Resolution of inflammation IN periodontal disease
While there are numerous factors that contribute to periodontal disease, the colonization of the cavity in the mouth by bacteria that are pathogenic and their following entry into the local epithelium layer is one of the triggers that have been most important (50).
This starts an inflammatory cascade characterized by an upsurge in the synthesis of multiple mediators of inflammation and adhesion molecules, all of that in turn activate and draw in macrophages as natural killer (NK), dendritic cells (DC), and polymorphonuclear neutrophils (PMN) to the damaged area. In typical circumstances, the microbial organisms are phagocytosed by neutrophils and macrophages, after which they go through apoptosis at the inflamed sites (23).
The elimination of cells that are apoptotic facilitates it being simpler for macrophage phenotypes to change from pro- to anti-inflammatory, that begins with the end of inflammation, a coordinated signaling mechanism that returns cell health and functioning. Yet, failure to stop the inflammatory cascade after the pathogenic stimulus has been eliminated results in persistent inflammation, which is characteristic of many illnesses connected to inflammatory disorders. While infectious microorganisms persist in spreading and are unable to be stopped by the acute immune system attack, the process of inflammatory response particularly in PD grows chronic, resulting in persistent inflammation and damage of the surrounding alveolar bone and soft tissue (51,52).
Studies on humans using low-dose aspirin and supplements of omega-3 fatty acids as an adjuvant to periodontal therapy have shown encouraging results and suggest a synergistic interaction between these medications. There haven’t been any lengthy randomized clinical trials comparing the advantages of omega-3 fatty acids as an adjuvant to periodontal therapy to those of other widely used pharmaceutical drugs, such as antibiotics. Large-scale experiments investigating the benefits of RvE1 therapy in patients with periodontitis may also provide greater insight into the intricate molecular processes underlying the remission of periodontal inflammation. It is necessary to do more research to determine whether RvE1 is an appropriate treatment option for periodontitis, either on its alone or in conjunction with other regimens (53).