Destruction of gingival and periodontal tissue is mediated by a very large degree of host cells following stimulation by locally produced cytokines. These cytokines act as the initial mediators of the cellular component of inflammation. It has now been shown that a range of bacterial molecules is able to induce human cells to produce a variety Of pro and anti-inflammatory cytokines. It is clear that cytokines play a key role in the immune system, in hematopoiesis, and in immunoregulation. They also play a role in the pathophysiology, both in producing tissue destruction as well as in healing. Host cells such as keratinocytess fibroblasts, endothelial cells and tissue monocytes respond to certain bacterial proteins and lipopolysaccharides by generating primary proinflammatory cytokines. Their excessive production in chronic inflammation may have pathologic consequences in diseases su ch as periodontitis.
Cytoki nes are a significant and integral part of the host response to periodontal infection. Additionally, these molecules are important as physiologic mediators in the periodontium, serving in both normal processes and as pathogenic mediators. A therapeutic goal in clinical periodontics can be aimed at maintaining a physiological role for the cytokines while recognizing that their overproduction results in pathologic changes.
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