While biofilm is the clear etiological agent of gingivitis, progression to a chronic periodontal lesion is largely determined by the host response to microbial dysbiosis. Disproportionate or uncontrolled immunologic and inflammatory responses lead to the tissue destruction characteristic of periodontal disease. Recent research has identified both pro-inflammatory and pro-resolving compounds that serve as critical mediators of inflammation. Pro-inflammatory mediators include cytokines, chemokines, and metalloproteinases, which are significantly elevated in periodontitis. Pro-resolving mediators are endogenous lipid compounds that serve to resolve inflammation, promoting monocytic resolution of inflammation and clearance of apoptotic neutrophils by macrophages, as well as anti-microbial defense mechanisms. Pro-resolving lipid mediators primarily consist of resolvins derived from either omega-3 fatty acids or lipoxins from arachidonic acid. Interestingly, arachidonic acid also gives rise to the pro-inflammatory compounds, prostaglandins and leukotrienes. It was thought for many years that inflammation resolution was the result of a passive decay of proinflammatory signals, however, it now appears pro-resolving mediators are important to arrest disease progression and actively reverse periodontal inflammation.
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