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).