Ratio of pro-resolving and pro-inflammatory lipid mediator precursors as potential markers for aggressive periodontitis.
Aggressive periodontitis (AgP) is a rapidly progressing type of periodontal disease in otherwise healthy individuals which causes destruction of the supporting tissues of the teeth. The disease is initiated by pathogenic bacteria in the dental biofilm, and the severity of inflammation and attachment loss varies with the host response. Recently, there has been an increased interest in determining the role of lipid mediators in inflammatory events and the concept of pro-inflammatory and pro-resolution lipid mediators has been brought into focus also in periodontal disease. The present study aimed to determine the profile of omega-3 or n3- as well as omega-6 or n6- polyunsaturated fatty acids (PUFAs) and PUFA-metabolites of linoleic acid, arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in gingival crevicular fluid (GCF), saliva and serum in AgP patients and healthy controls. In total, 60 selected n3- and n6-PUFAs and various PUFA metabolites were measured using high performance liquid chromatography-tandem electrospray ionisation mass spectrometry (HPLC-ESI-MS-MS). Of these, 51 could be quantified in this study. The concentrations of the majority were low in saliva samples compared with serum and GCF, but were mainly higher in AgP patients compared with healthy controls in all three kinds of sample. Ratios of n3- to n6-PUFAs (DHA + EPA)/AA were significantly lower in the GCF of AgP patients than in the healthy controls. Furthermore, various ratios of the direct precursors of the pro-resolution lipid mediators (precursors of resolvins and protectins) were calculated against the precursors of mainly pro-inflammatory lipid mediators. These ratios were mainly lower in GCF and saliva of AgP patients, compared with healthy controls, but only reached significance in GCF (P<0.05). To conclude, the ratios of precursors of pro-resolution/pro-inflammatory lipid mediators seem to be more relevant for describing the disease status of AgP than the concentration of specific lipid mediators.
Department of Clinical Dentistry - Periodontics, University of Bergen, Bergen, Norway.
Hager R Zein
HR
Elabdeen
Manal
M
Mustafa
Monika
M
Szklenar
Ralph
R
Rühl
Raouf
R
Ali
Anne Isine
AI
Bolstad
D000293:Adolescent; D000328:Adult; D010520:Aggressive Periodontitis / Q000097:blood / Q000378:metabolism*; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D005260:Female; D005883:Gingival Crevicular Fluid / Q000378:metabolism*; D006801:Humans; D018836:Inflammation Mediators; D050356:Lipid Metabolism; D008084:Lipoxygenase / Q000378:metabolism; D008297:Male; D053858:Metabolic Networks and Pathways; D055442:Metabolome; D055432:Metabolomics; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D012463:Saliva / Q000378:metabolism; D055815:Young Adult
D015415:Biomarkers; D018836:Inflammation Mediators; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases