Abstract

Periodontal diseases are localized chronic inflammatory conditions of the gingival and underlying bone and connective tissue. Platelet-activating factor (PAF), a potent inflammatory phospholipid mediator that has been previously detected in elevated levels in inflamed gingival tissues, in gingival crevicular fluid and in saliva, is implicated in periodontal disease. Our results from previous studies showed that the biologically active phospholipid detected in gingival crevicular fluid is a hydroxyl-PAF analogue. In this study, hydroxyl-PAF analogue was detected for the first time in human blood derived from patients with chronic periodontitis as well as from periodontally healthy volunteers. The hydroxyl-PAF analogue was purified by high-performance liquid chromatography, detected by biological assays and identified by electrospray analysis. In addition, the quantitative determination of PAF and hydroxyl-PAF analogue (expressed as PAF-like activity) showed a statistically significant increase in the ratio of hydroxyl-PAF analogue levels to PAF levels in periodontal patients, suggesting that this bioactive lipid may play a role in oral inflammation.

Highlights

  • Periodontal disease is a chronic disorder that occurs in susceptible individuals and is initiated when microorganisms of dental plaque (i.e. Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Treponema dentocola ) colonize the gingival sulcus, and thereafter the periodontal pocket

  • Platelet-activating factor (PAF), a potent inflammatory phospholipid mediator that has been previously detected in elevated levels in inflamed gingival tissues and gingival crevicular fluid (GCF), is implicated in periodontal disease.[4,5]

  • Á 20 These findings suggest that inflammatory mediators such as the hydroxylPAF analogue, which was identified in GCF, may be present in blood

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Summary

Introduction

Periodontal disease is a chronic disorder that occurs in susceptible individuals and is initiated when microorganisms of dental plaque (i.e. Porphyromonas gingivalis , Actinobacillus actinomycetemcomitans, Treponema dentocola ) colonize the gingival sulcus, and thereafter the periodontal pocket. Several reviews have summarized the role of activated inflammatory cells (e.g. polymorphonuclears, macrophages and lymphocytes) when challenged by bacterial lipopolysaccharide, as a key regulator of periodontal disease expression. These cells produce and secrete proinflammatory mediators such as interleukin-1b and tumour necrosis factor-g that induce and enhance the production of prostaglandin E2 and matrix metallo-proteinases. These molecules mediate destruction of the extracellular matrix of periodontal tissues and resorption of the alveolar bone.[2,3]. Platelet-activating factor (PAF), a potent inflammatory phospholipid mediator that has been previously detected in elevated levels in inflamed gingival tissues and gingival crevicular fluid (GCF), is implicated in periodontal disease.[4,5]

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