6-ketoprostaglandin-f1-alpha and Pulpitis

To study the change of the levels of 6-keto-prostaglandin F1 alpha (6-K-PGF1 alpha) and thromboxane B2 (TXB2) in deep caries and pulpitis pulp.. The levels of 6-K-PGF1 alpha and TXB2 were determined by radioimmunoassay (RIA) in 44 pulp tissues from subjects with healthy pulp (H), deep caries (DC), chronic pulpitis (CP) and acute pulpitis(AP). The 6-K-PGF1 alpha/TXB2 ratio(K/T) was calculated.. The lconcentrations of 6-K-PGF1 alpha in Group AP were highest and those in Group H were lowest. The levels of TXB2 in Group DC were lower than Group CP and those in Group H were lowest. Significant differences in K/T ratio were found among the groups except those between Group H and DC. The value of Group AP was highest and that of Group CP was lowest.. The dysbolism and dysequilibrium of PGI2 and TXA2 may be closely related to the genesis of pulp diseases.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Dental Caries; Dental Pulp; Humans; Pulpitis; Radioimmunoassay; Thromboxane B2

Using formalin-fixed and EDTA-decalcified cryostat sections, the immunohistochemical localization of prostaglandin (PG) E2, PGF2 alpha, and 6-keto-PGF1 alpha (a stable metabolite of PGI2) was examined in normal rat and inflamed dental pulp. Inflammation was induced by opening the pulp chamber. There was no immunoreactivity for prostaglandins in normal dental pulp, whereas positivities for PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were demonstrated in the cytoplasm of macrophages and endothelial cells in the inflamed dental pulp. In addition to these cells, numerous pulp cells and odontoblasts existing in the inflamed pulp and its apical noninflamed area also were intensely stained for PGF2 alpha. Such an area with positive cells gradually extended in an apical direction with the progression of inflammation. These findings suggested that PG production from these host cells is involved in development of inflammation of rat dental pulp.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Dental Pulp; Dinoprost; Dinoprostone; Immunohistochemistry; Macrophages; Male; Prostaglandins; Pulpitis; Rats; Rats, Wistar

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.

Topics: 12-Hydroxy-5,8,10,14-eicosatetraenoic Acid; 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acid; Arachidonic Acids; Capillary Permeability; Chromatography, High Pressure Liquid; Dental Pulp; Dinoprostone; Dose-Response Relationship, Drug; Hydroxyeicosatetraenoic Acids; Indomethacin; Lipopolysaccharides; Male; Pulpitis; Rats; Rats, Inbred Strains; Thromboxane B2

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.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Arachidonic Acid; Arachidonic Acids; Dental Pulp; Dinoprostone; Hydroxyeicosatetraenoic Acids; In Vitro Techniques; Male; Prostaglandin D2; Prostaglandins D; Prostaglandins E; Pulpitis; Rats; Rats, Inbred Strains; Thromboxane B2