Abstract

Dental plaque bacteria along with its products such as lipopolysaccharides (LPS) cause the destruction of the periodontal tissue directly and indirectly by activating the host’s defensive cells of the immune system, which in turn produce and release mediators that stimulate the effects of connective tissue expansion. Microbial plaque components have the capacity to induce initial inflammation and infiltration of inflammatory cells, including lymphocytes, macrophages, and polymorph nuclear leucocytes (PMNl). Microbial components, in particular LPS, activate macrophages to synthesize and secrete various proinflammatory molecules, including cytokines-IL-1 and tumor necrosis factor-alpha (TNF-alpha); prostaglandins, especially prostaglandin E2 (PGE2) and hydrolytic enzymes. The bacteria activate T lymphocytes for the production of IL-1 and lymphotoxin (LT), a molecule with similar properties of TNF-alpha. These cytokines manifest potent proinflammatory and catabolic activities and play a key role in the formation of periodontal pockets through collagenolytic enzymes such as matrix metalloproteinases (MMP). These latent collagenolytic enzymes are activated by reactive oxygen species in the inflammatory environment, leading to increased levels of interstitial collagenase in the inflamed gingiva, which deepens the gingival sulcus, creating a parodontal pocket [1]. A periodontal pocket with a depth of 4 to 12mm is a port of 107 to 109 bacterial cells.