1986
DOI: 10.1016/s0099-2399(86)80052-8
|View full text |Cite
|
Sign up to set email alerts
|

Arachidonic acid metabolism in canine tooth pulps and the effects of nonsteroidal anti-inflammatory drugs

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

0
6
0
1

Year Published

1987
1987
2012
2012

Publication Types

Select...
7
2
1

Relationship

0
10

Authors

Journals

citations
Cited by 36 publications
(7 citation statements)
references
References 10 publications
0
6
0
1
Order By: Relevance
“…Other than thrombin, arachidonic acid metabolites also have crucial roles in regulating functions of normal and inflamed dental pulp tissues, including blood flow, vascular permeability, hemostasis, inflammatory response, pain sensation and bone resorption (19,20,31). Elevation of tissue PGEz levels by mechanical and thermal irritation of the pulp and in symptom-atic pulp tissues have been reported (21,32).…”
Section: Discussionmentioning
confidence: 99%
“…Other than thrombin, arachidonic acid metabolites also have crucial roles in regulating functions of normal and inflamed dental pulp tissues, including blood flow, vascular permeability, hemostasis, inflammatory response, pain sensation and bone resorption (19,20,31). Elevation of tissue PGEz levels by mechanical and thermal irritation of the pulp and in symptom-atic pulp tissues have been reported (21,32).…”
Section: Discussionmentioning
confidence: 99%
“…High levels of prostaglandins have been reported to be present in Inflamed dental pulps and periradicular tissues of humans and experimental animals (Cohen et al 1985, Lessard et al 1986, McNicholas et al 1991, Leukotrienes are produced through the 5-Iipoxygenase pathway of arachidonic acid; five metabolites known as leukotriene A4 (LTA4), LTB4, LTC4, LTD4 and LTE4 have been identified through the activation of the 5-Mpo3cygenase pathway of arachidonic acid (Samuelsson 1983), (Fig, 1), In a recent study it was found that the levels of LTB4, a potent chemotactic agent for PMNS and pain mediator, were significantly higher in human periradicular lesions associated with symptoms of pain and swelling than in asymptomatic lesions (Torabinejad et al 1992), Leukotriene C4 together with its metabolites LTD4 and LTE4, formerly known as 'slow reacting substance of anaphylaxis', can be released from mast cells during a type I hypersensitivity reaction (Dahlen et al 1980). As an inflammatory mediator, LTC4 has a vasodilatory action at low concentrations and causes vasoconstriction at very high doses, it also increases vascular permeability and plasma leakage by acting on the endothelial lining of the postcapillary venule (Peck et al 1981, Bisgaard et al 1982, Samuelsson 1983, Soter et al 1983.…”
Section: Introductionmentioning
confidence: 99%
“…Regarding the dental pulp, PGE 2 is considered an important modulator of inflammation, because PGE 2 synthesis increases in experimentally inflamed pulps of rats (11)(12)(13) and dogs (14), and PGE 2 levels in pulp blood samples are higher in inflamed pulps than in clinically intact teeth (15). NSAIDs reduce the increase of PGE 2 synthesis and vascular permeability in lipopolysaccharide (LPS)-stimulated rat incisor pulps (12), which might implicate PGE 2 in the increase of vascular permeability.…”
mentioning
confidence: 99%