Journal of Osaka Dental University
Online ISSN : 2189-6488
Print ISSN : 0475-2058
ISSN-L : 0475-2058
Volume 33, Issue 1
Displaying 1-5 of 5 articles from this issue
  • Akinori Hayashi, Mitsuko Shinohara, Kiyoshi Ohura
    Article type: Article
    1999 Volume 33 Issue 1 Pages 1-7
    Published: 1999
    Released on J-STAGE: November 21, 2016
    JOURNAL FREE ACCESS
    It is well known that diabetes mellitus aggravates both the severity and progression of periodontal disease. We sought to further explore biologic mechanisms of this relationship using naturally occurring gingivitis rats (ODUS/Odu) rendered diabetic by 65 mg/kg intravenous injection of streptozotocin (STZ). Insulin was administered daily to one group of the rats beginning 4 weeks after STZ injection (STZ-insulin group). Others received no insulin (STZ group). A third group that received no STZ was kept as controls. Eight weeks after STZ injection, sterilized liquid paraffin was injected peritoneally into all three groups, and peritoneal macrophages were collected 4 days later. Macrophage chemotaxis was measured by the membrane filter method using a 48-well microchemotaxis chamber with zymosan activated serum used as a chemotactic stimulant. Blood glucose levels, body weight, plaque indices, pocket depths, serum triglyceride and hemoglobin A1C levels were also determined.
    We found that blood glucose levels, body weight and triglycerides recovered to normal values in the STZ-insulin group. Further, control of blood glucose resulted in diminished plaque indices, and pocket depths returned to values seen in the controls. Chemotaxis and phagocytosis of peritoneal macrophages improved slightly in the STZ-insulin group, but did not return to levels seen in the pretreatment state. Although insulin resulted in some improvement in leukocyte function damaged by induced diabetes mellitus, recovery was incomplete. (J Osaka Dent Univ 1999; 33: 1-7)
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  • Takaharu Ishii, Yasuo Nishikawa
    Article type: Article
    1999 Volume 33 Issue 1 Pages 9-21
    Published: 1999
    Released on J-STAGE: November 21, 2016
    JOURNAL FREE ACCESS
    Nociceptive neurons receiving afferent input from the tooth pulp (TP) were recorded from the nucleus ventralis posteromedialis proper (VPM) and intralaminar nuclei of the thalamus in cats anesthetized with urethane and chloralose. The effects of stimulating theperiaqueductal gray (PAG), or the nucleus raphe dorsalis (NRD) on responses of thalamic nociceptive neurons were investigated.
    Eight tooth pulp specific (TPS) and 7 wide dynamic range (WDR) neurons with TP input were observed around the periphery (shell region) of the posterior half of VPM. Following electrical stimulation of either the ventral PAG or the NRD, responses to TP stimulation were inhibited in all TPS and WDR neurons tested. Responses of these neurons to electrical stimulation of trigeminothalamic tract (TTT) fibers in the trigeminal medial lemniscus were also inhibited following PAG/NRD stimulation. These results suggest that PAG/NRD stimulation-produced inhibition of both TPS and WDR neurons may be partially mediated by an ascending antinociceptive mechanism.
    Intralaminar nociceptive neurons with TP input were observed in the nucleus centralis lateralis (CL), and parafascicularis (Pf). The effects of conditioning electrical stimulation of either the ventral PAG or the NRD on responses of intralaminar nociceptive neurons were studied. Of 15 intralaminar nociceptive neurons tested, 6 neurons were inhibited, 5 neurons were excited and 4 were unaffected following the conditioning stimulus. In neurons in which responses to TP stimulation were inhibited, responses elicited by electrical stimulation of the mesencephalic reticular formation (MRF) were also inhibited. These data suggest that although there is an ascending inhibitory pathway from PAG/NRD to intralaminar nuclei, this system is far less potent compared with the ascending inhibitory system acting upon the VPM. ( J Osaka Dent Univ 1999; 33: 9-21)
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  • Hirotaka Murakami, Kenji Uchihashi, Yo Yoshida
    Article type: Article
    1999 Volume 33 Issue 1 Pages 23-33
    Published: 1999
    Released on J-STAGE: November 21, 2016
    JOURNAL FREE ACCESS
    We examined the relationship between E-cadherin (E-CD), protein kinase C (PKC) and assembly of the tight junction (Tj) in rat submandibular gland acinar cells. The junctional complex of the acinar cells was double-labeled with anti-ZO-1 antibody and anti-E-CD antibody. When Ringer's solution was intraductally injected into the main duct, ZO-1 labels were highly concentrated at the Tj zone, and the adherens junction (Aj) was exclusively labeled by E-CD. In addition, the Tj was impermeable to microperoxidase. Neither intraductal injection of anti-E-CD antibody solution nor infusion of carbachol produced labels for ZO-1 at the Tj zone, although these proteins were occasionally intermixed at the Aj zone. In these cases, the Tj was permeable to microperoxidase. lntraductal injection of anti-E-CD antibody solution with PKC agonist, resulted in a reduction of E-CD labels in the Aj zone, while the ZO-1 was labeled exclusively in the Tj zone. In this case, Tj was impermeable to microperoxidase. These results suggest that E-CD plays a major role in mediating intercellular physical adhesion, and that PKC may be active in signaling the pathway activated by E-CD-mediated cell-cell adhesion. (J Osaka Dent Univ 1999; 33: 23-33)
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  • Tadashi Sagawa, Mitsuko Shinohara
    Article type: Article
    1999 Volume 33 Issue 1 Pages 35-41
    Published: 1999
    Released on J-STAGE: November 21, 2016
    JOURNAL FREE ACCESS
    It is well known that there are several coagulation factors and fibrinolysis factors, and these inhibitors are also present in blood and tissues. Normally, these factors balance each other. We measured antithrombin III (AT III), an important inhibitor of coagulation and α2-plasmin inhibitor (α2-Pl), a factor inhibiting fibrinolysis in blood and gingival tissue of naturally occurring gingivitis rats (ODUS/Odu) and control rats (Res). Blood plasma and supernatants of gingival homogenate from ODUS/Odu and Res were used assamples. And concentrations of α2-Pl and AT III were measured by colorimetric assay using commercially available reagents. We found no difference in blood concentrations of α2-Pl or AT III between ODUS/Odu and Res groups. However, AT III in the gingiva showed a significantly higher value in the ODUS/Odu group versus that in the controls (p< 0.001). There was a high positive correlation between AT III in gingival tissue and pocket probing depth. Moreover, the fibrinolytic activity in saliva and the gingiva from ODUS/Odu increased with each passing month. Results suggest that both the decrease in blood coagulability and systemic enhancement of fibrinolytic activity due to increased AT III in gingival tissue are associated with the bleeding tendency and inflammatory response in the gingiva of ODUS/Odu. (J Osaka Dent Univ 1999; 33: 35-41)
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  • Fazal H. Tabassam, Hisanori Umehara, Naochika Domae
    Article type: Article
    1999 Volume 33 Issue 1 Pages 43-51
    Published: 1999
    Released on J-STAGE: November 21, 2016
    JOURNAL FREE ACCESS
    Accumulation of T cells at inflammatory sites is one of the characteristic features of infection, autoimmune and chronic inflammatory diseases. Optimal activation of T cells requires the binding of the MHC/Ag complex with T cell receptor, as well as a secondary signal initiated by costimulatory molecules such as CD2, CD28 or integrins. Focal adhesion kinase, pp125FAK(FAK) has been previously shown to be localized in focal adhesions in fibroblasts and to be involved in integrin-mediated cellular activation. Although signaling through β1- or β3-integrins induces tyrosine phosphorylation of FAK, there has been no evidence that activation of T cells through the β2-integrin, lymphocyte functionassociated antigen (LFA) -1, involves FAK. We report here that crosslinking of LFA-1 induces tyrosine phosphorylation of FAK in PHA-activated T cells. Moreover, cocrosslinking with anti-LFA-1 monoclonal antibody (mAb) and suboptimal concentration of anti-CD3 mAb markedly increases tyrosine phosphorylation of FAK in an antibody-concentration and time-dependent manner compared with stimulation through CD3 alone. Furthermore this increased phosphorylation correlates well with the enhanced proliferation of PHA-activated T cells. Results indicate that signals mediated by LFA-1 can regulate FAK, suggesting that LFA-1-mediated T cell costimulation may be involved in T cell activation at least partially through FAK. (J Osaka Dent Univ 1999 ; 33 : 43-51)
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