In the progression of the Temporomandibular Joint Disorder(TMD), not only deformation and perforation of disc occur. But also fibrotic adhesion and inflammatory changes to the retrodiscal tissue can be seen in addition to the condylar degenerative change (e.g. osteoarthritis). However, the correct diagnosis,?planning for appropriate treatment, and prediction of prognosis are limited, because there are no means to stage the progression of the disorder. In this study relative signal intensity of retrodiscal tissue in MRI and the synovial fluid concentration of matrix metalloproteinase-2 (MMP-2), MMP-9, and Interleukin-6 (IL-6) in the 23 temporomandibular joints(TMJ), from 17 patients with TMD were evaluated as a possible diagnostic marker. The relative signal intensity of retrodiscal tissue was referenced to brain gray matter with same region of interest(ROI) size. The concentrations of MMP-2, MMP-9, and IL-6 were evaluated by Enzyme Linked Immunosorbent Assay (ELISA). The collected data were compared with condylar degenerative change, joint effusion and disc position observed in MRI. The relative signal intensity of the retrodiscal tissue was increased significantly when degenerative changes were present. In addition, there was significantly high signal intensity in the presence of a disc displaced without reduction. The concentration of IL-6 was significantly increased when condylar degenerative change was no observed. And there were no changes in the levels of IL-6 according to disc position and joint effusion measurement. Moreover, there were no significant relevance between the concentration of total MMP-2 and active MMP-9 in synovial fluid, relative to degenerative changes in the mandibular condyle, to joint effusion, and to disc position observed on MRI images. In conclusion, the relative signal intensity of the retrodiscal tissue can be regarded as a mean of diagnosing the procession of TMD in a non-invasive manner. But more additional studies are required for the levels of MMP-2. MMP-9, and IL-6 to determine their potentials as a diagnostic marker for TMD.
Brain ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-6* ; Joints ; Magnetic Resonance Imaging* ; Mandibular Condyle ; Matrix Metalloproteinase 2 ; Prognosis ; Synovial Fluid* ; Temporomandibular Joint Disorders* ; Temporomandibular Joint*

The purpose of this study was to amount of the frictional forces with the brackets and wires, ligation methods, dry/wet, offsets, interbracket distances, velocity and to compare them each other by different conditions. This study tested 0.018" x 0.025" slot sized 8 types of orthodontic bracket systems and 0.016", 0.016" x 0.022" sized stainless steel, NiTi, Cu-NiTi orthodontic wires. One cuspid bracket were positioned on the slide glass and archwire was engaged into bracket and ligated with elastomeric modules. The values of frictional forces were measured with the Instron universal testing machine. The results were as follows; 1. Polycrystalline ceramic bracket had the highest mean frictional forces and followed and by ceramic reinforced plastic bracket, metal bracket, plastic bracket with metal slot, monocrystalline ceramic bracket, single bracket, self-ligating bracket, friction free bracket in descending order. The self-ligating bracket showed low frictional forces in the round wires and high frictional forces in the rectangular wires. 2. Stainless steel wires had the least frictional forces and followed by NiTi, Cu-NiTi wires in descending order. Round wires had lower frictional forces then that of rectangular wires. 3. The stainless steel ligation method had significantly greater mean frictional forces them the elastomeric module ligation method. 4. Artificial saliva statistically increased the frictional forces in stainless steel wire, NiTi wire and Cu-NiTi wire. 5. There was a statistically significant difference with offset change. 6. There was no statistically significant difference with interbracket distance in stainless steel wires but a significant difference in NiTi wires as the interbracket was decreased.
Ceramics ; Cuspid ; Elastomers ; Friction* ; Glass ; Ligation ; Orthodontic Brackets* ; Orthodontic Wires ; Plastics ; Saliva, Artificial ; Stainless Steel

Microglial cell activation is known to contribute to neuropathic pain following spinal sensory nerve injuries. In this study, I investigated its mechanisms in the case of trigeminal sensory nerve injuries by which microglial cell and p38 mitogen-activated protein kinase (p38 MAPK) activation in the medullary dorsal horn (MDH) would contribute to the facial pain hypersensitivity following mandibular nerve transection (MNT). And also investigated the changes of trigeminal ganglion neurons and ERK, p38 MAPK manifestations. Activation of microglial cells was monitored at 1, 3, 7, 14, 28 and 60 day using immunohistochemical analyses. Microglial cell activation was primarily observed in the superficial laminae of the MDH. Microglial cell activation was initiated at postoperative 1 day, maximal at 3 day, maintained until 14 day and gradually reduced and returned to the basal level by 60 days after MNT. Pain hypersensitivity was also initiated and attenuated almost in parallel with microglial cell activation pattern. To investigate the contribution of the microglial cell activation to the pain hypersensitivity, minocycline, an inhibitor of microglial cell activation by means of p38 MAPK inhibition, was administered. Minocycline dose-dependently attenuated the development of the pain hypersensitivity in parallel with inhibition of microglial cell and p38 MAPK activation following MNT. Mandibular nerve transection induced the activation of ERK, but did not p38 MAPK in the trigeminal ganglion. These results suggest that microglial cell activation in the MDH and p38 MAPK activation in the hyperactive microglial cells play an important role in the development of facial neuropathic pain following MNT. The results also suggest that ERK activation in the trigeminal ganglion contributes microglial cell activation and facial neuropathic pain.
Animals ; Facial Pain ; Horns* ; Hypersensitivity ; Mandibular Nerve* ; Minocycline ; Neuralgia ; Neurons* ; p38 Mitogen-Activated Protein Kinases ; Protein Kinases ; Trigeminal Ganglion*

Carcinoma, Squamous Cell ; Cell Differentiation ; Humans ; Immunohistochemistry ; Korea ; Lymph Nodes ; Mouth Neoplasms ; Neoplasm Metastasis ; Peptide Hydrolases ; Prognosis ; Radiotherapy ; Saints ; Tissue Inhibitor of Metalloproteinase-1 ; Tongue