The morphology of the muscle bundle in the deep layer of the anterior temporal muscle was observed using cadavers for anatomical practice. With regard to the infratemporal crest, which is the origin of the muscle bundle, its cranial bone surface morphology was also observed, and the following results were obtained:
1. This muscle bundle was thought to be part of the anterior muscle bundle of the temporal muscle, considering the innervation and fascial conditions.
2. In elderly specimens, processes were noted on the bone surface of the infratemporal crest, which is the origin of this muscle bundle.
3. The length of this muscle bundle was 36.85±2.78mm, and the width was 12.49±1.37mm, with an inclination angle of 80.83±2.46° to the auriculo-orbital plane (FH. plane).
These findings suggested that although the deep muscle bundle is part of the anterior muscle bundle in the superficial layer, the muscle bundle developed as an independent muscle fascicle, causing changes in the bone surface in the adhesion area of the muscle, due to strong force applied during mandibular movement.

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This study was designed to investigate the effects of experimental traumatic occlusion on the temporomandibular joint (TMJ) in rats. Composite resin 2mm thick was built up on the occlusal surface of the maxillary left first molar (experimental group) and then traumatic occlusion was induced in 7-weekold Wistar rats. Untreated rats were used as the control. Rats in each group were sacrificed at 3, 7, 14, 28, 42, and 56 days after the induction of traumatic occlusion. For the histopathological analysis the sections were stained with hematoxylin and eosin. The cell proliferative activity in the condylar cartilage was identified by immunohistochemistry after injection of 5-bromo-2′-deoxyuridines (BrdU) and examined histopathologically and histometrically. At both sides in the experiment group, the thickness of condylar cartilage and the number of labelled cells with BrdU in the cartilage decreased at 7 days, but increased at 14 days. At 28 days, the thickness of condylar cartilage and the number of labelled cells with BrdU in the cartilage in the experimental group decreased to the same level as that in the control group. Thus, the results indicate that the histological and cytological responses of both sides of TMJ are influenced by the induction of traumatic occlusion of only one tooth.

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To determine whether clenbuterol, a β₂-adrenergic agonist, affects the mass and fiber type of the mouse masseter muscle by altering the expressions of insulin-like growth factors (IGFs), their receptors (IGFRs), and their binding proteins (IGFBPs), we analyzed changes in the myofiber diameter, the expressions of myosin heavy chain (MHC) mRNAs, the markers for muscle fiber type, and the expressions of IGF, IGFR, and IGFBP mRNAs. In addition, to identify a possible contribution of muscle satellite cells in the change of the mouse masseter induced by clenbuterol, we analyzed the expressions of the myoD family (myf5, myoD, myogenin, and MRF4) and myocyte nuclear factor (MNF) mRNAs, and performed immunolocalization for proliferating cell nuclear antigen (PCNA), because they are all markers for activated and quiescent satellite cells. Clenbuterol (40 μg/ml) was orally administered to 6-month-old mice via their drinking water for 2 weeks. The relative amounts of mRNAs were analyzed by competitive polymerase chain r action in combination with reverse-transcription. The administration of clenbuterol increased the myofiber diameter by 26% (p<0.001), but it did not significantly change the amounts of MHC mRNAs, suggesting that clenbuterol induced hypertrophy but did not alter the fiber type. The administration of clenbuterol increased the amount of mRNA for IGF-I by 219% (p<0.05), but it decreased that for IGFBP3 by 21% (p<0.001). The amounts of mRNAs for all genes except for IGF-I and IGFBP3, and the immunolocalization for PCNA were not significantly changed by clenbuterol. These results suggest that clenbuterol induces hypertrophy in the mouse masseter muscle and that IGF-I and IGFBP3 are involved in the clenbuterol-induced hypertrophy, but the satellite cells might not be involved.

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Bisphosphonates are widely known as inhibitors of formation and resorption of mineralized tissues. However, it is uncertain how bisphosphonates affect calcium phosphate precipitation and matrix synthesis in mineralized tissues. Several histological approaches have been done to study hard tissues affected by bisphosphonates. In this study, we used a bisphosphonate for biochemical investigation to study the mechanisms of biological mineralization and considered the effects of the bisphosphonates.
Hydroxyethylidene-1, 1-bisphosphonate (HEBP) was administered to rats by subcutaneous injection of 10mg P/kg for seven weeks. The incisors of the rats were removed and the dentin matrix proteins were analyzed biochemically. The amount of matrix proteins was relatively increased in the incisors of the experimental rats, though mineralization of the incisors of the those rats was reduced compared with that of the control rats. Dentin phosphophoryns, unique phosphoproteins of dentin, were also elevated in the experimental rats. Nevertheless, the composition of other non-collagenous proteins of dentin was essentially unchanged by the treatment.
Inhibition of mineralization by bisphosphonate may not be mediated by inhibition Of synthesis of noncollagenous matrix proteins, but mainly by inhibition of calcium phosphate deposition. Moreover, it is possible that the synthesis of phosphophoryns was promoted by the treatment.

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Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflammatory cytokines. Recently, it has been shown that A 2 a adenosine receptor (A 2 aR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory responses. It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the inflammation. However, very little, if anything, is known about the effect of bacterial LPS on the expression of A 2 aR during an infection of bacteria. The aim of this study is to evaluate the effects of adenosine, ATP and LPS on the expression of A 2 aR and toll-like receptor 4 (TLR 4), which is a receptor for LPS, in the mouse macrophage cell line RAW 264. Adenosine and ATP failed to affect proliferation in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly potentiated the expression of TLR 4, but not of A 2 aR. ATP and LPS markedly potentiated the expression of A 2 aR and TLR 4, respectively. Moreover, adenosine and ATP did not affect the expression of A 2 aR and TLR 4 in the presence of LPS, respectively. This study revealed that adenosine, ATP and LPS affect the expression of A 2 aR and TLR 4 in macrophages.

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