The oral microbiome modulates oral and systemic immune development that creates a sustainable balanced relationship with the host tissues to maintain homeostasis (Cornejo Ulloa, van der Veen, & Krom, 2019). A disturbance that creates an imbalance in this relationship will trigger an inflammatory response that activates host cellular and molecular responses to control the microbial challenge and protect host tissues against exogenous and endogenous danger to reestablish homeostasis (Abbas, Lichtman, & Pillai, 2022; Mechnikov, 1988). Innate immunity, which is comprised of physical and chemical barriers, neutrophils, tissue-resident sentinel cells such as macrophages and dendritic cells (DCs), and blood proteins including the complement system and other soluble mediators of inflammation, controls this response that leads to increased blood flow, vascular dilation, increased vascular permeability, and cell recruitment (Abbas et al., 2022; Kaur & Secord, 2021). An effective immune response is triggered by the innate immune cells' Pattern Recognition receptors (PRR) that sense the presence of pathogens or foreign bodies within the tissues to induce the production of cytokines, chemokines, and inflammatory lipid mediators (LMs) (Mogensen, 2009).

Inflammation is a protective response in the oral cavity; however, the presence of a prolonged and exaggerated response is damaging to the host tissues and results in the stimulation of dysbiosis of the resident local microbiome. Many commonly occurring chronic diseases, such as chronic inflammatory diseases of the intestine, type 2 diabetes, cardiovascular diseases, Alzheimer's disease, and periodontal diseases, are the consequence of inflammation's failure to resolve (Agrawal & Kant, 2014; Gewirtz et al., 2002; Hasturk et al., 2006; Herrera et al., 2015; Kantarci et al., 2018). The resolution of inflammation depends on active biochemical mechanisms regulated by mediators that switch gene expression, protein function, and tissue resident cells that stimulate the host tissues to return to homeostasis. Among the mediators that regulate this process are essential polyunsaturated fatty acid (PUFA)-derived lipid mediators (LMs) also known as Specialized Pro-resolving Mediators (SPMs) that activate the resolution process (Serhan, 2014). SPMs are capable of regulating the acute inflammatory response and dictate the temporal progression of inflammation from initiation by proinflammatory eicosanoids (prostaglandins and leukotrienes), through a lipid mediator class switching phase, to active termination by pro-resolving LMs, the SPMs (Campbell et al., 2007; Levy, Clish, Schmidt, Gronert, & Serhan, 2001; Rock & Kono, 2008; Serhan, 2011, Serhan, 2017). In this review, we will discuss the fundamental concepts of resolution, and the physiology of SPMs in the oral cavity, and review studies in periodontology and endodontolgy to gain a profound understanding of the resolution of inflammation in oral tissues.