Abstract
Polyunsaturated fatty acid-derived specialized pro-resolving lipid mediators (SPMs) play an important role in modulating inflammation. The aim of the study was to compare profiles of SPMs, SPM related lipid mediators and SPM receptor gene expression in gingiva of subjects with periodontitis to healthy controls. A total of 28 subjects were included; 13 periodontally healthy and 15 periodontitis before or after non-surgical periodontal therapy. Gingival tissues were collected from two representative posterior teeth prior to and 8 weeks after scaling and root planning; only once in the healthy group. Lipid mediator-SPM metabololipidomics was performed to identify metabolites in gingiva. qRT-PCR was performed to assess relative gene expression (2−ΔΔCT) of known SPM receptors. Intergroup comparisons were made using Wilcoxon tests. Thirty-six omega-6 or omega-3 fatty acid-derived lipid mediators and seven receptor genes were identified in gingiva. Profiles of lipid mediators and receptor gene expression were significantly different between the three groups. Levels of six lipid mediators, 5-HETE, 15-HETE, 15(S)-HEPE, 4-HDHA, 7-HDHA, and 17-HDHA in periodontitis before treatment were significantly higher than in periodontitis after treatment. The expression of BLT1 in the healthy group was significantly higher than periodontitis subjects before and after treatment. The expression of GPR18 in periodontitis before treatment was significantly higher than in periodontitis after treatment while the expression of GPR32 in periodontitis before treatment was significantly lower than in periodontitis after treatment. Elevated levels of SPM biosynthetic pathway markers in periodontitis subjects before treatment indicated inflammation induced pro-resolution activity in gingiva, but receptors for these molecules were deficient in periodontitis pre-treatment suggesting that failure of resolution of inflammation contributes to excess, chronic inflammation in periodontitis.
Highlights
Periodontitis is a biofilm-induced chronic inflammatory disease that is characterized by gingival inflammation, loss of connective tissue attachment and alveolar bone, which if severe enough, can potentially lead to tooth loss
According to a power analysis of preliminary results of lipid mediators (LMs)-specialized pro-resolving lipid mediators (SPMs) metabololipidomics, at least 12 subjects per group were needed to detect a difference in the level of 14-hydroxydocosahexaenoic acid (14-HDHA), the maresin pathway marker, with 1.27 effect size and 80% power
Varying levels of SPM pathway markers including 5-hydroxyeicosatetraenoic acid (5-HETE), 5(S),12(S)-DiHETE, 12HETE, 12(S)-HHTrE, 12-hydroxyeicosatetraenoic acid (15-HETE), 11-HEPE, 12-hydroxyeicosapentaenoic acid (12-HEPE), 18hydroxyeicosapentaenoic acid (18-HEPE), 4-hydroxydocosahexaenoic acid (4-HDHA), 17-HpDHA, 14-HDHA, prostaglandin E2 (PGE2), prostaglandin F2a (PGF2a), and TXB2 were identified in all samples
Summary
Periodontitis is a biofilm-induced chronic inflammatory disease that is characterized by gingival inflammation, loss of connective tissue attachment and alveolar bone, which if severe enough, can potentially lead to tooth loss. The disproportionate host response and dysbiosis of the oral microbiome are the two major etiologic factors in the pathogenesis of periodontitis [3]. Subjects initially develop an acute inflammatory response in the gingiva characterized by the presence of mostly neutrophils and macrophages. Persistence of inflammation leads to the development of a chronic lesion characterized by the predominance of plasma cells. The continued inflammation induced by concomitant stimulation by bacteria and their byproducts triggers the host response to mediate irreversible destruction of the affected periodontal tissues [3, 4]
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