AIM: Periodontitis is an @entity32 initiated by microbial biofilm. The host response to the biofilm destroys the periodontium mediated by an overly robust inflammatory response in susceptible individuals. Whether the excessive host response is genetic, epigenetic or mediated by environment is unknown. New pathways of resolution of @entity32 have been discovered. Resolution of @entity32 is an active, agonist-mediated, programmed return to tissue homeostasis. MATERIALS AND METHODS: Various computer-based search engines were employed to identify papers relevant to resolution of @entity32 . RESULTS: Recent data suggest that chronic @entity2520 may be a failure of resolution pathways as well as overexpression of proinflammatory pathways. In this review, the biology of resolution of @entity32 will be examined in normal tissues and periodontal disease. Anti-inflammatory pharmacologic agents [non-steroidal anti-inflammatory drugs (NSAIDs)] have been shown to prevent and slow the progression of @entity2521 in animals and @entity1 . However, the side effect profile of NSAIDS or other inhibitors or receptor antagonists preclude their use in periodontal therapy. CONCLUSION: The isolation and characterization of proresolving lipid mediators that are receptor agonists has opened a new area of research for potential therapeutic agents for the management of inflammatory @entity2521 .

Proresolving lipid mediators: potential for prevention and treatment of XXXX .

@entity1 :: ('9606', 'Species') :: ['humans'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation', 'inflammatory disease'] @entity2521 :: ('MESH:D010518', 'Disease') :: ['periodontitis'] @entity2520 :: ('MESH:D010510', 'Disease') :: ['inflammatory periodontal disease']
@entity2521 :: (MESH:D010518,Disease) :: ['periodontitis']
