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T Okiji

Publications and source records attributed to T Okiji.

24 records · Page 2Linked to original sources
PubMed1991

The role of leukotriene B4 in neutrophil infiltration in experimentally-induced inflammation of rat tooth pulp.

Inflammation was induced in rat dental pulp by applying bacterial lipopolysaccharide (LPS). Extirpated tissue samples from inflamed pulps were incubated in vitro in a Krebs buffer containing Ca2+ ionophore A23187, and leukotriene (LT) B4 released into the medium was determined by radio-immunoassay. Production of LTB4 could be detected three to 24 h after the application of LPS and showed a maximum at 12 h. Histologically, marked infiltration of neutrophils, but not other leukocytes, was characteristically observed in the LPS-applied pulps, and the temporal change in neutrophil infiltration was almost parallel, but somewhat more delayed than LTB4 production. When BW755C, a dual inhibitor of cyclo-oxygenase and lipoxygenase, was given to the animals before the application of LPS, both the production of LTB4 and the number of infiltrated neutrophils were significantly decreased, whereas administration of indomethacin had no effect. These results suggest that LTB4 may be involved in neutrophil infiltration in pulpal inflammation. It was also suggested that a major early source of LTB4 in experimental pulpitis was leukocytes, primary neutrophils, because the synthesis of LTB4 in the inflammed pulp was diminished by depletion of circulating leukocytes with cyclophosphamide prior to the application of LPS.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1989

Involvement of arachidonic acid metabolites in increases in vascular permeability in experimental dental pulpal inflammation in the rat.

Pulp was experimentally inflamed by applying bacterial lipopolysaccharide (LPS). Changes in arachidonic acid (AA) metabolites were determined by measuring the conversion of exogenously added AA in pulp homogenates. The inflamed pulp produced 12-hydroxy-eicosatetraenoic acid (12-HETE), 6-keto-prostaglandin (PG) F1 alpha greater than PGE2, thromboxane B2 and 11-HETE, which was further identified with high-performance liquid chromatography. The LPS treatment caused a 2.0-fold increase in 12-HETE production at 1 h, a 3.8-fold increase in 6-keto-PGF1 alpha production at 12 h and increases in PGE2 and 11-HETE production of 8.8- and 5.5-fold, respectively, at 24 h. Vascular permeability in the inflamed pulp was measured by quantifying the amount of an extravasated dye; it increased markedly from 6 h and reached a peak at 12 h after the LPS application. When indomethacin (0.3-30 mg/kg, s.c.) was given before LPS, both the production of 6-keto-PGF1 alpha and PGE2 and the increase in vascular permeability were inhibited dose dependently. Exogenously applied PGE2 and PGI2 methyl ester reduced the inhibition of the increase in vascular permeability caused by indomethacin. Thus PGE2 and PGI2 may be involved in increases in vascular permeability in pulpal inflammation.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1987

Arachidonic-acid metabolism in normal and experimentally-inflamed rat dental pulp.

Pulp homogenates were incubated with [14C]-arachidonic acid and the metabolites separated by thin-layer chromatography. The main products of normal pulp were 6-keto-prostaglandin (PG) F1 alpha and 12-hydroxy-eicosatetraenoic acid (12-HETE), further identified by high performance-liquid chromatography. Thromboxane (TX) B2, and PGD2, E2 and F2 alpha were also detected at less than 30 per cent of 6-keto-PGF1 alpha. When the pulp was inflamed by applying bacterial lipopolysaccharide, production of all these metabolites increased; in particular, PGE2 was increased 9.3-fold compared with normal, and 6-keto-PGF1 alpha and HETE 3.8- and 2.0-fold, respectively. An unidentified product, slightly more polar than 12-HETE, was also markedly produced by the inflamed pulp. Thus arachidonic-acid metabolites including lipoxygenase products may be involved in the development of pulpal inflammation.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

Effect of ascorbic acid deficiency on primary and reparative dentinogenesis in non-ascorbate-synthesizing ODS rats.

Ascorbic acid is essential to the biosynthesis of collagen, the major organic matrix component of dentine. The ODS rat is a mutant strain of Wistar rat characterized by hereditary lack of L-gulono-gamma-lactone oxidase and thus is unable to synthesize ascorbic acid. ODS rats were given an ascorbic acid-free diet to investigate how ascorbic acid deficiency affects dentine formation in vivo. Histomorphometric analysis on their growing molars and incisors showed a significant reduction in both size and mineral apposition rate of dentine, as revealed by contact microradiography and fluorescent time-marking, respectively. A similar reduction in bone formation was simultaneously demonstrated in the mandible, confirming the previously reported osteopathic effects of ascorbic acid deficiency. When pulp inflammation was induced in lower first molars by making unsealed pulp exposures, specimens from control animals showed continuous deposition of an osteodentine-like tissue in the radicular pulp chamber; this type of mineralized tissue formation was greatly reduced in ascorbic acid-deprived animals. These results indicate that ascorbic acid deficiency hampers dentine formation under both physiological and pathological conditions of the dentine/pulp complex. ODS rats could be useful in investigating in vivo effects of ascorbic acid deficiency on the formation of dentine and other dental mineralized tissues.

Animals↗