title: Proresolving lipid mediators: potential for prevention and treatment of periodontitis.
abstract: OBJECTIVE
  Periodontitis is an inflammatory disease 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 inflammation have been discovered. Resolution of inflammation is an active, agonist-mediated, programmed return to tissue homeostasis.
  
  
  METHODS
  Various computer-based search engines were employed to identify papers relevant to resolution of inflammation.
  
  
  RESULTS
  Recent data suggest that chronic inflammatory periodontal disease may be a failure of resolution pathways as well as overexpression of proinflammatory pathways. In this review, the biology of resolution of inflammation 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 periodontitis in animals and humans. However, the side effect profile of NSAIDS or other inhibitors or receptor antagonists preclude their use in periodontal therapy.
  
  
  CONCLUSIONS
  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 periodontitis.
authors.affiliation: Department of Periodontology and Oral Biology, Boston University, Boston, MA, USA. tvandyke@forsyth.org
authors.forename: Thomas E
authors.initials: TE
authors.lastname: Van Dyke
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D018441:Biofilms; D018957:CD59 Antigens / Q000627:therapeutic use; D004281:Docosahexaenoic Acids / Q000627:therapeutic use*; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D044045:Lipoxins / Q000627:therapeutic use*; D010518:Periodontitis / Q000382:microbiology / Q000517:prevention & control* / Q000628:therapy
chemical_list: D000893:Anti-Inflammatory Agents; D018957:CD59 Antigens; D018836:Inflammation Mediators; D044045:Lipoxins; D004281:Docosahexaenoic Acids