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 to: 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 and experimental literature relating to degenerative joint disease is presented. Epidemiology, pathogenesis, diagnosis, treatment, and prognosis are described witb particular emphasis given to the temporomandibular joint. Tbis article describes factors affecting tbe temporomandibular joint remodeling/degeneration parity and presents rationale for approacbes to diagnosis and treatment.
J OROFACIAL PAIN 1995;9:I68-13O,

key words: temporomandibular joint, degenerative joint disease, osteoarthriris

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 parity and, in doing so, present rationale for diagnosis and treatment. 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 displacement with or without reduction; (3) dislocation; (4) inflammatory 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 musculoskeletai disease and reactive processes""" have been commonly implicated in the progression of DJD, Diagnoses of DJD reflect disease processes of tissue deterioration in which soft tissue, cartilage, and bone are converted into or replaced hy tissue of inferior quality,'" Generally, DJD appears to be the manifestation of an imbalance between an adaptive response (remodeling) and a nonadaptive response (degeneration).

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without sustaining damage.'" Repetitive cyclic microtrauma has heen implicated in the etiology of DJD.-. may facilitate rhe pathogenesis of DJD." Incongruities between loaded TMJ articular surfaces predispose to stress concentrations that are observed more frequently in the temporal component where degenerative lesions more commonly occur.•'•^" Attrition has also. resulting in loss of proliferative zone potential.'" histochemical studies of articular surfaces that macroscopically demonstrate DJD have shown a reduction in sulfated glycosammoglycan.^'"'* Intensity and direction of Stresses generated hy various occlusal forces have been analyzed utilizing three-dimensional math- ematical""'" and finite element-analysis models.Data support the concept that aging women seem co be more prone to DJD than are men.Kamelchuk/Major Epidemiology Literature relating to epidemiology of degenerative disease of the TMJ is descriptive and retrospective. Joint Loading and Stress Distribution Strong evidence exists to suggest the TMJ is loaded during function."'-*"" hut vi'hen age is controlled." heen associated with TMJ osteoarthritis despite irs questionable etiologic role. however." Such age-related changes in the articular tissues affect their mechanical properties and. 8% to 12% receive diagnoses of DJD. however. may increase the susceptibility of articular cartilage to trauma caused hy impact."''°'"-^ Pathogen es is Role of Aging There is a general association between the incidence of DJD and increasing age.'"'' with osteoarthritis of the TMJ commonly appearing asymptomacically. and that damage occurs only if cartilage is subjected to less frequent but much higher stress.'"' Although age may be correlated with observations of temporomandibular DJD.""'" Each TMJ is a pressure-bearing. While synovial fluid aspirates of joints that show arthroscopic evidence of DJD contain elevated levels of keratin sulfate. double-synovial joint." Whether or not DJD can be attributed to the cumulative effect of repetitive minor trauma to normal TMJ articular tissue remains debatable. In the TMJ. of increased stiffness.""-'-'"" suggesting that age is a predisposmg factor. infrastructural alterations occur.''" Kopp et al*" conclude. Major trauma to synovial joints may progress to DJD. in turn. Age-related changes in articular tissues have been documented. reducing disc displacements may potentiate repetitive impact loading*' and consequently lead to a subchondrai sclerosing known to occur prior to the onset of DJD." with loss or degeneration of cartilage normally resistant to compressive stress. Schiffman et al''' conclude that approximately 7% of the general population may benefit from treatment for TMJ problems and that tnost symptomatic subjects can function adequately without treatment.significantly decrease with aging.""'" Autopsy results confirm TMJ degenerative disease prevalence that varies from 22% to greater than 40% of the population. Repeated impact loading of cartilage-lined articular surfaces results in an increased rate of osteogenesis in subchondrai hone evidenced radiographicaily as subchondrai sclerosis.'"' Excessive |oint loading may disrupt the normal adaptive capacity of articular tissue.'"-''" Lesions are markedly fewer in the condyle than in the temporal component. independently of age. Studies indicate that the frequency of DJD increases in older persons. The mcidence of tooth loss and osteoarthritis is associated with increasing age." Arthritic lesions of the TMJ are most often localized in the lateral aspect of the temporal fossa. TMJ cellularity generally decreases with aging.'" Affected hone." Adequate lubrication of the TMJ components is required to facilitate the mechanics of joint mo- Joumal of Orofscial Pain 169 . the stress to which it is most regularly subjected. compound. In mice. resulting in eventual cartilage breakdown and elevated proteoglycan levels in the synovial fluid.'" Articular tissue thickness and distribution probably reflect areas of stress concentration in the condylar and temporal components. The fibrous component of the matrix of aged articular tissue of the TMJ consists of a well-organized collagen network occasionally dispersed with elastic fibers. Of patients treated at cemporomandihulat dysfunction clinics." The overall amount of collagen does not . Proteoglycan content decreases and binding quality is altered. the associarion is coincidental." it was hypothesized that articular cartilage adapts mechanically to transmit. that degenerative changes described in their autopsy material are probably mostly due to local factors. In a study of location of osteoarchritic lesions in patellofemoral compartments of 39 cadaveric knee joints.*^' with the lateral part of the joint exposed to the largest functional and parafunctional loads. compared to the medial aspect. the possible correlation does not elucidate etiology.

1995 . The tipper joint compartment is subject to transktory movenietit while the lower undergoes rotational movement. Stegenga et al*' hypothesized that TM joints are subject to a continual process of articular surface breakdown and repair.'™-'"^ Proteases such as collagenaselike (CL) peptidase"""'™ and prolyl endopeptidase (PEP)'"""''. In addition to mediators of inflammation.'"-"" Westesson" conducted a radiographie study including arthrograms on 12S patients with internal derangements. Stegenga et ai"suggested that internal derangement is an accompanying sign of DJD and is capable of causing a rapid progression of the disorder. Nitzan and Dolwick'^ suggest that a lack of gliding in the joint can be attributed to disc adherence to the fossa by a reversible effect stich as vacuum and/or decreased volume of high-viscosity synovial fluid. The cytokmes interleukin1 (IL-1) and interleukin-6 (IL-6) mediate chondrocyte protease production causing cartilage destruction in DJD."' However."'"'' The TMJ articular surfaces are covered with fibrous connective tissue. The gliding capacity of the articular disc may become impaired. thus predisposing to internal derangement.Kameichuk/Major tion.'" Articular cartilage is also an estrogen-sensitive tissue. Internal Derangement Internal derangement of the TMJ. but 39% of the patients with nonreducing disc displacement and 60% of the patients with perforation had degenerative changes. Anderson and Katzberg"' obtained comparable findings with a tomographic and arthrographic study of 141 patients with temporomandibular dysfunction. Position and configuration of the articular disc has been related to DJD. but research suggests*'**'" that inflammatory changes in articular matrix components are (1) responsible for impairment of the physicochemical properties of the articular surfaces and (2) likely to contribute to the development of DJD. Degenerative changes were consistently found in joints with disc perforation. Decreased synthesis of the glycoprotein luhricin. may be involved in the etiology of DJD. These observations suggest it is more likely that DJD is the cause and perforation is rhe effect."' Differences in the freqtiency of degenerative lesions hetween the condylar anid temporal components may he dtic to greater frictiona! loading between the disc and temporal components than hetween the condyle and disc. If the degradarive response exceeds the reparative response. may progress to DJD."*"". internal derangement of the TMJ precedes degenerative disease. Schellhas"' regards internal derangement of the TMJ as an irreversible and generally progressive disorder that may he staged clinically. early stages of DJD show fibrillation and fissures at the articular surface level that will eventually progress to a complete erosion of rhe cartilage. Stegenga et al*^ concluded that in many cases of temporomandibular dysfunction." other biochemical mediators have been identified with DJD and osteoarthrosis. Only 9% of the patients with a reducing displacement showed signs of degeneration. These authors*"'"' conclude that. and that the accompanying muscle pain and internal derangement is secondary.*""'" In appendicular joints with cartilage articular surfaces."'"' In humans.'^ Inflammatory/Histochemical Considerations Histologie studies of synovium of degenerative joints show a significant amount of inflammation""*" and proteoglycan turnover." Pathologic changes appear ro be related to increased levels of metalloproteinases that produce both a breakdown of the collagen network""'" and a size reduction of the proteoglycan monomer. DJD is the primary disorder. then a DJD process is initiated. perforations were found only in cases with DjD.'"" In a blind study of joints with normally positioned discs.increase in serum concentration in mice inbred for osteoarrhrosis of the TMJ. Osseous changes were seen in 50% of the patients with anterior disc displacement without reduction but seldom in patients with disc displacement with reduction. displaced but reducing discs."" Despite the relationship between disc displacement and disc perforation. observed perforations localized ro the posterior attachment of the disc" suggest the attachment does not have the same resistance to compressive loading as does the disc Itself. normally associated with the lubrication fraction of synovial fluid.^'"*•'" rhe concept that DJD IS the result of displacement and perforation of the disc is disputed.'' Lack of joint lubrication may exacerbate articular tissue failure by increasing frictional resistance during loaded joint movements. an estrogen 170 Volume 9."•' It has been demonstrated that tamoxifen. and displaced nonredticing discs. in many cases. 73% of the cases with DJD did not have perforations.Surgical creation of hilateral disc perforation in Macaca fascicularis monkeys produces pathologic alterations consistent with DJD in the majority of experimental joints. Number 2. There is a relationsbip between disc perforation and degenerative disease of the TMJ. as opposed to hyaline cartilage. particularly with disc deformation.

localized surface changes were common." the variable presence of adaptive remodeling alone cannot predict a progression to active degenerative disease. In one study."' only one half of joints with confirmed DJD exhibited ctepims. Different functional demands made on the mandibular complex contribute to the variable nature of remodeling changes. If crepitation is used as the only diagnostic criteria. under certain circumstances. and proteoglycaiiase production hy cartilage cells. Rohlin et al'" found that 10 of 12 joints with crepitation had degenerative changes while the remaining two had extensive remodeling. restricted joint mobility and limited excursive movements ate accompanied by tenderness of the joint capsule and pain in the masticatory muscles. is a normal biologic adaptation to continual functional demands made on the TMJ.'" The specific etiologic role of occlusion. They concluded that features such as anterior open bite in patients with osteoarthrosis are the consequence of.Kamelch ui</Major antaguriLSt. is a common precipitating factor. There is a potentially asymptomatic DJD population segment who.'"Unilateral loss of tooth support will increase loading in the contralateral Clinical findings vary with the course of degenerative disease of the TMJ. however. Distal placement of the condyle wirh Class III orthodontic forces produces regressive remodeling of the posterior condyiar surface and anterior surface of the post gienoid tubercle. as a result ot remodeling. DJD."''•'" Although the etiologic contribution of excessive joint loading to onset of osteoarthtosis is plausible. may appear.'-" Pullinger et al"^ analyzed occlusal variation in an osteoarthrotic sample of patients and reported that occlusion was neither a unique nor a dominant factor in defining the sample. remains to be proven. It is currently open to speculation whether specific occlusal factors predispose to DJD"'-'--" or rather result from intracapsular or capsular changes. Although DJD usually occurs in an articular area formerly subjected to remodeling. The remodeling capacity of the TMJ demonstrates that the joint can accommodate and adapt to various occlusal conditions. the clinical signs and symptoms of patients with TMJ degenerative disease do not differ from those of other patients with mandibular dysfunction. estradiol facilitares the process. Journal of Orofacisl Pain 171 . mobility improves and crepitation."" Local modifications of both the condylar surface and the overall condylar shape appear to be interrelated adaptive responses to functional stimuli.'" Crepitus is an accurate predictive sign of DJD'''''"" but has low sensitivity as a diagnostic sign. if not already present. Remodeling changes.'^' Biomechanical analyses of the mandibular complex predict that joint loading is increased as the point of application of bite force is moved anteriorly. the direct etioiogic effect oí occlusion is debatable.'^'" Rasmussen'""-'" reported that during the early painful phases. Animal studies indicate that changes in mandibular position obtained by intraoral or extraoral devices induce characteristic remodeling changes in the articular surfaces. Characteristics of the occlusal scheme may depict patterning and intensity of forces transferred to the articular surfaces of the joints. Different presentations of remodeling may be observed between the lateral and medial aspects of the joint components within the same joint. reduced range of motion. present with high variability. whereas posterior disc displacement IS accompanied by flattening of or concavities in the posterior aspect of the condyle."'"" Anterior condyle placement caused by the application of Class II orthodontic forces is accompanied by osteogenesis on the posterior aspect of the condyle and increased periostea! deposition on the post glenoid tubercle. by altered occlusal relationships."^ Limitations of Remodeling Change in condylar morphology. rathet than an etiology for. As the pain ceases. in conrrasr.'-" Contribution of Occlusion joint/' as does unilateral chewing."' Internal derangement viiith anterior disc displacement may lead to flattening of the anterior condyiar surface."" Trauma. Both estradiol and tamoxifen affect proteoglycan. and crepitus. in part. may suddenly become symptomatic. joint tenderness to palpation. prostaglandin. Principal clinical findings in osteoarthrosis of the TMJ include pain on movement or biting. reduces the developmenr of experimentally induced DJD in rabbits. Except for crepitation. In a study of 96 joint specimens from young adults. with tespect to TMD in general. in general. Seligman and Pullinger'" stated that epidemioiogic studies may demonstrate associations between occlusa! factors and DJD but fail to prove the etiologic contributions of occlusion. joints with DJD will not be properly diagnosed.'-''•'" DiagnosJs Clinical Considerations Functional demands may be imposed on the TMJ.

'"'•""• Results of synovial fluid assays suggest that the enzyme activities of N-acetyl-beta-glucosaminidase and N-acetyl-beta-galacrosaminidase reflect rhe degree of TMJ dysfunction.''.''"'"''' If pain relief is inadequate. early degenerative changes in rhe articular soft tissue may occur long before radiographie signs are visible. utilizing various modalities to control inflammation. visible witb MRI. Kopp and Rockier"" concluded that redticed ¡oint space is probably not an indicator of DJD if molar support is present and the radiographs are exposed with the mandible in the intercnspal position. and improve joint mobility.'"*'•'•' Reduced joint space.'* and may be adaptive responses to increased functional loading. erosions or loss of cortical lintng. are potentially quantifiable."* Splint Therapy Existing concepts of DJD etiology suggest treatment should attempt to reduce loading in the TMJ.''" tbus. However."' It is often difficult. to radiographically differentiate between degenerative changes and adaptive remodeling. Distraction of the TMJ may be an effective means of eliminating ¡oint loading and has been attempted with spring mechanics.'"""' Osseous changes must be pronounced to be detected radiographically. Number 2. and gum chewing should be undertaken. osteopbytes and lipping may be found in the anterior part of the condyle.'" Management is primarily symptom directed.'" In rhesus macaques knees.Histochemically detectable entities may be useful as early biochemical markers of tbe onset of osteoarthrosis."'' Researchers have also shown correlarional trends between areas of decreased signal mtensity and histologie degenerative changes in cartilage of goat knees." •'•" Condylar and eminential flattening are frequently associated witb bony condensation or subchondral sclerosis. condylar flattening and subchondral sclerosis are usually representative of remodeling.'"'" Histochemical markers of cartilage metabolism have been identified. the absence of radiographie changes cannot exclude the presence of degenerative lesions.". based on the understanding that DJD appears to run a clinical course of 1 to 3 years generally followed by a natural regression of symptoms.'"' splints with increased vertical dimension."' Especially in the absence of degenerative signs such as surface erosions or irregularities. observed increases in serum collagenaselike (CL) peptidase and prolyl endopeptidase (PEP) occurred at an earlier stage tban histologie changes.'" '"' In mice inbred for osteoarthrosis. MR relaxation times and proton density values have been sbown to vary with tbe severity of osteoarthrttts.'•"""' Cartilage erosions.Kamelchuk/Msjot Imaging Considerations Histochemical Considerations Radiograpliic observattons characteristic of DJD include reduced joint space.''•"•""•''' Modification of parafunctional habits sucb as clenching. short-term analgesic and anti-inflammatory medication may be helpful. Osteoarthritic hard and soft tissue ahnormahttes have been identified using magnetic resonance imaging (MRI). the effect of sphnt therapy on condylar distraction has been shown to be questionable. sbould be undertaken and followed by home exercises. particularly in association with crepitation.""'''' Although MRI of tbe TMJ may confirm disc displacement. In advanced cases. and perforations. if not impossible. Apparettt osteophytes can be caused by either apposition of bone or simulated apposition due to destruction of adjacent areas.'" In tbe human hip. MRI may be sensitive for specific early degenerative change'"''' but may underestimate cartilage and osseous abnormalities.Rasmussen'" reported that treat- 172 Volume 9. Patients should be advised tbat the joints may be easily irritated.'"' Physiotherapy."""".'"'' and unnecessary mechanical stresses on the joint may be avoided by changing the diet to softer. smaller food. Treatment Palliative Treatment Palliative care should begin with an explanation of the nature and prognosis of TMJ degenerative disease.it has been shown to underdiagnose osseous changes. tnay represent articular soft ttssue destruction. 1995 . and presence of osteophytes. tbey are predotninantly located in the lateral pole.'"' In other antmal models.'""'"" However. subchondral sclerosis. If condylar surface erosions or irregularities are observed.'~' and pivoting splints. independent of arthrosis. However. reduce secondary muscle spasm. and they correlate with early soft tissue changes associated with onset of osteoarrhritis. bruxing. osseous flattening. adhesions.'" Fibronectin fragments are detectable in synovial fluid aspirates of parients with osteoarthritis and are known to potentiate release of meta II o protein ases resulting in proteoglycan depletion. MRI is positive for accutnulation of synovial fluid and cartilage degradation.

there is more than one pathogenesis helps to explain many of the apparent conflicts regarding etiology. provide continued rationale for open and arthroscopic surgical techniques. Residual symptoms such as mild restriction of movement and crepitus remain in many patients long after rhe subjective symptoms subside. however. and subjects generally complete the healing phase by 3 years. Treatment included flat plane splints. Bilateral centric stops on posterior teeth appear important for protecting the joints from excessive loading.'™ Intra-articular corticosteroid injecrions have been associated wirh both beneficial and adverse effects. Occlusal splint therapy remains a common treatmenr modality. No statistically significant difference was found in rhe duration of presence of symptoms with the different treatment modalities in the study population. and a subsequent reparative phase. Occlusai splint therapy can reduce joint loading indirectly by reducing muscle hyperactivity. Surgical Treatmenf Temporomandibular joint surgery is restricted to patients with long-sranding. Likewise. Ito et al". Corticosteroid injections have also been shown to suppress enzyme synrhesis in experimental osteoarthritis. sodium hyaluronate.'"" However. Splints without posterior tooth support result in increased joint loading during clenching.'" Short-term results of intra-articuiar injections inro painful shoulders have produced rapid symptom relief from pain.'"'"' and the joints appear clinically stable. Rasmussen"'estimated that the destructive and reparative phases last 1 to 1. intraanicular corticosteroid injection is known to give short-term symptom relief'*" but is also controversial. using animal and human models.investigated joint loading associated with several different splint designs. and no treatment. A second group is composed of an older population where internal derangement is secondary to the DJD process. compared with nonsurgery patients.5 years each.'"'™ Long-term studies confirm that the majority of DJD parients with crepirus show no clinical change in crepitation.'"''""* Injection Modalities ment. that terminates in healing.-'" Rasmussen". In 75% of subjects examined.Kamelchuk/Malor ment of DJD with pivotal splints resulted in relief from pain but increased the extent of the radiographically observed degenerative disease. diagnosis. pivotal splints. The concept that although the end result is similar. with distraction of the ipsilateral joint. Despite improvement in subjective symptonis.^"^-'" Prognosis Degenerative joint disease appears to have an itiitial destructive phase. is a high-molecular weight polysaccharide'" that functions as a lubricant in normal synoviai fluid."'' The sodium salt of hyaluronic acid.-"'-^"' Generally. and it compares favorably witb open surgical techniques. splmts with unilateral posterior contact create increased loading in rhe contralateral joint. and management of patients presenting with DJD.'"-'" Intracapsular injections of hyaluronic acid have been shown ro provide relief from TMJ pain.-"' In experimental models. however. radiographie evidence of healing is minimal.'™ Arthroscopy also has diagnostic merit with the potential to provide highly tissue-specific pathologic information. Intra-articular injections bave been proposed as a possible treatment modality for some types of TMD.'"' Short-term outcome of patients treated with arthroscopic surgery."" Arthroscopy has been introduced into standard therapy for TMJ internal derangement and osteoarthritis.^"' Different approaches. compared to placebo injections. subjective symptoms subside. arthroscopic intervention may cause irreversible changes in TMJ articular tissues. steroid injection.'"" Clinically. One group is mainly composed of patients under 35 years of age where internal derangement precedes onset of DJD. includes subjective reports of increased mobility and pain relief.'''"'" and it may provide symptom relief by decreasing coexistent neuromuscular symptoms. particularly during parafunctional activities. Pullinger and Seligman'""-"' suggested that there are two distinct populations of patients with DJD.'" Human osteoarthritic synovial membranes experimentally treated with hydrocortisone demonstrate decreased production of alpha and beta IL-l'"" known to be involved in the osteoarthritis pathophysiologic process. sbow no significant difference in treatment outcome. the entire course is estimated to be less than 18 months. Bertolami er al"* reported that patients with temporomandibukr DJD who received intracapsular sodium hyaluronate. severe pain and restricted range of mandibular movement who show no favorable response to conservative treat- Journal of Orofacial Pain 173 .compared effects of various treatment modalities on subjective symptoms of patients wirh DJD.

Blackwood HJJ. Bijlsma JW.106:75-77. Vanden-Berg WB. Granados JI. Temporomandibulat Disorders. 12. and Eagle's syndrome. Bayliss MT. Osteoarthrosis. 24. References 1. Hodges DC. Jones JW. most likely. Surface and form changes in the temporomandibular joinrs of 18th century Londoners. Diagnosis.10:289-296.29i349-384. and Management. Swed Dent J 1987.3:72-79.40. Fricton jR. Temporomandibular Disorders. Acta Orrhop Beig 92-. Dixon DC. Ishigaki S.37:263-272. 30. Thorkeldsen A. Mejers)o C. and prevent or minimize deformity. Mittlmeier T. Acta Odontol Scand 1977. Weslesson P-L. 7. 3. Bell WE. 5. Shapiro BL.11^155200. 8. ] Ptosthet Res 1989. treatment is aimed at minimizing TMJ loading. 18. Age-related changes in the composition and structure of human articular-cartilage proteoglycans. Management. 20. mandibular joint clinic. McNeill C (ed). Fajers CM. J Prostbet Dent 1979. Assessment. Maruyama T. and Management. 9. Kopp S. 13. 27. best achieved with a multiprofessionai approach. Br Dent J I963.39:2O7-2I1.Ksmelchuk/Major Conclusion Temporomandibular DJD is a pathologic response to mechanical stress placed upon the articular surfaces of the joint. Avascular necrosis of the humeral head after dislocation with fracture of the greater tuberosity. The distribution of internal derangement in patients witb temporomandibular joint dysfunction—Prevalence. 16. 6. Association between tooth loss and TMJ dysfunction. Curr Med Res Opin 1992^13:1-12. Rohlin M. McNeill C (ed). Idiopathic osreonecrosis of the hip. J Craniomand Pract 1992. Hellsing G. Whittaker DK. Arthtotic changes and deviation in form of the temporomandibular joint—An autopsy study. Cantlllon V. 32. Radiography of the temporomandibular joint in female parients with TMJ pain or dysfunction. Molleson T. ed 3. The aim of treatment of DJD is to shorten its natural course or at least to make it more tolerable.12:189-194. NZ Dent J 1991:87:113-llS. J Am Denf Assoc 1990. Heloe B. Agents A<. Classification. 21.n5:317-32é. Am J Phys Anthropol 1991. 31. 15. 1990:166-176. 25. Wbittaker DK. 134:223-231.tions SuppI I993. 26. Arthroscopy 1992. 14. 10. Griffiths MJ. 28. 1990. Plitz W. Once the disease process has stabilized. Oberg T. Br Rheumatol l993. The temporomandibular ioint: A morpbologic study on human autopsy material Acta Odontol Scand 1971. J Oral Rehabd 199Üil7:89-97. Bell WE. Chicago: Quintessence. Haley DP.Neiad F. Carlsson GE. Studies on tbe temporomandibular joints of eighteenthcentury London population (Spitalfields). 4S-53. Suso S. RepotI of the president's conference on examination. the temporomandibular joint. Hollender L. Glazer PA. Davies G. The prevalence and treatment needs of subjects wiih temporomandibular disorders. Biocbem J 1978. 19. 1989il01-113. The correlation of tempotomandibular joint sounds with morphology in fifty-five autopsy specimens. Guidelines for Classification. J Oral Rehabil 198i. Articular surface breakdown can occur because of increased mechanical stress or reduced ability of the tissue to withstand and adapt to the applied stress. Br DentJ 1973. Vandcr-Kraan PM. Guidelines for Evaluation. J Am Dent Assoc 1994. 122. Chicago: Year Book Medical. 23. The in yivo effects of naproxen on canine experimental osteoarthriric articular cartilage: Composition. Hagena FW. Whittaker DK. Osteoarthrosis of tbe mandibular condyle. and tteatments. 2.120: 29. Axelsson S.5-303. Alanen P. Toller PA. 29. Heloe LA. Internal detangement related to osteoartbrosis in temporomandibular joint autopsy specimens. Mohl ND. Hauf W. J Manipulative Physiol Ther 1993. Rohlin M. Community Dent Oral Epidemiol l?7S.43 i 194-200. Chicago: Quintessence. I Am Dent Assoc 1983. Griffiths RH. Ericksson L. looth loss. ease simulating impingement syndrome: Arthroscopic findings. diagnosis and management of tempotomandibular disorders. Ratcliffe A. 11. 22. Barrett AW.32:281-286. Edwards PW. Lafeber FP. Kay SP. Mahmud F. Rosenwasser MP. Cutrent status of diagnostic procedures for temporomandibular disorders. Schiffman EL. The influence of the loss of teeth and attrition on the articular eminence. These objectives are. Huber-Bruning O. Lane N. 1995 . J Oral Maxillufac Surg 19 85. Ali SY. American Academy of Craniomandibuiar Disorders. Management. preserve function. Craniomandibulat Disorders.I6:37^2. Chicagoi Yeat Book Medical. Kirveskari P. Double-blind comparison of etodolac SR and diclofenac SR in the treatment of patients with degeneraiive joint disease of the knee. 41. diagnosis. There is a delicate balance between adaptive response (remodeling) and nonadaptive response (degeneration) to functional demands. Khan FM. Fitins D. Clinical presentation and final diagnosis of patients referred to a tempoto. Ferguson JW. Subjective symptoms in temporomandibular joint osteoarthtosis.25:169-176.125:56-64. 12:407-419.75:273-275. Biomed Tech (Berlin) 1992. 4.Si-A$l^59. Saed. 33. Scully C. Oral Surg Oral Med Oral Pathol 1993. Diagnosis. Peidro L.42: 78-85. Oste o arthritic human cartilage is more sensitive to transforming growth factor beta than is normal canilage.176:683-693. Bessette RW.85:367-377.i7i17-22. ed 4. Williams PI. Number2. Oral Surg Oral Med Oral Path 1984. Arthritis of the mandibular joint. Harris E. Mow VC. 17. Acta Radiol [Diagl 1984. Temporomandibular joint (isreoarchritis in a British skeletal population. J Oral Rebabil 1985. 1993:11-13. Method for patella. Ameticati Academy of Orofacial Pain. Brown M. attrition. Westesson P-L. Edwards JL.8:482^87. 174 Volume 9. and temporomandibular joint changes in Romano-British population.68(special issue): [abstract 1211]. Ellman H.35:207-215. Early degenerative joint dis. Ramon R. Classification. Characteristics of a group of patients with temporomandibular joint disorders. Diagnosis. Orofadal Pains. It is hoped that treatment during the active phases of the disease will reheve pain. 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Es wird eine Übersicht über klinische und experimentelle Literatur zu degenerativen Geienkerkrankungen vorgestellt. im allgemeinen. California 94549. patogénesis. Diagnose. Lafayette. La progresión de la enfermedad degenerativa de la artioulación depende de los procesos patológicos subyacentes y/o reactivos envueltos. der. Se describe la epidemiología. und Prcgncse werden beschrieben. Therapie. Epidemiologie. The ABOP will offer annual certification examinations to dentists licensed in the United States. mit speziellem Schwergewicht auf dem Kiefergelenk Der Artikel behandelt Faktoren. The application for the 1996 examination will be available on June 1. com pro nieten la adaptabilidad tisutar. For more information. die das Gleichgewicht zwischen Remodeling und Degeneration im Kiefergelenk beeinflussen kónnen und stellt Grundprinzipien zur Diagnose und Therapie vor. 1995. die Adaptationsfáhigkeit des Gewebes einschränkt. 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 pain management. Number 2. y pronóstico con jn énfasis particular en la articulación temporomandibular (ATM) Este articulo describe los factores 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. 1995 .Kamele hu k/M ai or Resumen Enfermedad Degenerativa Temporomsndibular de la Articulación Zusammenf assu ng Degenerative Eriírankungen des Kiefergelenkes Das Fortschreiten einer degenerativen Gelenkerkrankung hangt vom ihr zugrundeliegenden palhoiogischen und/oder reaktiven Prozess ab. diagnóstico. Pathogenese. Se presenta una revisión de literatura clínica y eïpenmental relacionada a la enfermedad degenerativa de la articulación. •sao Volume 9. please write to: The American Board of Orofacial Pain. 10 Jopliti Court. y que en general.