title: Osteoclast activation in inflammatory periodontal diseases.
abstract: OBJECTIVE
  In this paper, we review the mechanisms thought to be involved in the activation of osteoclasts in periodontitis.
  
  
  CONCLUSIONS
  Osteoclasts are regulated by both microbial and host factors. Some factors act directly on cells of the osteoclast lineage, whereas others act indirectly through other cell types in the bone environment. The proinflammatory cytokines (interleukins 1 and 6, tumor necrosis factors) have been implicated in the stimulation of osteoclastic resorption. The roles of the immunoregulatory cytoknes (interleukins 2 and 4, interferon gamma) are less clear, but decreased levels of these factors may contribute to periodontitis. A number of lipid mediators may be involved in stimulation of bone resorption. These include bacterial lipopolysaccharide and host-derived platelet-activating factor and prostaglandins. More recently, reactive oxygen intermediates and extracellular nucleotides, both present at sites of inflammation, have been investigated as possible modulators of osteoclast activity. The potential use of antiresorptive therapies in periodontitis is reviewed.
  
  
  CONCLUSIONS
  A wide range of host and bacterial factors contribute to the loss of alveolar bone in periodontitis. However, much remains to be understood about the complex mechanisms through which these factors regulate osteoclast activity. Further studies at the cellular and molecular level will lead to a better understanding of these processes and perhaps suggest new approaches for periodontal therapy.
authors.affiliation: Department of Physiology, Faculty of Dentistry, University of Western Ontario, London, Canada.
authors.forename: S H
authors.initials: SH
authors.lastname: Wiebe
authors.forename: M
authors.initials: M
authors.lastname: Hafezi
authors.forename: H S
authors.initials: HS
authors.lastname: Sandhu
authors.forename: S M
authors.initials: SM
authors.lastname: Sims
authors.forename: S J
authors.initials: SJ
authors.lastname: Dixon
mesh_terms: D016301:Alveolar Bone Loss / Q000503:physiopathology*; D000818:Animals; D016207:Cytokines / Q000502:physiology*; D018450:Disease Progression; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology*; D007371:Interferon-gamma / Q000502:physiology; D007378:Interleukins / Q000502:physiology; D008070:Lipopolysaccharides / Q000276:immunology / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism / Q000502:physiology*; D010518:Periodontitis / Q000276:immunology* / Q000378:metabolism / Q000503:physiopathology*; D010972:Platelet Activating Factor / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D007378:Interleukins; D008070:Lipopolysaccharides; D010972:Platelet Activating Factor; D011453:Prostaglandins; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma