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Home , Osteoarthritis

Degenerative of the Temporomandibular

Lome S. Kamelchuk, DDS, MSc Progression of degenerative joint disease is dependent on the Clinical Instructor, Research Fellow underlying patbotogic and/or reactive processes involved that, in Department of Stomatology general, compromise tissue adaptability. A review of clinical and Paul W, Major, DDS, MSc, MRCDtC) experimental literature relating to degenerative joint disease is pre- Associate Professor sented. Epidemiology, pathogenesis, diagnosis, treatment, and Department of Stomatology prognosis are described witb particular emphasis given to the tem- poromandibular joint. Tbis article describes factors affecting tbe university of Alberts remodeling/degeneration parity and pre- Edmonton, Alberta sents rationale for approacbes to diagnosis and treatment. Canada J OROFACIAL 1995;9:I68-13O, Correspondence to: Dr Lorne S, Kamelchuk key words: temporomandibular joint, degenerative joint disease, University of Alberta osteoarthriris 4068 Dentistry Pharmacy Centre Edmonton, Alberia T6G 2N8 Canada

reakdown of temporomandibular joint (TMj) tissues, and articular surfaces in general, may occur due to an increased Bmechanical 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 and capsulitis; (5) arthritides including osteoarthrosis, osteoarthritis, and ; and (6) ,'' 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 commonly implicated in the progression of DJD, Diagnoses of DJD reflect dis- ease processes of tissue deterioration in which soft tissue, , and 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 nonadaptive response (degeneration).

168 Volumes, Number 2, 1995 Kamelchuk/Major

Epidemiology ematical""'" and finite element-analysis mod- els.""'" Each TMJ is a pressure-bearing, compound, Literature relating to epidemiology of degenerative double-.'" disease of the TMJ is descriptive and retrospective, Repetitive cyclic microtrauma has heen impli- Schiffman et al''' conclude that approximately 7% cated in the etiology of DJD. Repeated impact of the general population may benefit from treat- loading of cartilage-lined articular surfaces results ment for TMJ problems and that tnost symp- in an increased rate of osteogenesis in subchondrai tomatic subjects can function adequately without hone evidenced radiographicaily as subchondrai treatment. Of patients treated at cemporomandihu- sclerosis.'" Affected hone, of increased stiffness, lat dysfunction clinics, 8% to 12% receive diag- may increase the susceptibility of articular carti- noses of DJD.""'" Autopsy results confirm TMJ lage to trauma caused hy impact," with loss or prevalence that varies from degeneration of cartilage normally resistant to 22% to greater than 40% of the population,'"'' compressive stress. In the TMJ, reducing disc dis- with osteoarthritis of the TMJ commonly appear- placements may potentiate repetitive impact load- ing asymptomacically.-- Data support the concept ing*' and consequently lead to a subchondrai scle- that aging women seem co be more prone to DJD rosing known to occur prior to the onset of DJD." than are men."''°'"-^ Whether or not DJD can be attributed to the cumulative effect of repetitive minor trauma to normal TMJ articular tissue remains debatable. Pathogen es is Major trauma to synovial may progress to DJD,'"' Excessive |oint loading may disrupt the nor- Role of Aging mal adaptive capacity of articular tissue, resulting in eventual cartilage breakdown and elevated pro- There is a general association between the incidence teoglycan levels in the .''" Kopp et of DJD and increasing age. Studies indicate that the al*" conclude, however, that degenerative changes frequency of DJD increases in older persons,""-'-'"" described in their autopsy material are probably suggesting that age is a predisposmg factor. The mostly due to local factors. While synovial fluid mcidence of tooth loss and osteoarthritis is associ- aspirates of joints that show arthroscopic evidence ated with increasing age,"'-*"" hut vi'hen age is con- of DJD contain elevated levels of keratin sulfate,'" trolled, the associarion is coincidental.•'•^" Attrition histochemical studies of articular surfaces that has also, independently of age," heen associated macroscopically demonstrate DJD have shown a with TMJ osteoarthritis despite irs questionable eti- reduction in sulfated glycosammoglycan." ologic role.'"' Although age may be correlated with Arthritic lesions of the TMJ are most often observations of temporomandibular DJD, the pos- localized in the lateral aspect of the temporal sible correlation does not elucidate etiology. fossa, compared to the medial aspect.'"-''" Lesions Age-related changes in articular tissues have been are markedly fewer in the condyle than in the tem- documented. The fibrous component of the matrix poral component. In a study of location of osteo- of aged articular tissue of the TMJ consists of a archritic lesions in patellofemoral compartments of well-organized network occasionally dis- 39 cadaveric joints," it was hypothesized that persed with elastic fibers." The overall amount of articular cartilage adapts mechanically to transmit, collagen does not .significantly decrease with aging; without sustaining damage, the stress to which it is however, infrastructural alterations occur. Proteo- most regularly subjected, and that damage occurs glycan content decreases and binding quality is only if cartilage is subjected to less frequent but altered. In mice, TMJ cellularity generally decreases much higher stress.'" Articular tissue thickness and with aging, resulting in loss of proliferative zone distribution probably reflect areas of stress concen- potential." Such age-related changes in the articular tration in the condylar and temporal compo- tissues affect their mechanical properties and, in nents,*^' with the lateral part of the joint exposed to turn, may facilitate rhe pathogenesis of DJD, the largest functional and parafunctional loads." Incongruities between loaded TMJ articular sur- faces predispose to stress concentrations that are Joint Loading and Stress Distribution observed more frequently in the temporal compo- Strong evidence exists to suggest the TMJ is loaded nent where degenerative lesions more commonly during function.^'"'* Intensity and direction of occur," Stresses generated hy various occlusal forces have Adequate lubrication of the TMJ components is been analyzed utilizing three-dimensional math- required to facilitate the mechanics of joint mo-

Joumal of Orofscial Pain 169 Kameichuk/Major

tion. The tipper joint compartment is subject to but reducing discs, and displaced nonredticing transktory movenietit while the lower undergoes discs, perforations were found only in cases with rotational movement."' Differences in the fre- DjD."' However, 73% of the cases with DJD did qtiency of degenerative lesions hetween the condy- not have perforations. These observations suggest lar anid temporal components may he dtic to it is more likely that DJD is the cause and perfora- greater frictiona! loading between the disc and tion is rhe effect. temporal components than hetween the condyle Schellhas"' regards internal derangement of the and disc. Nitzan and Dolwick'^ suggest that a lack TMJ as an irreversible and generally progressive of gliding in the joint can be attributed to disc disorder that may he staged clinically. Stegenga adherence to the fossa by a reversible effect stich as et al*' hypothesized that TM joints are subject to vacuum and/or decreased volume of high-viscosity a continual process of articular surface break- synovial fluid. Decreased synthesis of the glycopro- down and repair. If the degradarive response tein luhricin, normally associated with the lubrica- exceeds the reparative response, then a DJD pro- tion fraction of synovial fluid, may be involved in cess is initiated. The gliding capacity of the artic- the etiology of DJD.'' Lack of joint lubrication may ular disc may become impaired, thus predispos- exacerbate articular tissue failure by increasing fric- ing to internal derangement. Stegenga et ai"- tional resistance during loaded joint movements. suggested that internal derangement is an accom- panying sign of DJD and is capable of causing a rapid progression of the disorder. Stegenga et al*^ Internal Derangement concluded that in many cases of temporoman- Internal derangement of the TMJ, particularly dibular dysfunction, DJD is the primary disor- with disc deformation, may progress to DJD. der, and that the accompanying muscle pain and Position and configuration of the articular disc has internal derangement is secondary.'^ been related to DJD.'"-"" Westesson" conducted a radiographie study including arthrograms on 12S patients with internal derangements. Osseous Inflammatory/Histochemical Considerations changes were seen in 50% of the patients with Histologie studies of synovium of degenerative anterior disc displacement without reduction but joints show a significant amount of inflamma- seldom in patients with disc displacement with tion""*" and turnover.*""'" In appen- reduction. Degenerative changes were consistently dicular joints with cartilage articular surfaces, found in joints with disc perforation. Anderson early stages of DJD show fibrillation and fissures and Katzberg"' obtained comparable findings with at the articular surface level that will eventually a tomographic and arthrographic study of 141 progress to a complete erosion of rhe cartilage." patients with temporomandibular dysfunction. Pathologic changes appear ro be related to in- Only 9% of the patients with a reducing displace- creased levels of metalloproteinases that produce ment showed signs of degeneration, but 39% of both a breakdown of the collagen network""'" and the patients with nonreducing disc displacement a size reduction of the proteoglycan monomer."'"'' and 60% of the patients with perforation had The TMJ articular surfaces are covered with fi- degenerative changes. These authors*"'"' conclude brous connective tissue, as opposed to hyaline car- that, in many cases, internal derangement of the tilage, but research suggests*'**'" that inflammatory TMJ precedes degenerative disease. changes in articular matrix components are (1) There is a relationsbip between disc perforation responsible for impairment of the physicochemical and degenerative disease of the TMJ."*""- Surgical properties of the articular surfaces and (2) likely to creation of hilateral disc perforation in Macaca contribute to the development of DJD. fascicularis monkeys produces pathologic alter- In addition to mediators of ," other ations consistent with DJD in the majority of biochemical mediators have been identified with experimental joints."'"' In humans, observed perfo- DJD and osteoarthrosis. The cytokmes interleukin- rations localized ro the posterior attachment of the 1 (IL-1) and interleukin-6 (IL-6) mediate chondro- disc" suggest the attachment does not have the cyte protease production causing cartilage destruc- same resistance to compressive loading as does the tion in DJD.'™-'"^ Proteases such as collagenaselike disc Itself."" Despite the relationship between disc (CL) peptidase"""'™ and prolyl endopeptidase displacement and disc perforation,^'"*•'" rhe concept (PEP)'"""''- increase in serum concentration in mice that DJD IS the result of displacement and perfora- inbred for osteoarrhrosis of the TMJ.'" Articular tion of the disc is disputed.'"" In a blind study of cartilage is also an estrogen-sensitive tissue."•' It has joints with normally positioned discs, displaced been demonstrated that tamoxifen, an estrogen

170 Volume 9. Number 2, 1995 Kamelch ui

antaguriLSt, reduces the developmenr of experimen- joint/' as does unilateral chewing."''•'" Although tally induced DJD in rabbits, in conrrasr, estradiol the etiologic contribution of excessive joint loading facilitares the process. Both estradiol and tamoxifen to onset of osteoarthtosis is plausible, the direct affect proteoglycan, prostaglandin, and proteogly- etioiogic effect oí occlusion is debatable. The caiiase production hy cartilage cells."^ remodeling capacity of the TMJ demonstrates that the joint can accommodate and adapt to various Limitations of Remodeling occlusal conditions.'-" Pullinger et al"^ analyzed occlusal variation in an Change in condylar morphology, as a result ot osteoarthrotic sample of patients and reported that remodeling, is a normal biologic adaptation to con- occlusion was neither a unique nor a dominant fac- tinual functional demands made on the TMJ. In a tor in defining the sample. They concluded that fea- study of 96 joint specimens from young adults, tures such as anterior open bite in patients with localized surface changes were common."" Local osteoarthrosis are the consequence of, rathet than modifications of both the condylar surface and the an etiology for, DJD. Seligman and Pullinger'" overall condylar shape appear to be interrelated stated that epidemioiogic studies may demonstrate adaptive responses to functional stimuli. Re- associations between occlusa! factors and DJD but modeling changes, however, present with high vari- fail to prove the etiologic contributions of occlusion. ability. Different presentations of remodeling may It is currently open to speculation whether specific be observed between the lateral and medial aspects occlusal factors predispose to DJD"'-'--" or rather of the joint components within the same joint. result from intracapsular or capsular changes.'" The Although DJD usually occurs in an articular area specific etiologic role of occlusion, with tespect to formerly subjected to remodeling," the variable TMD in general, remains to be proven.'-''•'" presence of adaptive remodeling alone cannot pre- dict a progression to active degenerative disease. Different functional demands made on the man- DiagnosJs dibular complex contribute to the variable nature of remodeling changes. Animal studies indicate that changes in mandibular position obtained by intra- Clinical Considerations oral or extraoral devices induce characteristic Clinical findings vary with the course of degenera- remodeling changes in the articular surfaces."'"" tive disease of the TMJ. There is a potentially Anterior condyle placement caused by the applica- asymptomatic DJD population segment who, under tion of Class II orthodontic forces is accompanied certain circumstances, may suddenly become symp- by osteogenesis on the posterior aspect of the tomatic."" Trauma, in general, is a common precip- condyle and increased periostea! deposition on the itating factor. Principal clinical findings in osteo- post glenoid tubercle. Distal placement of the arthrosis of the TMJ include pain on movement or condyle wirh Class III orthodontic forces produces biting, reduced , joint tenderness to regressive remodeling of the posterior condyiar sur- palpation, and .'^'" Rasmussen'""-'" re- face and anterior surface of the post gienoid tuber- ported that during the early painful phases, cle."' Internal derangement viiith anterior disc dis- restricted joint mobility and limited excursive placement may lead to flattening of the anterior movements ate accompanied by tenderness of the condyiar surface, whereas posterior disc displace- and pain in the masticatory muscles. ment IS accompanied by flattening of or concavities As the pain ceases, mobility improves and crepita- in the posterior aspect of the condyle.'-" tion, if not already present, may appear. Except for crepitation, the clinical of patients with TMJ degenerative dis- Contribution of Occlusion ease do not differ from those of other patients with Functional demands may be imposed on the TMJ, mandibular dysfunction.'" Crepitus is an accurate in part, by altered occlusal relationships. Charac- predictive sign of DJD'''''"" but has low sensitivity teristics of the occlusal scheme may depict pattern- as a diagnostic sign. Rohlin et al'" found that 10 of ing and intensity of forces transferred to the articu- 12 joints with crepitation had degenerative changes lar surfaces of the joints.'^' Biomechanical analyses while the remaining two had extensive remodeling. of the mandibular complex predict that joint load- In one study,"' only one half of joints with con- ing is increased as the point of application of bite firmed DJD exhibited ctepims. If crepitation is used force is moved anteriorly.'"Unilateral loss of tooth as the only diagnostic criteria, joints with DJD will support will increase loading in the contralateral not be properly diagnosed.

Journal of Orofacisl Pain 171 Kamelchuk/Msjot

Imaging Considerations Histochemical Considerations Radiograpliic observattons characteristic of DJD Histochemical markers of cartilage metabolism include reduced joint space, osseous flattening, have been identified, and they correlate with early subchondral sclerosis, erosions or loss of cortical soft tissue changes associated with onset of osteo- lintng, and presence of ,'"*'•'•' Reduced arrhritis.'"'•""• Results of synovial fluid assays suggest joint space, particularly in association with crepi- that the enzyme activities of N-acetyl-beta-glu- tation, tnay represent articular soft ttssue destruc- cosaminidase and N-acetyl-beta-galacrosaminidase tion. However, Kopp and Rockier"" concluded reflect rhe degree of TMJ dysfunction,'" Fibronectin that redticed ¡oint space is probably not an indica- fragments are detectable in synovial fluid aspirates of tor of DJD if molar support is present and the parients with osteoarthritis and are known to poten- radiographs are exposed with the mandible in the tiate release of meta II o protein ases resulting in pro- intercnspal position. In advanced cases, osteo- teoglycan depletion,'" '"' In mice inbred for pbytes and lipping may be found in the anterior osteoarthrosis, observed increases in serum collage- part of the condyle. Apparettt osteophytes can be naselike (CL) peptidase and prolyl endopeptidase caused by either apposition of bone or simulated (PEP) occurred at an earlier stage tban histologie apposition due to destruction of adjacent areas. If changes,"- Histochemically detectable entities may condylar surface erosions or irregularities are be useful as early biochemical markers of tbe onset observed, tbey are predotninantly located in the of osteoarthrosis. lateral pole."' It is often difficult, if not impossible, to radio- graphically differentiate between degenerative Treatment changes and adaptive remodeling.'"""' Osseous changes must be pronounced to be detected radio- Palliative Treatment graphically;''" tbus, early degenerative changes in rhe articular soft tissue may occur long before Palliative care should begin with an explanation of radiographie signs are visible." •'•" Condylar and the nature and prognosis of TMJ degenerative dis- eminential flattening are frequently associated witb ease,'" Management is primarily symptom directed, bony condensation or subchondral sclerosis, inde- based on the understanding that DJD appears to pendent of arthrosis,'* and may be adaptive re- run a clinical course of 1 to 3 years generally fol- sponses to increased functional loading."' Espe- lowed by a natural regression of symptoms.''•"•""•''' cially in the absence of degenerative signs such as Modification of parafunctional habits sucb as surface erosions or irregularities, condylar flatten- clenching, bruxing, and gum chewing should be ing and subchondral sclerosis are usually represen- undertaken. Patients should be advised tbat the tative of remodeling. However, the absence of joints may be easily irritated,'"'' and unnecessary radiographie changes cannot exclude the presence mechanical stresses on the joint may be avoided by of degenerative lesions, changing the diet to softer, smaller food,'"' Physio- Osteoarthritic hard and soft tissue ahnormahttes therapy, utilizing various modalities to control have been identified using magnetic resonance inflammation, reduce secondary muscle spasm, and imaging (MRI).'•"""' Cartilage erosions, visible improve joint mobility, sbould be undertaken and witb MRI, are potentially quantifiable,'" In rhesus followed by home ,''"'"''' If pain relief is macaques , MR relaxation times and proton inadequate, short-term and anti-inflam- density values have been sbown to vary with tbe matory medication may be helpful."* severity of osteoarthrttts.'"' In other antmal mod- els, MRI is positive for accutnulation of synovial Splint Therapy fluid and cartilage degradation."'' Researchers have also shown correlarional trends between areas of Existing concepts of DJD etiology suggest treat- decreased signal mtensity and histologie degenera- ment should attempt to reduce loading in the TMJ. tive changes in cartilage of goat knees.'" In tbe Distraction of the TMJ may be an effective means human , MRI may be sensitive for specific early of eliminating ¡oint loading and has been degenerative change'"''' but may underestimate attempted with spring mechanics,'"' splints with cartilage and osseous abnormalities,""'''' Although increased vertical dimension,'~' and pivoting MRI of tbe TMJ may confirm disc displace- splints.'""'"" However, the effect of sphnt therapy ment,""""- it has been shown to underdiagnose on condylar distraction has been shown to be osseous changes, adhesions, and perforations.'"'" questionable,''- Rasmussen'" reported that treat-

172 Volume 9, Number 2, 1995 Kamelchuk/Malor ment of DJD with pivotal splints resulted in relief ment,"" has been introduced into from pain but increased the extent of the radio- standard therapy for TMJ internal derangement graphically observed degenerative disease, and osteoarthritis, and it compares favorably witb Occlusal splint therapy remains a common treat- open surgical techniques,'™ Arthroscopy also has menr modality, Ito et al"- investigated joint loading diagnostic merit with the potential to provide associated with several different splint designs. highly tissue-specific pathologic information.'"' Splints without posterior tooth support result in Short-term outcome of patients treated with increased joint loading during clenching. Likewise, arthroscopic surgery, compared with nonsurgery splmts with unilateral posterior contact create patients, includes subjective reports of increased increased loading in rhe contralateral joint, with mobility and pain relief.-"' In experimental models, distraction of the ipsilateral joint. Bilateral centric however, arthroscopic intervention may cause irre- stops on posterior teeth appear important for pro- versible changes in TMJ articular tissues.^"' Dif- tecting the joints from excessive loading, particu- ferent approaches, using animal and human mod- larly during parafunctional activities, Occlusai els, provide continued rationale for open and splint therapy can reduce joint loading indirectly arthroscopic surgical techniques,^"^-'" by reducing muscle hyperactivity,'''"'" and it may provide symptom relief by decreasing coexistent neuromuscular symptoms.'"''""* Prognosis

Injection Modalities Degenerative joint disease appears to have an itii- tial destructive phase, and a subsequent reparative Intra-articular injections bave been proposed as a phase, that terminates in healing. Rasmussen"'esti- possible treatment modality for some types of mated that the destructive and reparative phases TMD.'" Human osteoarthritic synovial membranes last 1 to 1,5 years each. In 75% of subjects exam- experimentally treated with demon- ined, the entire course is estimated to be less than strate decreased production of alpha and beta 18 months, and subjects generally complete the IL-l'"" known to be involved in the osteoarthritis healing phase by 3 years. Despite improvement in pathophysiologic process. Corticosteroid injections subjective symptonis, however, radiographie evi- have also been shown to suppress enzyme synrhesis dence of healing is minimal,-"'-^"' Generally, subjec- in experimental osteoarthritis.'"" Clinically, intra- tive symptoms subside,'"'"' and the joints appear anicular corticosteroid is known to give clinically stable. Residual symptoms such as mild short-term symptom relief'*" but is also controver- restriction of movement and crepitus remain in sial.'™ Intra-articular corticosteroid injecrions have many patients long after rhe subjective symptoms been associated wirh both beneficial and adverse subside.'"'™ Long-term studies confirm that the effects.'"-'" majority of DJD parients with crepirus show no Intracapsular injections of have clinical change in crepitation,-'" been shown ro provide relief from TMJ pain,"'' Rasmussen"- compared effects of various treat- The sodium salt of hyaluronic acid, sodium ment modalities on subjective symptoms of hyaluronate, is a high-molecular weight polysac- patients wirh DJD, Treatment included flat plane charide'" that functions as a lubricant in normal splints, pivotal splints, injection, and no synoviai fluid,'" Short-term results of intra-articu- treatment. No statistically significant difference iar injections inro painful shoulders have produced was found in rhe duration of presence of symp- rapid symptom relief from pain,'"" However, toms with the different treatment modalities in the Bertolami er al"* reported that patients with tem- study population. Pullinger and Seligman'""-"' sug- poromandibukr DJD who received intracapsular gested that there are two distinct populations of , compared to injec- patients with DJD, One group is mainly composed tions, sbow no significant difference in treatment of patients under 35 years of age where internal outcome. derangement precedes onset of DJD, A second group is composed of an older population where internal derangement is secondary to the DJD pro- Surgical Treatmenf cess. The concept that although the end result is Temporomandibular joint surgery is restricted to similar, there is more than one pathogenesis helps patients with long-sranding, severe pain and to explain many of the apparent conflicts regard- restricted range of mandibular movement who ing etiology, diagnosis, and management of show no favorable response to conservative treat- patients presenting with DJD.

Journal of Orofacial Pain 173 Ksmelchuk/Major

13. Ratcliffe A, Rosenwasser MP, Mahmud F, Glazer PA, Conclusion Saed.Neiad F, Lane N, Mow VC. The in yivo effects of on canine experimental osteoarthriric articular Temporomandibular DJD is a pathologic response cartilage: Composition, metalloproleinase activities and to mechanical stress placed upon the articular sur- metabolism. Agents A<;tions SuppI I993;39:2O7-2I1. faces of the joint. There is a delicate balance 14. Schiffman EL, Fricton jR, Haley DP, Shapiro BL. The prevalence and treatment needs of subjects wiih temporo- between adaptive response (remodeling) and non- mandibular disorders. J Am Denf Assoc 1990;120: adaptive response (degeneration) to functional 29.5-303. demands. Articular surface breakdown can occur 15. Toller PA. Osteoarthrosis of tbe mandibular condyle. Br because of increased mechanical stress or reduced DentJ 1973; 134:223-231, ability of the tissue to withstand and adapt to the 16. Heloe B, Heloe LA. Characteristics of a group of patients with temporomandibular joint disorders. Community applied stress. The aim of treatment of DJD is to Dent Oral Epidemiol l?7S;3:72-79. shorten its natural course or at least to make it 17. Mejers)o C, Hollender L. of the temporo- more tolerable. It is hoped that treatment during mandibular joint in female parients with TMJ pain or dys- the active phases of the disease will reheve pain, function. Acta Radiol [Diagl 1984;25:169-176. preserve function, and prevent or minimize defor- 18. Crooks MC, Ferguson JW, Edwards JL. Clinical presenta- tion and final diagnosis of patients referred to a tempoto. mity. Once the disease process has stabilized, treat- mandibular joint clinic, NZ Dent J 1991:87:113-llS. ment is aimed at minimizing TMJ loading. These 19. Oberg T, Carlsson GE, Fajers CM. The temporomandibu- objectives are, most likely, best achieved with a lar ioint: A morpbologic study on human autopsy mate- multiprofessionai approach. rial Acta Odontol Scand 1971;29i349-384. 20. Rohlin M, Westesson P-L, Ericksson L. The correlation of tempotomandibular joint sounds with morphology in fifty-five autopsy specimens. J Oral Maxillufac Surg References 19 85;43 i 194-200. 21. Blackwood HJJ. of the mandibular joint. Br Dent 1. Bell WE. Orofadal . Classification, Diagnosis, Man- J I963;n5:317-32é. agement, ed 4. Chicago: Year Book Medical, 1989il01-113. 22. Barrett AW, Griffiths MJ, Scully C. Osteoarthrosis, the 2. Bell WE. Temporomandibulat Disorders. Classification, temporomandibular joint, and Eagle's syndrome. Oral Diagnosis, Management, ed 3. Chicagoi Yeat Book Surg Oral Med Oral Pathol 1993;75:273-275. Medical, 1990:166-176. 23. Ishigaki S, Bessette RW, Maruyama T. The distribution of 3. Griffiths RH. 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Whittaker DK, Davies G, Brown M. looth loss, attrition, the hip. J Manipulative Physiol Ther 1993;I6:37^2. and temporomandibular joint changes in Romano-British 10, Khan FM, Williams PI. Double-blind comparison of population. J Oral Rehabil 198i; 12:407-419, SR and SR in the treatment of patients 31. Wbittaker DK. Surface and form changes in the temporo- with degeneraiive joint disease of the knee. Curr Med Res mandibular joinrs of 18th century Londoners. ] Ptosthet Opin 1992^13:1-12. Res 1989;68(special issue): [abstract 1211]. 11, Ellman H, Harris E, Kay SP, Early degenerative joint dis. 32. Whittaker DK, Jones JW, Edwards PW, Molleson T. ease simulating impingement syndrome: Arthroscopic Studies on tbe temporomandibular joints of eighteenth- findings. Arthroscopy 1992;8:482^87. century London population (Spitalfields). J Oral Rehabd 12, Lafeber FP, Vandcr-Kraan PM, Huber-Bruning O, 199Üil7:89-97. Vanden-Berg WB, Bijlsma JW. Oste o arthritic human carti- 33. Hodges DC. 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34. Pullinger AG, Seligman DA. The degree to which attrition 54. Gardner DL. The nature and causes of osleoarrhtosis. Bt characterises differentiated patient groups of temporo- Med J Clin Res Ed ]983;286:418-424. mandibular disotders. J Orofacial Pain 1993;7:196-208. 55. Lohmander LS, Dahlberg L, Ryd L. Increased levels of 35. deBont LG, Liem RS, Boeting G. Ulttastructute of the artic. proteoglycan fragments in knee joint fluid aftet . ulat cartilage of the mandibular condyle: Aging and degener- Arthritis Rheum 1989;32:1434-1442. ation. Oral Surg Oral Med Oral Pathol 1985;60:631-641. 56. Lsrael HA, Saed Nejad F, Ratcliffe A. Early diagnosis of 36. Silberman M. Livne E. Age related degenerative changes in osteoarthrosis of the temporomandibular joint: Cor- the mouse mandibular joint. J Anat 1979;129:507-520. relation between arthroscopic diagnosis and keratin sul- 37. Hekneby M. The load of the temporomandibular joint: fate levels in synovial fluid. 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73. Helmy E, Bays R, Sharawy M. Osteoartbrosis of tbe tem- Montella A, Manunta A, Espa E, Gasparini G, De Santis poromandibular joint following experimental disc perfora- E, Gulisano M. Human articular cartilage in tion in Macaca fascicularis. J Oral Maxillofac Surg osteoarthrosis. 1. The matrix. Transmission electron 1938;46:979-990. microscope srudy. Arch Itat Anat Enibriol 1992;97: 74. Helmy E, Bays R, Sharawy M. Synovial chondromatosis 1-12. associated with experimental osteoarthritis in adult mon- Richard M, Broquet P. Vignon E, Pescbard MJ, Garret keys. J Oral Maxillofac Surg 1989i47:823-827. JP, Louisot P. Galmodulin-dependent collagenase and 75. Scapino RP. The posterior attachment: Its structure, proteoglycanase activities in cbondrocytes from human function, and appearance in TMJ imaging studies. Patt I. osteoarthritic cartilage. Biochem Biophys Res Commun J Craniomandib Disord Facial Oral Pain 1991;5: 199T;174:1204-1207. S3-95. Gruz TF, Mills G, Pritzket KP, Kandel RA. 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Campbell J. Extension of the temporomandibular ioint 196. Radin EL, Paul IL, Swann DA, Schottstaedt ES. Lubri- space by methods derived from general orthopedic pro- cation of synovial membrane. Ann Rheum Dis 1971;30: cedures. J Prosthet Dent 19S7;7Í3 86-399. 322-325. Sears VH. Occlusal pivotal splints. J Prosthet Dent 1956- 197. Leardini G, Perbellini A. Franceschini M, Mattara L. 6:332-338. Intra-articular injections of hyaluronic acid in the treat- Berry DC. Occlusal pivots. A cas eport. Dent Pr ment of painful shoulder. Clin Ther 1988;10:i21-526. 1962;I2:337-338. 198. Bertolami CN, Cay T, Clark GT, Rendell J, Shetty V, Rasmussen OC. Treatment of tempotomandibular Liu C, Swann DA. Use of sodium hyalutonate in treating arthroparhy. Scand J Dent Res 1982^90:64-68. temporomandibular joint disorders: A randomized, Clark GT, Beemsterboer PL, Soiberg WK, Rugh JD. double-blind, placebo-controlled clinical trial. J Oral Nocturnal electromyographic evaluation of myofascial Maxillofac Surg 1993;S 1:232-242. pain dysfunction in patients undergoing occlusal splint 199. Mejersjo C. Therapeutic and prognostic consideration therapy. J Am Dent Assoc 1979;99:607-611. in TMJ osteoarthrosis: A literature review and long Chung SC, Kim HS. The effect of rhe stabilization splint term study of 11 subjects. J Craniomand Pract 1987; on the TMJ closed lock. J Craniomand Pract 1993- 5i69-7S. 11:95-101. 200. Reich RH. Temporomandibular joint surgery. Curr Soiberg WK, Clark GT, Rugh JD. Nocturnal elec- OpinDent 1992;2:17-24. tromyographic evaluation of bruxism patients undergo- 201. Murakami K, Clark GT. Diagnosis of inrracapsular ing short term splint treatment. J Oral Rehabil 1975; pathology associated with tempotomandibular joint dis. 2:215-223. otders. Adv Dent Res 1993;7a20-126. Ahlqvist J, Legrell PE. A technique for the accurate 202. Stegenga B, deBont LG, Dijkstra PU, Boering G. 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Journal of Orofscial Pain 179 Kamele hu k/M ai or

Resumen Zusammenf assu ng

Enfermedad Degenerativa de la Articulación Degenerative Eriírankungen des Kiefergelenkes Temporomsndibular Das Fortschreiten einer degenerativen Gelenkerkrankung hangt La progresión de la enfermedad degenerativa de la artioulación vom ihr zugrundeliegenden palhoiogischen und/oder reaktiven depende de los procesos patológicos subyacentes y/o reac- Prozess ab. der. im allgemeinen, die Adaptationsfáhigkeit des tivos envueltos, y que en general, com pro nieten la adaptabilidad Gewebes einschränkt. Es wird eine Übersicht über klinische und tisutar. Se presenta una revisión de literatura clínica y eïpen- experimentelle Literatur zu degenerativen Geienkerkrankungen mental relacionada a la enfermedad degenerativa de la articu- vorgestellt. Epidemiologie. Pathogenese, Diagnose. Therapie, lación. Se describe la epidemiología, patogénesis, diagnóstico, und Prcgncse werden beschrieben, mit speziellem Schwerge- tratamiento, y pronóstico con jn énfasis particular en la articu- wicht auf dem Kiefergelenk Der Artikel behandelt Faktoren, die lación temporomandibular (ATM) Este articulo describe los fac- das Gleichgewicht zwischen Remodeling und Degeneration im tores que afectan ia paridad en la re m o dei ación/degene ración y Kiefergelenk beeinflussen kónnen und stellt Grundprinzipien zur presenta i a rajón funda m en ta i de ios enfoques de diagnóstico y Diagnose und Therapie vor. tratamiento.

ABOP Certification

The American Board of Orofacial Pain (ABOP} was founded in 1994 in response to the need for a valid certification process for dentists practicing orofacial . The ABOP will offer annual certification examinations to dentists licensed in the United States. The application for the 1996 examination will be available on June 1, 1995. For more information, please write to: The American Board of Orofacial Pain, 10 Jopliti Court, Lafayette, California 94549.

•sao Volume 9. Number 2, 1995