Inflammatory Mediators in periodontal disease
Inflammatory mediators, which are generated by immune and inflammatory cells in reaction to the accumulation of biofilm on the teeth, have a role in both the beginning and progression of periodontal disease. It has become obvious that the bulk of tissue destruction in the periodontium is caused by host-derived enzymes and mediators including cytokines and other inflammatory mediators like PGE2. Paradoxically, tissue breakdown is also a function of the host systems that protect against certain diseases. Therefore, the spatial course of the inflammation that spreads to the cartilage and periodontal ligaments is an essential variable which could determine whether the damaging impact is predominant over infection administration, and the contribution of pro-inflammatory mediators in the inflammatory process is crucial (23).
Cytokines are crucial in a myriad of physiological tasks, but when cytokines circulation improperly, they may induce disease. The ratio of pro- and anti-inflammation in periodontal conditions is tilted towards proinflammatory activity. “Interleukin-1 (IL-1) and IL-6”, as well as the tumor necrosis factor (TNFα), appears to have critical functions in periodontal tissue degeneration (24,25).
The host is composed of tissue cells (neutrophils and monocytes) expressing IL-1 and -1, IL-6, TNFα, and prostanoids; ultimately opening the route for further destruction of periodontal tissues. Hence, the host reaction has a dual role that motivates tissue enzymes known as proteolytic enzymes to produce them overly, ultimately driving the host to self-destruct (26).