thromboxane-b2 and Gingivitis

A clinical trial was undertaken to examine the effects of a potent cyclooxygenase inhibitor, flurbiprofen, on both developing and established gingivitis in humans. 21 subjects with healthy gingiva abstained from all oral hygiene procedures for 21 days. 7 subjects were prescribed flurbiprofen, 50 mg b.d. beginning from baseline and a control group (Cl, n = 14) were given placebo. Gingival redness and bleeding on probing were assessed at baseline, 7, 14 and 21 days. Crevicular fluid (GCF) samples were also taken to determine concentrations of PGE2, TxB2 and LTB4 at baseline and at 21 days. Results show that flurbiprofen significantly inhibited the development of redness and bleeding (p < 0.001) effects which were associated with a significant inhibition of TxB2 (p < 0.05). There were no apparent flurbiprofen effects on GCF-PGE2 or GCF-LTB4 during this 21-day gingivitis, model To assess the effects of flurbiprofen on established experimental gingivitis, the model was extended to 28 days. On day 21, the Cl group was subdivided into 2 groups of 7 subjects. One group was prescribed flurbiprofen (50 mg b.d.) for 7 days and controls (C2) continued to take placebo. All subjects continued to abstain from tooth cleaning. Pretreatment (day 21) and post-treatment (day 28) comparisons showed that flurbiprofen again significantly inhibited bleeding (p < 0.001), but did not affect redness. Control subjects demonstrated a significant elevation in gingival bleeding on day 28, and this was associated with significant rises in GCF-PGE2 (p < 0.001), GCF-TxB2 (p < 0.01) and GCF-LTB4 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Dinoprostone; Female; Flurbiprofen; Gingival Crevicular Fluid; Gingivitis; Humans; Leukotriene B4; Thromboxane B2

We conducted a study to localize and quantify the thromboxane B2 (TXB2) in human gingival tissue obtained from clinically healthy sites and patients with gingivitis and periodontitis. Human gingival samples were assayed for TXB2 by immunofluorescence on slides and enzyme-immunoassay (EIA). We found that concentrations of TXB2 in gingivitis sites are at mean 10-fold higher than in the healthy sites and histologically show a consistently intracytoplasmic staining with a significant increase in gingivitis. This argues in favour of a local production of TXB2. Concentrations of TXB2 at periodontitis sites are only 3-fold higher than in healthy sites and histologically show a stronger staining as for the gingivitis sections, with principally an extracellular localization. Thus, TXB2 could be released in large quantities in the crevicular fluid when the periodontitis stage has reached. These data suggest that the epithelial cells of the gingival tissue are involved in synthesis and secretion of TXB2, which occurred during the development of gingival inflammation.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Coloring Agents; Cytoplasm; Epithelial Cells; Extracellular Matrix; Female; Fluorescent Antibody Technique, Direct; Gingiva; Gingival Crevicular Fluid; Gingivitis; Humans; Immunoenzyme Techniques; Male; Middle Aged; Periodontitis; Thromboxane B2

Ketoprofen creams were evaluated for the treatment of periodontal disease in a placebo-controlled, double-blind study in the rhesus monkeys, Macaca mulatta. Two formulations containing ketoprofen (1%), with or without vitamin E, were evaluated against appropriate controls (8 monkeys per group). Two weeks prior to treatment, the animals received prophylaxis on only the left side of the mouth (spontaneous model). Selected teeth on the right side of the mouth were ligated (ligature model). The creams were administered to the gingiva once daily at a standard dose of 1.8 ml per monkey for 6 months. Clinical assessments were made 2 wk before initiation, at baseline and 1, 2, 3 and 6 months post-treatment. The clinical parameters included plaque formation, gingival redness, edema, bleeding on probing and Ramfjord Attachment Level measurements (RAL). Radiographs were taken at 2 wk before initiation, baseline and at 3 and 6 months post-treatment. Digital, subtraction radiography was used to measure vertical linear bone loss along the interproximal root surfaces of the left and right mandibular first molars. Gingival crevicular fluid (GCF) was collected for biochemical assays on PGE2, TxB2, LTB4, IL-1 beta and TNF alpha. There were no significant differences among groups with respect to gingival indices. Radiographic data demonstrated significant positive effects on bone activity in both groups treated with ketoprofen formulations with improvement over time in the ligature model (0.01 < or = p < or = 0.04). The placebo group exhibited bone loss of 1.96 +/- 0.48 and 1.40 +/- 0.56 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream showed an apparent bone gain of 0.28 +/- 0.41 and 0.78 +/- 0.47 mm per site at 3 and 6 months, respectively. The group treated with ketoprofen cream containing vitamin E showed a mean bone loss of 0.41-0.48 mm per site at 3 months with improvement to an apparent bone gain of 0.31 +/- 0.44 mm per site at 6 months. The biochemical data demonstrated early and significant suppression of GCF-LTB4 by both ketoprofen formulations at 1 month, which preceded the significant suppression of GCF-PGE2 at 2 and 3 months in the ligature model (p < 0.003) and at 2 to 6 months in the spontaneous model (p < 0.02). We conclude that ketoprofen at 1% level in suitable topical vehicles can effectively inhibit GCF-LTB4 and GCF-PGE2 and positively alter alveolar bone activity in the ligature-induced model of periodontitis in the m

Topics: Administration, Topical; Alveolar Bone Loss; Animals; Anti-Inflammatory Agents, Non-Steroidal; Dental Plaque; Dinoprostone; Double-Blind Method; Edema; Emollients; Female; Follow-Up Studies; Gingival Crevicular Fluid; Gingival Hemorrhage; Gingivitis; Interleukin-1; Ketoprofen; Leukotriene B4; Macaca mulatta; Male; Molar; Periodontal Attachment Loss; Periodontitis; Placebos; Radiographic Image Enhancement; Random Allocation; Subtraction Technique; Thromboxane B2; Tumor Necrosis Factor-alpha; Vitamin E

We conducted a study to determine the sequence of cytokine and lipid mediator activation within the periodontium during the development of experimental gingivitis in humans. Crevicular fluid samples were collected from 7 previously cleaned, healthy patients at baseline, 1, 2, 3 and 4 weeks following the cessation of all oral hygiene measures. Gingival and plaque scores were taken at each visit to follow the development of gingivitis and plaque retention. Crevicular fluid samples were assayed in quadruplicate for prostaglandin E2 (PGE2), thromboxane B2 (TxB2), leukotriene B4, interleukin-1 beta (IL-1 beta) and tumour necrosis factor alpha (TNF alpha) by RIAs or ELISAs, maintaining site pairing to examine temporal changes. Redness scores (expressed as mean percentage of sites with redness present) increased almost linearly from a baseline value of zero to approximately 40% at 1 week, 59% at 2 weeks, 83% at 3 weeks and 100% at 4 weeks. The mean % of sites with bleeding on probing increased gradually from zero at baseline to 5% at 3 weeks and then rose abruptly to 25% at 4 weeks. CF-PGE2 and CF-TxB2 levels remained fairly stable at baseline levels for the first 3 weeks then rose sharply by 2.5- and 2-fold, respectively, at 4 weeks. CF-LTB4 levels increased 2-fold by 1 week and 4-fold by 4 weeks. The CF levels of IL-1 beta increased abruptly from mean baseline values of 16.5 +/- 9.3 ng/ml to 131 +/- 76.0 ng/ml at 1 week and remained at this level for the duration of the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Analysis of Variance; Autacoids; Dinoprostone; Gingival Crevicular Fluid; Gingivitis; Humans; Interleukin-1; Leukotriene B4; Thromboxane B2; Tumor Necrosis Factor-alpha

This study was undertaken to determine the ability of inflamed and normal gingival tissues to synthesize prostaglandins (PGs) from the precursor arachidonic acid. Thirteen samples of inflamed human gingival tissue and six samples of normal human gingival tissue were studied. The inflammation was characterized histologically. After incubation of the tissue with [14C]arachidonate, PG metabolites were separated by thin-layer chromatography and identified by comparison with co-chromatographed standards. Inflamed gingival tissue synthesized significantly larger amounts, compared to normal tissue, of 6-keto-PGF1 alpha (P less than 0.05), thromboxane B2 (P less than 0.01), PGD2 (P less than 0.05), and PGA2 (P less than 0.001). Some unidentified metabolites, possibly lipoxygenase products were detected in significantly (P less than 0.001) larger amounts in inflamed than in normal tissue.

Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acid; Arachidonic Acids; Carbon Radioisotopes; Dinoprost; Dinoprostone; Gingiva; Gingivitis; Humans; Periodontitis; Prostaglandin D2; Prostaglandins; Prostaglandins A; Prostaglandins D; Prostaglandins E; Prostaglandins F; Thromboxane B2

Topics: Animals; Dogs; Gingiva; Gingival Crevicular Fluid; Gingivitis; Periodontitis; Thromboxane B2; Thromboxanes