Pathogenesis of Degenerative Joint Disease in the Human Temporomandibular Joint

Abstract

ABSTRACT:The wide range of disease prevalences reported in epidemiological studies of temporomandibular degenerative joint disease reflects the fact that diagnoses are frequently guided by the presence or absence of non-specific signs and symptoms. Treatment is aimed at alleviating the disease symptoms rather than being guided by an understanding of the underlying disease processes. Much of our current understanding of disease processes in the temporomandibular joint is based on the study of other articular joints. Although it is likely that the molecular basis of pathogenesis is similar to that of other joints, additional study of the temporomandibular joint is required due to its unique structure and function. This review summarizes the unique structural and molecular features of the temporomandibular joint and the epidemiology of degenerative temporomandibular joint disease. As is discussed in this review, recent research has provided a better understanding of the molecular basis of degenerative joint disease processes, including insights into: the regulation of cytokine expression and activation, arachidonic acid metabolism, neural contributions to inflammation, mechanisms of extracellular matrix degradation, modulation of cell adhesion in inflammatory states, and the roles of free radicals and heat shock proteins in degenerative joint disease. Finally, the multiple cellular and molecular mechanisms involved in disease initiation and progression, along with factors that may modify the adaptive capacity of the joint, are presented as the basis for the rational design of new and more effective therapy.

Pushing the limit: masticatory stress and adaptive plasticity in mammalian craniomandibular joints

“…Rather, the duration of dietary manipulation in our study greatly exceeds that of previous investigations and it is well known that cartilage exhibits accelerated degradation in response to elevated and/or repetitive loading (Guerne et al, 1994;Guerne et al, 1995;Bae et al, 1998). Such changes in cartilage composition reflect the early onset and progression of degenerative effects that compromise the structural integrity of a joint (Mankin et al, 1971;Newton and Nunamaker, 1985;Haskin et al, 1995;Kamelchuk and Major, 1995;Ishibashi et al, 1996;Ostergaard et al, 1999;Fujimura et al, 2005). This interpretation is consistent with patterns of change noted for rabbit TMJ ·8.…”

“…Lower proteoglycan content throughout the FC pad and in the lower two layers of the condylar cartilage of O-diet rabbits mirrors findings for the articular surface of mammal limb elements, where age-related onset of cartilage degradation is linked to decreases in proteoglycan content (Mankin et al, 1971;Newton and Nunamaker, 1985;Haskin et al, 1995;Ostergaard et al, 1999). Due to the elevated viscoelasticity of proteoglycan-rich tissues in joints subjected to cumulatively low postnatal stresses (i.e.…”

The effect of loss of occlusal support on mandibular morphology in growing rats

“…The influence of tooth loss, especially loss of molar support, on the etiology of degenerative changes is a topic of long-standing controversy. 4 Reduced occlusal support below the normal value, which is 12-14 pairs of contacting teeth in an adult, affects muscle activity, bite force, and jaw movements. 5 Also, premature tooth loss often leads to space loss, alteration in the proper contact of the inclined planes of the teeth, and disturbance of masticatory function.…”

Functional Lateral Shift of the Mandible Effects on the Expression of ECM in Rat Temporomandibular Cartilage

“…4 Although the relationship between functional malocclusion and temporomandibular joint disorder (TMD) is still debatable, a high incidence of TMD signs and symptoms has been reported frequently in children and adolescents with a functional lateral shift of the mandible. 5,6 Nonphysiologic mechanical loading 7 and TMJ structural abnormalities 8 are considered factors that contribute to TMD. These factors suggest that an underlying biological link between the loading from unilateral functional crossbite and TMD still is not understood.…”