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Degenerative Disease of the Temporomandibular Joint

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Degenerative Disease of the Temporomandibular Joint Degenerative Disease of the Temporomandibular Joint 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 temporomandibular joint remodeling/degeneration parity and pre- Edmonton, Alberta sents rationale for approacbes to diagnosis and treatment. Canada J OROFACIAL PAIN 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 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 commonly 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- 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-synovial joint.'" 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 degenerative disease 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 joints 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 synovial fluid.''" 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 collagen network occasionally dis- 39 cadaveric knee 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
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