Prostaglandin E₂ concentrations in gingival crevicular fluid: observations in untreated chronic periodontitis

Abstract

A trend for gradually increasing GCF-PGE2 concentrations in the absence of any clinical signs of disease progression was noted in a group of patients monitored longitudinally. We suggest that this phenomenon is to be expected in longitudinal clinical trials, and propose a new model for the role of PGE2 in the pathogenesis of periodontal destruction. We feel that if GCF mediators are to be monitored in clinical studies, then both concentrations and absolute mediator content should be calculated, and a standardised sampling protocol should be employed.

Involvement of the P2X₇ Purinergic Receptor and c-Jun N-Terminal and Extracellular Signal-Regulated Kinases in Cyclooxygenase-2 and Prostaglandin E₂ Induction by LL-37

“…Moreover, because of the clinical observations that the concentrations of LL-37 are raised to the low µg/ml levels in the GCF of patients with chronic periodontitis [9], which are in the same range of LL-37 concentrations used to treat HGFs in this study, and that the levels of PGE 2 are elevated in the GCF of patients with periodontitis [27], it is likely that elevated levels of LL-37 in the GCF of patients with chronic periodontitis may further enhance the production of PGE 2 from gingival fibroblasts, causing greater inflammation in periodontitis. This warrants further investigation.…”

T Cell Replicative Senescence in Human Aging

“…Moreover, exposure of human T cells to PGE2 in concert with activation increases their RANKL production; if a similar process occurs in vivo , this would function to enhance osteoclast activity and bone breakdown. In support of this hypothesis, in patients with periodontitis, high levels of PGE2 were related to the severity of periodontal disease and the increase in alveolar bone loss [167, 168]. In addition, there is a greater production of PGE2 by old periodontal ligament cells [169], and this might promote recruited inflammatory T cells to acquire a senescent phenotype, enhancing the rate of alveolar bone resorption in elderly patients.…”

Gingival Crevicular Fluid Prostaglandin E2 and Thiobarbituric Acid Reactive Substance Levels in Smokers and Non‐Smokers With Chronic Periodontitis Following Phase I Periodontal Therapy and Adjunctive Use of Flurbiprofen

“…As an arachidonic acid metabolite, prostaglandin E 2 (PGE 2 ) is one of the most important biochemical mediators of periodontal inflammation and plays a significant role in the pathogenesis of periodontal diseases. PGE 2 stimulates bone resorption and increased PGE 2 levels were found in gingival crevicular fluid (GCF) samples of periodontitis sites compared to healthy or gingivitis sites 3,4 . Reactive oxygen species (ROS) can also cause inflammatory damage of the host tissue by a variety of different mechanisms, such as DNA damage, protein damage, oxidation of important enzymes, stimulation of cytokine release, and lipid peroxidation 5 .…”