Chronic periodontitis is a multi-factorial disease involving anaerobic bacteria and the generation of an inflammatory response, including the production of metalloproteinases, pro-inflammatory cytokines, and eicosanoids. Hypochlorous acid (HOCl) and taurine-N-monochloramine (TauCl) are the end-products of the neutrophilic polymorphonuclear leukocyte (PMN) respiratory burst. They act synergistically to modulate the inflammatory response. In the extracellular environment, HOCl and TauCl may directly neutralize interleukin 6 (IL-6) and several metalloproteinases, while HOCl increases the capacity of alpha(2)-macroglobulin to bind Tumor Necrosis Factor-alpha, IL-2, and IL-6, and facilitates the release of various growth factors. TauCl inhibits the production of inflammatory mediators, prostaglandins, and nitric oxide. HOCl activates tyrosine kinase signaling cascades, generating an increase in the production of extracellular matrix components, growth factors, and inflammatory mediators. Thus, HOCl and TauCl appear to play a crucial role in the periodontal inflammatory process. Taken together, these findings may offer opportunities for the development of novel host-modulating therapies for the treatment of periodontitis.