Molecular biology of temporomandibular joint disorders: Proposed mechanisms of disease
ABSTRACT PURPOSE: The biologic processes of temporomandibular joint adaptation and disease are poorly understood. However, recent technologic advances have provided methods that allow sophisticated studies of the molecular mechanisms that are relevant to the pathophysiology of degenerative temporomandibular joint diseases. This review examines current models of the molecular events that may underlie both adaptive and pathologic responses of the articular tissues of the temporomandibular joint to mechanical stress. It is hoped that an increased understanding of these complex biologic processes will lead to improved diagnostic and therapeutic approaches directed to the management of temporomandibular disorders.
- SourceAvailable from: Keiichiro Okamoto
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- "The basis for this sex difference is not certain; however, clinical findings suggest that changes in estrogen status may play a significant role (Suenaga et al., 2001; Isselee et al., 2002; LeResche et al., 2003). In those TMJD cases diagnosed with disc displacement or after overt injury to the TMJ elevated levels of pro-inflammatory agents are found within the joint space and may contribute to persistent TMJD pain (Milam and Schmitz, 1995; Lobbezoo et al., 2004; Ta and Dionne, 2004). Intra-articular administration of Complete Freund's Adjuvant (CFA) is a wellestablished animal model for monoarthritis that causes persistent joint inflammation (Wilson et al. 2006) and long-term changes nociceptive behavior in rodents (Butler et al. 1992; Schadrack et al. 1999; Luo et al. 2008). "
ABSTRACT: The mitogen-activated protein kinase/extracellular regulated kinase (MAPK/ERK) pathway plays a key role in mediating estrogen actions in the brain and neuronal sensitization during inflammation. Estrogen status is a risk factor in chronic temporomandibular muscle/joint (TMJ) disorders; however, the basis for this relationship is not known. The present study tested the hypothesis that estrogen status acts through the MAPK/ERK signaling pathway to alter TMJ nociceptive processing. Single TMJ-responsive neurons were recorded in laminae I-II at the spinomedullary (Vc/C(1-2)) junction in naïve ovariectomized (OvX) female rats treated for 2 days with high-dose (20 microg/day; HE2) or low-dose estradiol (2 microg/day; LE2) and after chronic inflammation of the TMJ region by complete Freund's adjuvant for 12-14 days. Intra-TMJ injection of ATP (1 mM) was used to activate Vc/C(1-2) neurons. The MAPK/ERK inhibitor (PD98059, 0.01-1 mM) was applied topically to the dorsal Vc/C(1-2) surface at the site of recording 10 min prior to each ATP stimulus. In naïve HE2 rats, low-dose PD98059 caused a maximal inhibition of ATP-evoked activity, whereas even high doses had only minor effects on units in LE2 rats. By contrast, after chronic TMJ inflammation, PD98059 produced a marked and similar dose-related inhibition of ATP-evoked activity in HE2 and LE2 rats. These results suggested that E2 status and chronic inflammation acted, at least in part, through a common MAPK/ERK-dependent signaling pathway to enhance TMJ nociceptive processing by laminae I-II neurons at the spinomedullary junction region.Neuroscience 09/2009; 164(4):1813-20. DOI:10.1016/j.neuroscience.2009.09.058 · 3.33 Impact Factor
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- "When its properties are altered, the functional effectiveness of the disc is reduced, presumably resulting in increased joint failure (Chen et al., 1999). Hence, degenerative joint disorders may be the result of mechanical joint overload, and there seems to be an association between the intensity and frequency of mechanical stress and the reaction of the cartilage matrix (Milam and Schmitz, 1995). Investigating joint load in vivo, however, requires invasive direct monitoring of joint forces, which has never been successfully performed due to technical challenges. "
ABSTRACT: Occlusal splints are used for the management of temporomandibular disorders, although their mechanism of action remains controversial. This study investigated whether insertion of an occlusal splint leads to condyle-fossa distance changes, and to mandibular rotation and/or translation. By combining magnetic resonance images with jaw tracking (dynamic stereometry), we analyzed the intra-articular distances of 20 human temporomandibular joints (TMJs) before and after insertion of occlusal splints of 3 mm thickness in the first molar region. For habitual closure, protrusion, and laterotrusion in the contralateral joint, occlusal splints led to minor--yet statistically significant--increases of global TMJ space and to larger increases at defined condylar areas. Condylar end rotation and translation in habitual closure were reduced. Hence, the insertion of a 3-mm-thick occlusal splint led to a change in the topographical condyle-fossa relationship, and therefore to a new distribution of contact areas between joint surfaces.Journal of Dental Research 10/2008; 87(9):877-81. DOI:10.1177/154405910808700903 · 4.14 Impact Factor
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- "Noise is created as dissipated energy from fibroelastic tissue, which gradually changes histomorphometrically and becomes incapable of absorbing the energy generated by dysfunctional torque. The influence of chronic unopposed tissue-destructive torque within the system most likely initiates the elevation of certain painful inflammatory and pain mediators via both oxidative and mechanical tissue destruction (Fig. 3)        . "
ABSTRACT: Biomechanical principles of temporomandibular joint (TMJ) loading are unique, particularly in an orthopedic system that exhibits curvilinear general plane motion. Certain type-specific derangements can be surgically challenging and may primarily require open arthrotomy techniques rather than arthroscopy. This article discusses the basic biomechanical principles in normal and pathologic function. Three-dimensional preoperative imaging of TMJs is necessary for appropriate assessment of all patients and when open techniques are necessary as the initial surgical procedure.Oral and Maxillofacial Surgery Clinics of North America 09/2006; 18(3):345-68, vi. DOI:10.1016/j.coms.2006.03.006 · 0.48 Impact Factor