raphs and m agnetic reso-nance imaging, J Rheumatoi 1994;21:é75-é79,Dreinbofer KE, Schwarzkopf SR, Haas NP, Tsclieriie H.Isolated t raumatic dis locat ion of the hip. Long-termresul ts in SO pat ients . J Bone Joint Surg [Br | 1994;
76:6-12,Murakami S, Takahashi A, Nishiyama H, Fujishita M,Fuchihata H, Magnetic resonance evaluation of the tem-poromandihular ]oint disc position and configuration,Dentomaxillofac Radiol 1993;22:2Ü5-2Ü7,
R a us t i a A M , T e r v one n O , P yh t i ne n J , T e m p or o -mandihular joint f indings obtained hy brain MRL JCraniomand Pract 1994;12:28-32,Bell KA, Miller KD, Jones JP. Cine magnetic resonanceimaging of the temporomandibular joint, J CraniomandPract 1992;10i313-317,Wa t t - S m i t h S , S a d l e r A . B a dde l e y H , R e n t on P ,Comparison of arthrotomographit and magnetic reso-nance images of SO tem por om and ihu lar joints withoperat ive f indings , Br J Oral Maxil lofac Surg 1993;31:139-143 ,Santler G, Karcher H, Simbrunner J. MR imaging of rheTM J , MR diagnos i s and in t raop era t ive f indings , JCraniomaxillofac Surg 1993;21;284-288,Thonar EJ , Shinmei M, Lobmander LS, Body f luidmarkers of cartilage changes in osteoarthritis. RheumDis Chn orth Am 1 9 9 3 ; 1 9 T 6 3 5 - 6 5 7 ,
Carney SL, Cartilage research, biochemical, histologie,and lmmunohistochemical markers in cartilage, and ani-mal models of os leoarthri t is , Curr Opin Rheumatoi1991;3 :669-675,
Kamada A, Fuj i ta A, Kakudo K, Okazaki J , Ida M,Sakaki T, Changes in synovial fluid N-acetyl-beta-glti-cosaminidase activity in the human temporomandibularjoint with dysfunction. J Osaka Dent Univ 1993;27:107-111 ,Homandberg GA, Hui E , Arg-Gly-Asp-Ser pept ideanalogs suppress cartilage chondrolytic activities in inte-grin-binding and nonbinding f ibronect in fragments .Arch Biodiem Biophys 1994;310:40-48,Hom andberg GA, Meyers R, Williams JM . Imraarticularinjection of fihronectin fragments causes severe depletionof cartilage pioteoglycans in vivo, J Rheumatoi 1993;20:1378-1382,
Xie DL, Meyers R, Homandberg GA, Fibronectin frag-ments in osteoarthritic synovial fluid. J Rheumatoi 1992;19:1448-14S2,Boering G, Stegenga B, deBont LG, Temporomandibularjoint osteoarthrosis and internal derangement. Part I,Clinical course and initial treatment, Int Dent J 1990;40:339-346,Magnusson T, Carlsson GE, Treatment of patients withfunctional disturbances df the masticatory system. A sur-vey of 80 consecut ive parients , Swed Denr J 198C;4i 145-1 S3 .
Poswillo D, Conservative management of degenerativetemporomandibular joint disease in the elderly, Irt DentJ 1 9 8 3 ; 3 3 : 3 2 5 - 3 3 1 ,
Stegenga B , Di jk s t ra PU, deBont LG, Boer ing G,Tempocomandibular joint os teoarthrosis and internalderangement. Part II, Additional treatment options, IntDent J 1990;40:347-353,Clark GT, Meriil RL, Diagnosis and non-surgical treat-ment of masticatory muscle pain and dysfunction. In:Sarnat BG, Laskin DM (eds]. The TemporomandibularJoint: A Biological Basis for Clinical Practice, Phila-delphia: Saunders, 1992:346-356,Rocabado M, Physical therapy for the postsurgical TMJpatient, J Craniomandib Disord Facial Oral Pain 1989;3:75-S2,Gray RJ , Quayle AA, Hal l CA, Schof ie ld MA,
Physiotherapy in the t reatment of temporomandibularjoint disorders: A comparative study of four tréarmentmethods, Br Dent J 1994; 176:257-2 61,Brown KE, Dynamic opening device for mandihular tris-mus, J Prosthet Dent 1968;20:438^42,
Campbell J. Extension of the temporomandibular iointspace by methods derived from general orthopedic pro-cedures. J Prosthet Dent 1 9 S 7 ; 7 Í 3 8 6 -3 9 9 .Sears VH. Occlusal pivotal splints. J Prosthet Dent 1956-6 : 3 3 2 - 3 3 8 .Berry DC. Occlusal pivots. A cas1 9 6 2 ; I 2 : 3 3 7 - 3 3 8 .R a s m u s s en O C . T r e a t m e n t o f t e m p o t o m a n d i b u l a rarthroparhy. Scand J Dent Res 19 82^90:64-68.Clark GT, Beemsterboer PL, Soiberg WK, Rugh JD.Nocturnal electromyographic evaluation of myofascialpain dysfunction in patients undergoing occlusal splinttherapy. J Am Dent Assoc 1979;99:607-611.Chung SC, Kim HS. The effect of rhe stabilization splinton the TMJ c losed lock . J Craniomand Prac t 1993-11: 95-101.Soiberg WK, C la rk GT, Rugh JD. Noc turna l e l ec -tromyographic evaluation of bruxism patients undergo-ing short term splint treatment. J Oral Rehabil 1975;2 : 2 1 5 - 2 2 3 .Ahlqvist J, Legrell PE. A technique for the accurate
a dm i n i s t r a t i on o f c o r t i c os t e r o i d s i n t he t e m por o -mandibula r jo in t . Dentomaxi l lofac Radiol 1993 ; 22:2 1 1 - 2 1 3 .Pelletier JP, Cloutier JM, Martel-Pellerier J. In vitroeffects of NSAfDS and corticosteroids on the synthesisand secretion of interleukin 1 by human osteoarthriticsynovia l membranes . Agent s Ac t ions SuppI 1993 ; 39 :1 8 1 - 1 9 3 .Pelletitr JP, Mineau E, Raynauld JP, Woessner JF Jr,Gunja-S mith Z, M art e I-Pelle tier J. Intra artic ular injec-t ions with methylprednisolone acetate reduce os teo-arthritic lesions in parallel with cbondrocyte strömelysinsynthesis in experimental osteoartbritis. Arthritis Rheum
1 9 9 4 ; 3 7 : 4 1 4 - ^ 2 3 .Schni tzer TJ . Osteoartht i t is t teatnient update. Mini-mizing pain while limiting panent risk. Postgrad Med1 9 9 3 ; 9 3 : 8 9 - 9 2 , 95Wada J , Kosbino T , Mor i i T , Sugimoto K. Na tura lcourse of osteoarthritis of the knee treated with or with-out inttaarticular corticosteroid injections. Bull Hosp Jt
191. Pelletier JP, Ma rtel-Pe lletier J. In vivo pro tective effectsof prophylac t i c t rea tment wi th t i aprofenic ac id orintraarticular corticosteroids on osteoarthritic lesions int h e e x p e r i m e n t a l d o g m o d e l . J R h e u m a t o l S u p p I1 9 9 1 ; 2 7 i l 2 7 - 1 3 0 .
192. Matteso n EL, M cCu ne WJ. S eptic arthritis caused bytreatment resistant Pseuom onas cepacia. Ann Rheum Dis1990^49:258-259 .
Agus B, Weisberg J, Friedman M H. Therapeu tic injec-t ion of the temporomandibular joint . Oral Surg OralMed Ora l Pa thol 19 83 ;55:553-555.
Fader KW, Grum mon s DC, Maijer R, Christensen LV.Pressurized infusion of sodium hyaluronate for closedlock of the temporomandibular joint . Part I : A caseStudy. J Craniomand Pract 19 9 3 ;11:68-7 2.
S wann DA. M acro mo iecul es of synov ia l f lu id . In :S okoloff I. ed¡. Tbe Joints and S ynovial Eluid. Orlan do,EL: Academic Press, 1 9 78:407 -43 5.
196 . Radin EL, Paul IL, S wann DA, S chottstaedt ES. Lub ri-cation of synovial membrane. Ann Rheum Dis 1971;30:3 2 2 - 3 2 5 .
1 9 7 . Leardini G, Perbellini A. Franceschini M, M attara L.Intra-articular injections of hyaluronic acid in the treat-ment of painful shoulder. Clin Ther 1988;10:i21-526.
Liu C, Swann DA. Use of sodium hyalutonate in treatingtemporomandibula r jo in t d i sorders : A randomized,doub le-blind, p lacebo-co ntrolled clinical trial. J OralMaxillofac Surg 993;S 1:232-242.
1 9 9 . Mejersjo C. Therapeutic and prognostic considerationin TMJ osteoarthrosis: A literature review and longterm study of 11 subjects. J Craniomand Pract 1987;5 i 6 9 - 7 S .
200. Re ich RH. Tem porom andibu la r jo in t surgery . CurrOpinDent 1992 ;2 :17-24.
201 . M urak am i K, Clark GT. Diagnosis of inrracapsularpathology associated with tempotomandibular joint dis.otders . Adv Dent Res 1993;7a20-126.
202. S tegenga B, deBont LG, Dijkstra PU, Boering G. S hort-
t e rm outcome of a r throscopic surgery of t emporo-mandibular joint osteoarthrosis and internal derange-ment: A randomized controlled clinical trial. Br J OralMaxil lofac Surg 1993;31:3-14.
2 0 3 . B j o r n l a nd T , R or v i k M , H a a na e s H R , T e i ge J .Degenerative changes in the temporomandibular jointafter diagnostic arthroscopy. An experimental study ingoats. Inl J Oral Maxillofac Surg 1994;23:4I--i5.
204. S harawy MM , Helmy ES , Bays RA, Larke VB. Repair oftemporomandibular joint disc perforation using a sy-novial membrane flap in Macaca fascicularis monkeys:Light and electron microscopy studies. J Oral MaxillofacS urg 19 94^52:25 9 -2 70;[discussion]270-271.
205 H a n s s on L G , P e t e r son A . V a l l on - C hr i s t e r s s on D .Clinical and radiographie six year follow-up study ofpat ients with crepi tat ion of the temporomandibularjoint . Swed Den tJ 19 84;g:277-287.
206 . Gteene CS , Marko vic MA. Response to nonsurgicaitreatment of patients with positive tadiographic findingsin the temporomandihular joint. J Oral Surg 1976;34:6 9 2 - 6 9 7 .
207. Yoshim ura Y, Yoshida Y, Oka M, Miyoshi M, Uem uraS. Long term evaluation of non-surgical treatment ofos teoarthrosis of the temporomandibular joint . Int JO r a l S u r g 1 98 2a i : 7 - 1 3 .
208. deLeeuw R, Boering C, Stegenga B, deBont LG. Clinicalsigns of TMJ osteoatthrosis and internal derangement
30 years after nonsurgicai treatment. J Orofacial Pain1994 ;8 :18-24.
2 0 9 . Pullinger AG, S eligman DA. TMJ osteaarth rosis: A dif-ferentiation of diagnostic subgroups by symptom historyand demographics. J Craniomandib Disord Facial OralP a i n l 9 8 7 ; l : 2 5 1 - 2 5 6 .
210 . S eligman DA, Pullinger AC. TMJ derangem ents andosteoarthrosis subgroups different iated according toactive range of mandibular opening. J CraniomandibDisord Facial Oral Pain 1988;2:35^0.
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 y
presenta i a rajón funda m en ta i de ios enfoques de diagnóstico y
tratamiento.
Das Fortschreiten einer degenerativen Gelenkerkrankung hangtvom ihr zugrundeliegenden palhoiogischen und/oder reaktivenProzess ab. der. im allgemeinen, die Adaptationsfáhigkeit des
Gewebes 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, die
das Gleichgewicht zwischen Remodeling und Degeneration im
Kiefergelenk beeinflussen kónnen und stellt Grundprinzipien zur
Diagnose und Therapie vor.
ABOP Cert i f icat ion
The American Board of Orofacial Pain ABOP}was founded in 1994 in response to the need for a
valid certification process for dentists practicingorofacial pain management. The ABOP will offerannual cert ification examinations to dentistslicensed in the United States. The application for
the 1996 examination will be available on June 11995. For more information, please write to: The
American Board of Orofacial Pain, 10 JoplitiCourt, Lafayette, California 94549.
