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  • 1
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inflammation of the airways contributes to the multicomponent disease known as asthma. The primary cells that infiltrate the airways in response to antigen exposure are PMNs and eosinophils, cells that can release cellular components, and damage the airways. We adapted a double-ballon endotracheal tube to study the cellular response to threede novo synthesized lipid mediators (LTB4, PAF-acether and 15 HETE) found in respiratory fluids following antigen exposure. In random repeat challenges in groups of 7 dogs using mongrel dogs at 240 min following exposure to 10−6 M agonists, the PMN content of the perfused fluid was 870±240, 1632±883, 515±395, and 1575±214 cells/ml/5 high power fields for vehicle, LTB4, PAF, and 15 HETE respectively. Eosinophils that infiltrated the lumen at 240 min were 162±23, 608±287, 502±23, 115±14 cells/ml/5 HPF for vehicle, LTB4, PAF, and 15 HETE respectively. Thus LTB4 and PAF-acether significantly (p〈0.05) increased eosinophils, and LTB4 and 15 HETE increased PMNs (p〈0.05). After determining the agonist response for the 3 agonists we included 2 specific antagonists in the perfusate. The LTB4 antagonist U-75,302 10−5 M, and the PAF antagonist L 652,731 10−5 M in chambers containing LTB4 and PAF-acether respectively blocked significantly the influx of PMNs and eosinophils compared to vehicle (p〈0.01). Methylprednisolone 5 mg/kg i.m.-18 hrs blocked eosinophilia to PAF and LTB4. Oral U-78,517F a Trolox amine lazaroid, active as an inhibitor of lipid peroxidation, 30 mg/kg-18 hrs significantly blocked eosinophilia to PAF-acether and LTB4 directed chemotaxis compared to vehicle (p〈0.05) but not 15 HETE. Specificity was shown for each antagonist since the PAF and LTB4 antagonists did not block the opposite agonist. Use of this novelin vivo chemotaxis model allows the additional advantage of studying chemotaxis in living tissue.
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  • 2
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Leukotrienes (C4, D4) have been shown to enhance mucus seeretion in both isolated human airway tissue and intact canine tracheain vivo. They also have been implicated as putative mediators in several airways diseases. In previous canine studies the mucus enhancing effect of leukotriene-C4 was blocked by atropine, FLP 55,712, and hexamethonium but not by cutting the superior laryngeal and vagus nerves. We anesthetized mongrel dogs with chloralose (100 mg/kg) and urethane (500 mg/kg) and ventilated them on a pump. To visualize the secretions from submucosal glands, we exposed the mucosa of the upper trachea and coated its surface with powdered tantalum. Seeretions from the glands formed elevation in the tantalum layer (hillocks) with time: the number of tracheal hillocks (an index of mucus secretion) was measured at one or more of the four time points on six dogs after each treatment of the treatment sequence: no LTC4, LTC4, no LTC4+ blocker, and LTC4+ blocker. The potential blocker was diphenhydramine, an H1 antagonist for histamine. LTC4 was injected into the cranial thyroid artery which directly feeds the tracheal segment. We observed hillocks through a dissecting microscope, and the number of hillocks per 1.2 cm2 were counted for a 1–4 min interval. In 6 dogs with 12 responses, LTC4 (10 μg) gave a positive response that was significantly different from control (p〈0.01–0.05) at 2–4 min. Diphenhydramine (n=6), 0.5 mg/kg, a dose which blocked a histamine challenge without blocking an acetylcholine challenge of secretion, gave a statistically significant (p〈0.01–0.05) reduction in mucus secretion at 1–4 min. These results support the conclusion that leukotriene C4 induces mucus secretion in dogs that is blocked by prior diphenhydramine administration. This would indicate histamine has a role, but as yet an unknown mechanism in the action of leukotriene-C4 in enhancing mucus.
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  • 3
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of the non-steroidal anti-inflammatory drug, ibuprofen, on the progression of periodontal disease was studied in 22 beagle dogs over a 13-month period. Standardized radiographs were used to measure the rate of bone loss. Following a 6-month pretreatment baseline period. 6 dogs were treated daily with 4 mg/kg ibuprofen, 5 dogs were treated with 4 mg/kg ibuprofen in a sustained release preparation, 5 dogs were treated with 0.4 mg/kg ibuprofen and 6 untreated dogs served as controls. In the untreated control dogs the rate of bone loss in the treatment period did not change significantly from baseline, although the rate was increased. In both the 4.0 mg/kg and sustained release 4.0 mg/kg ibuprofen-treated dogs the rate of bone loss in the treatment period was significantly less than the pretreatment period rate. In the 0.4 mg/kg ibuprofen-treated dogs the rate of bone loss, although reduced, was not significantly less than the pretreatment rate. When the rate of bone loss in the control dogs was compared with the rate of bone loss in the ibuprofen-treated dogs, all three ibuprofen-treated groups of dogs had significantly less bone loss than the control dogs. The untreated control dogs lost 10 teeth during the treatment period, whereas the 4.0 mg/kg and 0.4 mg/kg ibuprofen-treated dogs lost 6 teeth and the sustained release 4.0 mg/kg ibuprofen-treated dogs lost 2 teeth during the treatment period. The data indicate that a propionic acid derivative, the non-steroidal anti-inflammatory drug, ibuprofen, can significantly inhibit alveolar bone loss in beagles. Sustained release ibuprofen. which gave consistently greater blood levels over 24 h, was overall more effective.
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  • 4
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of the non-steroidal anti-inflammatory drug flurbiprofen, topically applied, on the progression of periodontal disease was studied in 12 beagle dogs over a 13-month period. Standardized radiographs were used to measure the rate of bone loss. Following a 6-month pretreatment baseline period, 6 dogs were treated daily with 0.3 mg flurbiprofen gently applied to the gingival margin in 1 ml of gel vehicle. Six untreated dogs served as controls. In the untreated control dogs the rate of bone loss in the treatment period did not change significantly from baseline, although the rate was elevated by 38%. In contrast, the rate of bone loss significantly decreased by 71% from baseline in the flurbiprofen-treated dogs. The untreated control dogs lost 10 teeth during the treatment period whereas the topical flurbiprofen-treated dogs lost only 1 tooth. The data indicate that topical application of flurbiprofen in a gel vehicle significantly inhibits alveolar bone loss in beagles over a 7-month treatment period. The data also indicate that topical flurbiprofen is associated with the loss of considerably less teeth than in untreated control dogs over the 7-month treatment period.
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  • 5
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of the nonsteroidal anti-inflammatory drug flurbiprofen has been studied in the ligature-induced and spontaneous periodontitis model in the rhesus monkey, Macaca mulatta. Twenty-four adult monkeys with incipient periodontitis were divided into three disease-matched groups. Two groups received flurbiprofen at dosages of either 0.27 mg/kg/d or 7.1 mg/kg/d delivered systemically via osmotic minipump. A split-mouth approach was used, placing ligatures on one side and monitoring the progression of periodontitis at regular intervals for 6 months. Clinical measurements included standardized radiographs, Ramfjord attachment level determinations and assessments of redness, edema and bleeding on probing. There was a statistically significant inhibition of attachment loss (p 〈 0.05), gingival redness (p 〈 0.05) and bleeding on probing (p 〈 0.05) in ligatureinduced and spontaneous periodontitis in the flurbiprofen-treated animals at 6 months. Eight of 8 ligated control monkeys lost significant attachment (mean loss of 1.06 mm/site). Only 3 of 15 flurbiprofen-treated ligated monkeys lost any significant attachment, with an overall mean loss of 0.34 mm/site, which was significantly less than the control loss of 1.06 mm/site at p = 4.46 times 10-3. The odds of a control ligated monkey undergoing significant attachment loss in 6 months are elevated 29.3-fold, as compared to the flurbiprofen-treated, cohort monkey group. Flurbiprofen treatment also significantly inhibited spontaneous attachment loss for 6 months as compared to control monkeys, at p 〈 0.05. These data provide further evidence for the central role of cyclooxygenase products in the progression of periodontal disease. The ability of flurbiprofen to inhibit periodontal attachment loss, even in the presence of gross plaque accumulation, has significant implications for the potential use of flurbiprofen as an adjunctive periodontal therapeutic modality.
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  • 6
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of lodoxamide ethyl, a mast cell release inhibitor on the progression of chronic periodontal disease in beagles was examined. Twelve adult female beagles with naturally occurring periodontitis were studied. Following a six-month pretreatment baseline period, six dogs were given 20 mg/kg lodoxamide ethyl orally for a twelve-month treatment period. In addition, at the beginning of the treatment period one-half’ mouth in each dog was treated with periodontal flap surgery. Thus, the experimental design allowed a comparison of the progression of periodontitis about premolar teeth in a pretreatment period with progression of periodontitis in a treatment period in which one of the following treatment protocols was used: no treatment, teeth treated with periodontal flap surgery, teeth treated with lodoxamide ethyl administration, and teeth treated with lodoxamide ethyl administration plus periodontal flap surgery.In the systemically untreated dogs the rate of alveolar bone loss increased in the treatment period, compared to the baseline pretreatment period about both teeth not treated locally and teeth treated with flap surgery. In contrast, the rate of alveolar bone loss was significantly reduced in the treatment period in those dogs administered lodoxamide ethyl daily. Lodoxamide ethyl administration combined with flap surgery was more effective than lodoxamide ethyl alone. Tooth mobility significantly increased in those dogs administered lodoxamide.The data indicate that administration of an orally active mast cell release inhibitor can decrease the rate of alveolar bone loss which occurs in beagle periodontitis. However, the clinical usefulness of this pharmacologic agent is not clear due to the increased tooth mobility which occurred in this study. Since the principle effect of lodoxamide ethyl is believed to be on mast cell degranulation, a role for mast cells in beagle alveolar bone loss is implied.
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  • 7
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The non-steroidal anti-inflammatory drug(NSAID) naproxen was studied in 11 beagle dogs over a 13-month period to determine its effect on the progression of periodontitis. Following a 6-month pretreatment period, 5 dogs received naproxen daily at a dosage of 2.0 mg/kg for 1 month, then 0.2 mg/kg for 6 months. Six control dogs received a gelatin capsule daily as placebo. Standardized radiographs were used to measure the rate of bone loss during the pretreatment and treatment periods. In the control dogs, the rate of bone loss was seen to increase during the treatment period although the increase was not statistically significant. In dogs treated daily with naproxen, the rate of bone loss in the treatment period was significantly less at 4 months of treatment; however, at 7 months the difference, though lower than pretreatment rate, was not significant. When the percent change in rate of bone loss during the overall 7-month treatment period was compared with pretreatment rate, the control dogs demonstrated a 38% increase in rate of bone loss during the treatment period contrasting with a 61% decrease in bone loss rate in naproxen-treated dogs. The data indicate that the non-steroidal anti-inflammatory drug naproxen can significantly inhibit alveolar bone loss in beagles. At 4 months of treatment the rate of bone loss in the naproxen-treated dogs was significantly less than pretreatment, but at 7 months of treatment the rate was no longer statistically significantly less than baseline. This probably reflects a dose response to naproxen treatment for, after 30 days of the treatment period, the naproxen dosage was reduced 10-fold due to tolerance by the beagle.
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  • 8
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effect of two non-steroidal anti-inflammatory drugs, indomethacin and flurbiprofen, on the progression of alveolar bone loss and on the crevicular fluid (CF) levels of four arachidonic acid metabolites was compared in 16 beagle dogs over a 12-month period. Standardized radiographs were used to measure the rate of bone loss. Radioimmunoassay was used to measure CF levels of PGE2, PGF2α, TxB2 and 6K-PGF1α. Following a 6-month pretreatment baseline period, 5 dogs were dosed daily with 1.0 mg/kg indomethacin, 5 dogs were dosed daily with 0.02 mg/kg flurbiprofen, and 6 dogs were dosed with empty gelatin capsules for a 6-month period. With the administration of either indomethacin or flurbiprofen. the CF levels of PGE2, PGF2α, and TxB2 were similarly significantly decreased; 6K-PGF1α levels were not altered. Indomethacin and flurbiprofen did not have a similar effect on reducing the rate of alveolar bone loss. Flurbiprofen significantly decreased rate of bone loss from baseline whereas indomethacin did not. The data indicate that indomethacin and flurbiprofen inhibit CF arachidonic acid metabolite levels in a similar manner, but not rate of bone loss. The data suggest that flurbiprofen's striking effect on inhibiting rate of bone loss cannot be solely attributed to simple cyclooxygenase inhibition with a reduction in CF prostaglandin levels.
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  • 9
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
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  • 10
    ISSN: 1600-0765
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: This investigation focuses on the changes in the concentrations of cyclooxygenase (CO) products present within the crevicular fluid in naturally-progressing periodontitis in the beagle and the effects of various non-steroidal anti-inflammatory drugs (NSAIDs) on these metabolite levels and disease progression. Six groups of 5–6 beagles with periodontitis were followed for 6 months to determine the pretreatment rate of radiographic bone loss. At baseline, groups of animals were placed on soft chow to promote disease progression. Groups were treated with either placebo, three different formulations of systemic ibuprofen, systemic naproxen or topical flurbiprofen. During the 6-month treatment phase, crevicular fluid (CF) samples and radiographs were taken at regular intervals. Radioimmunoassay of CF samples from untreated animals demonstrated a steady increase in prostaglandin E2 (PGE 2) over baseline values. At 1 month, CF-PGE2 levels increased 2-fold over baseline and, by 6 months, had reached a 5- to 6-fold elevation. Crevicular fluid thromboxane B2 (CF-TxB2) levels rapidly reached a 4- to 5-fold peak over baseline at 1 month and subsequently dropped to a 2-fold elevation for the remainder of the study. The rate of bone loss (BLOSS) in untreated animals increased 38% during the 6-month period, as compared to baseline pretreatment BLOSS rates. Overall, there was a significant depression in the CF levels of both PGE2 and TxB2 in all NSAID-treated groups. All NSAID treatments significantly retarded BLOSS, ranging from 21.0–36.9% of the control BLOSS rate. The topical application of flurbiprofen was as effective in depressing CF levels of PGE2 and TxB2 as systemic or sustained release formulations of other NSAIDs. The data further substantiate the concept that much of the BLOSS that occurs in periodontal disease is mediated by products of the cyclooxygenase pathway. Furthermore, CO activation represents a major regulatory step in bone destruction and may thereby serve as an important site for pharmacological modulation.
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