Levels of prostaglandin E<sub>2</sub>, thromboxane, and prostacyclin in periodontal tissues

Dewhirst, Floyd E.; Moss, D.; Offenbacher, Steven; Goodson, J. Max

doi:10.1111/j.1600-0765.1983.tb00348.x

Cited by 80 publications

(35 citation statements)

References 32 publications

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“…This suggests that there is an activation process which enhances tis-sue CO activity. Furthermore, inflamed periodontal tissues which are undergoing attachment loss and bone resorption contain elevated levels of CO products, particularly PGE 2 and to a lesser extent, thromboxane A2 (TxA2) [7][8][9]. Finally, there are considerable data which demonstrate that drugs which block ARA metabolism serve to both diminish the levels of CO products present within the periodontal tissues and inhibit periodontal inflammation, attachment loss and bone resorption [10][11][12][13][14][15][16][17][18][19][20].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

et al. 1990

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Considerable evidence has demonstrated the importance of PGE2 synthesis in the pathogenesis of periodontal disease. Although various cyclooxygenase inhibitors have been known to block periodontal PGE2 synthesis and prevent disease progression in animal models, there are few reports comparing relative efficacies of various inhibitors of arachidonic acid (ARA) metabolism. We have developed a sensitive in vitro assay to measure PGE2 synthesis in periodontal tissues. The apparent IC50 values (i.e. the concentration of drug which causes 50% inhibition of maximum PGE2 synthesis) have been determined for a series of arachidonic acid analogues as well as competitive and non-competitive cyclooxygenase inhibitors. Periodontal tissue homogenates were incubated in the presence of 3H-arachidonic acid for 45 min at 37 degrees C. Inhibitors were tested at 10(-10)-10(-4) M and at zero concentration to measure conversion of 3H-arachidonate to 3H-PGE2. Log or half log dilutions of inhibitors were tested in triplicate for each assay. Radiolabeled PGE2 was extracted from homogenates, purified by reverse phase chromatography and quantitated by double antibody capture. RIA was performed on each homogenate to determine the amount of endogenous unlabeled PGE2 present in the sample to correct for antibody capture recovery. The apparent IC50 values were determined for each drug by averaging two or more replicate assays. Specific total enzymatic activity of periodontal tissue homogenates was typically 5-11 pg PGE2/min/mg tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Introductionmentioning

confidence: 99%

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

et al. 1990

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“…Levels of PGE 2 are elevated in the gingival tissue and gingival fluid of patients with periodontitis, compared with periodontally healthy subjects. [2][3][4][5] It has also been reported that the inhibition of PGE 2 using selective or nonselective nonsteroidal anti-inflammatory drugs decreases periodontal disease progression and reduces alveolar bone resorption, which highlights the significance of PGE 2 in the pathogenesis of periodontal disease. 6 -8 In addition to these findings, bone resorption in lipopolysaccharide-treated mice has been shown to be dependent on PGE 2 synthesis, a finding that might be explained by the observation that PGE 2 stimulates the formation of osteoclasts.…”

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confidence: 99%

Expression of Prostaglandin E Synthases in Periodontitis

Båge

Kats

Lopez

et al. 2011

The American Journal of Pathology

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The inflammatory mediator prostaglandin E 2 (PGE 2 ) is implicated in the pathogenesis of chronic inflammatory diseases including periodontitis; it is synthesized by cyclooxygenases (COX) and the prostaglandin E synthases mPGES-1, mPGES-2, and cPGES. The distribution of PGES in gingival tissue of patients with periodontitis and the contribution of these enzymes to inflammationinduced PGE 2 synthesis in different cell types was investigated. In gingival biopsies, positive staining for PGES was observed in fibroblasts and endothelial, smooth muscle, epithelial, and immune cells. To further explore the contribution of PGES to inflammation-induced PGE 2 production, in vitro cell culture experiments were performed using fibroblasts and endothelial, smooth muscle, and mast cells. All cell types expressed PGES and COX-2, resulting in basal levels of PGE 2 synthesis. In response to tumor necrosis factor (TNF-␣), IL-1␤, and cocultured lymphocytes, however, mPGES-1 and COX-2 protein expression increased in fibroblasts and smooth muscle cells, accompanied by increased PGE 2 , whereas mPGES-2 and cPGES were unaffected. In endothelial cells, TNF-␣ increased PGE 2 production only via COX-2 expression, whereas in mast cells the cytokines did not affect PGE 2 enzyme expression or PGE 2 production. Furthermore, PGE 2 production was diminished in gingival fibroblasts derived from mPGES-1 knockout mice, compared with wild-type fibroblasts. These results suggest that fibroblasts and smooth muscle cells are important sources of mPGES-1, which may contribute to increased PGE 2 production in the inflammatory condition periodontitis.

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“…Therefore, the presence of elevated GCF-PGE 2 levels in periodontal tissues undergoing active inflammatory destruction may represent a potential diagnostic concept for the determination of disease activity. In addition to PGE 2 , the levels of TxB 2 and 6-keto-prostaglandin F 1α were measured in human biopsies adjacent to shallow and deep periodontal pockets [50]. Control gingival samples were gained from retromolar distal wedge samples that did not yield clinical evidence of periodontal inflammation.…”

Section: B Arachidonic Acid Metabolite Levels In Periodontal Tissuesmentioning

confidence: 99%

The Effects of Non-Steroidal Anti-Inflammatory Drugs (Selective and Non-Selective) on the Treatment of Periodontal Diseases

Salvi

Lang

2005

CPD

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The objective was to review the literature on the effects of selective and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) on the treatment of periodontal diseases. A search of MEDLINE was conducted and articles published in English until December 2003 were included. The results from in vitro and animal experiments as well as from human clinical trials are presented. Non-selective cyclooxygenase-1 (COX-1) inhibitors used in periodontal research include compounds such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam. Selective cyclooxygenase-2 (COX-2) inhibitors represent a new group of pharmaceutical products termed "coxibs" that include meloxicam, nimesulide, etodolac and celecoxib. Evidence from animal experiments and clinical trials documents that selective and non-selective NSAIDs are mainly responsible for the stabilization of periodontal conditions by reducing the rate of alveolar bone resorption. This is achieved through local inhibition of both enzymes (e.g. COX-1 and COX-2) responsible for the synthesis of arachidonic acid metabolites. Evidence shows that the effects of NSAIDs drop off rapidly after drug withdrawal. One of the major advantages of selective COX-2 inhibition is the reduction of adverse systemic effects. Although some studies present promising results, no data from long-term, multicenter prospective clinical trials are yet available for determining whether these therapeutic effects can be retained on a long-term basis. Many of these compounds, such as flurbiprofen, are readily absorbed through the gingival tissues. Therefore, the development of topical NSAIDs formulations (e.g. gels, toothpastes, rinses) with a daily application seems to be of particular interest. This may help to further reduce adverse systemic effects of non-selective NSAIDs in the long-term host modulation of periodontitis-susceptible patients.

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Levels of prostaglandin E₂, thromboxane, and prostacyclin in periodontal tissues

Cited by 80 publications

References 32 publications

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

Expression of Prostaglandin E Synthases in Periodontitis

The Effects of Non-Steroidal Anti-Inflammatory Drugs (Selective and Non-Selective) on the Treatment of Periodontal Diseases

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Levels of prostaglandin E2, thromboxane, and prostacyclin in periodontal tissues

Cited by 80 publications

References 32 publications

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

Inhibition of human periodontal prostaglandin E2 synthesis with selected agents

Expression of Prostaglandin E Synthases in Periodontitis

The Effects of Non-Steroidal Anti-Inflammatory Drugs (Selective and Non-Selective) on the Treatment of Periodontal Diseases

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Levels of prostaglandin E₂, thromboxane, and prostacyclin in periodontal tissues