Abstract
Inflammatory response is a protective biological process intended to eliminate the harmful effect of the insulting influx. Resolution of inflammation constitutes an active sequence of overlapping events mediated by specialized proresolving mediators, such as lipoxins, resolvins, protectins, and maresins, which originate from the enzymatic conversion of polyunsaturated fatty acids (PUFAs). An unresolved acute inflammatory response results in chronic inflammation, which is a leading cause of several common pathological conditions. Periodontitis is a biofilm-induced chronic inflammatory disease, which results in loss of periodontal connective tissue and alveolar bone support around the teeth, leading to tooth exfoliation. An inadequate proresolving host response may constitute a mechanism explaining the pathogenesis of periodontal disease. An emerging body of clinical and experimental evidence has focused on the underlying molecular mechanisms of resolvins and particularly Resolvin E1 (RvE1) in periodontitis. Recently, RvE1 has been directly correlated with the resolution of inflammation in periodontal disease. Herein, we provide a comprehensive overview of the literature regarding the role and possible mechanisms of action of RvE1 on different cell populations recruited in periodontal inflammation as well as its potential therapeutic implications. Along with recent data on the benefits of PUFAs supplementation in periodontal clinical parameters, we touch upon suggested future directions for research.
Highlights
Inflammation constitutes an essential biological process of the immune host response, which is activated when the natural tissue homeostasis is disturbed after infection or injury
When incubated with increasing concentrations of Resolvin E1 (RvE1) and subsequently challenged with N-formyl-methionyl-leucyl-phenylalanine, polymorphonuclear neutrophil (PMN) from localized aggressive periodontitis (LAgP) patients and controls responded with an 80% reduction in superoxide generation [16], providing an indication that this lipid mediator counteracts the collateral tissue damage induced by PMNs in periodontal inflammation (Figure 2)
Resolution of inflammation is a well-orchestrated active process mediated by a variety of specialized lipid mediators
Summary
Inflammation constitutes an essential biological process of the immune host response, which is activated when the natural tissue homeostasis is disturbed after infection or injury. In 1994, Marsh proposed the “Ecological Plaque Hypothesis,” suggesting that an imbalance in the total microflora, due to ecological stress, allows for the overgrowth of disease-related microbes [13] This hypothesis underlined the interaction between the local environment and the composition of dental plaque. Recent evidence provided by animal studies has confirmed that regulating inflammation through resolution pathways can result in a beneficial shift in the microflora and reduce the relative abundance of disease-related genera [17]. The pathogenesis of the disease is characterized by an altered or aberrant host response to the present microflora, leading to immune cell-mediated selfdestruction of periodontal tissues [15, 16]. A rapidly emerging body of evidence has focused on the role of SPMs in periodontitis and has provided a window to explore the pathophysiology of this chronic inflammatory disease. The enzymatic conversion of EPA leads to the generation of E-series resolvins, whereas DHA constitutes the parent substrate for the formation of D-series resolvins, protectins, and maresins [25]
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