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).